PERIODONTAL DISEASE A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Periodontal Disease: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84158-6 1. Periodontal Disease-Popular works.I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on periodontal disease. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON PERIODONTAL DISEASE ............................................................................ 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Periodontal Disease..................................................................... 26 E-Journals: PubMed Central ....................................................................................................... 83 The National Library of Medicine: PubMed ................................................................................ 85 CHAPTER 2. NUTRITION AND PERIODONTAL DISEASE ................................................................ 129 Overview.................................................................................................................................... 129 Finding Nutrition Studies on Periodontal Disease.................................................................... 129 Federal Resources on Nutrition ................................................................................................. 133 Additional Web Resources ......................................................................................................... 133 CHAPTER 3. ALTERNATIVE MEDICINE AND PERIODONTAL DISEASE .......................................... 137 Overview.................................................................................................................................... 137 The Combined Health Information Database............................................................................. 137 National Center for Complementary and Alternative Medicine................................................ 138 Additional Web Resources ......................................................................................................... 141 General References ..................................................................................................................... 145 CHAPTER 4. DISSERTATIONS ON PERIODONTAL DISEASE ............................................................ 147 Overview.................................................................................................................................... 147 Dissertations on Periodontal Disease......................................................................................... 147 Keeping Current ........................................................................................................................ 148 CHAPTER 5. CLINICAL TRIALS AND PERIODONTAL DISEASE ...................................................... 149 Overview.................................................................................................................................... 149 Recent Trials on Periodontal Disease......................................................................................... 149 Keeping Current on Clinical Trials ........................................................................................... 152 CHAPTER 6. PATENTS ON PERIODONTAL DISEASE....................................................................... 155 Overview.................................................................................................................................... 155 Patents on Periodontal Disease.................................................................................................. 155 Patent Applications on Periodontal Disease .............................................................................. 170 Keeping Current ........................................................................................................................ 198 CHAPTER 7. BOOKS ON PERIODONTAL DISEASE .......................................................................... 199 Overview.................................................................................................................................... 199 Book Summaries: Federal Agencies............................................................................................ 199 Book Summaries: Online Booksellers......................................................................................... 201 The National Library of Medicine Book Index ........................................................................... 204 Chapters on Periodontal Disease................................................................................................ 206 CHAPTER 8. MULTIMEDIA ON PERIODONTAL DISEASE ............................................................... 215 Overview.................................................................................................................................... 215 Video Recordings ....................................................................................................................... 215 Bibliography: Multimedia on Periodontal Disease .................................................................... 216 CHAPTER 9. PERIODICALS AND NEWS ON PERIODONTAL DISEASE ............................................ 219 Overview.................................................................................................................................... 219 News Services and Press Releases.............................................................................................. 219 Newsletter Articles .................................................................................................................... 224 Academic Periodicals covering Periodontal Disease .................................................................. 225 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 227 Overview.................................................................................................................................... 227 U.S. Pharmacopeia..................................................................................................................... 227 Commercial Databases ............................................................................................................... 228 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 233
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Overview.................................................................................................................................... 233 NIH Guidelines.......................................................................................................................... 233 NIH Databases........................................................................................................................... 235 Other Commercial Databases..................................................................................................... 241 APPENDIX B. PATIENT RESOURCES ............................................................................................... 243 Overview.................................................................................................................................... 243 Patient Guideline Sources.......................................................................................................... 243 Finding Associations.................................................................................................................. 257 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 259 Overview.................................................................................................................................... 259 Preparation................................................................................................................................. 259 Finding a Local Medical Library................................................................................................ 259 Medical Libraries in the U.S. and Canada ................................................................................. 259 ONLINE GLOSSARIES................................................................................................................ 265 Online Dictionary Directories ................................................................................................... 265 PERIODONTAL DISEASE DICTIONARY .............................................................................. 267 INDEX .............................................................................................................................................. 347
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with periodontal disease is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about periodontal disease, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to periodontal disease, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on periodontal disease. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to periodontal disease, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on periodontal disease. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON PERIODONTAL DISEASE Overview In this chapter, we will show you how to locate peer-reviewed references and studies on periodontal disease.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and periodontal disease, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “periodontal disease” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Acupuncture: A Unique Effort to Treat Periodontal Disease: Case Report Source: JADA. Journal of the American Dental Association. 132(12): 1705-1706. December 2001. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. Summary: Acupuncture, a technique for conscious sedation, was introduced as a modality for pain control in 1958 in the United States. Acupuncture has been used to treat illnesses in Asia for more than 3,000 years. This case report describes the use of acupuncture as a treatment for periodontal disease as prescribed and administered by a Korean practitioner. The patient was treated in 1991 by the insertion of multiple
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acupuncture needles in response to a diagnosis of 'gum pain.' Chronic, low grade discomfort, diagnosed as a symptom of the disease, disappeared after the acupuncture treatment. The patient had minimal professional care in this country since the acupuncture therapy. The patient had experienced low grade, but persistent, discomfort over the previous two years. The oral diagnosis is moderate to advanced generalized chronic periodontitis with primary occlusal trauma. The present findings tend to implicate parafunction as the etiology for the current pain and perhaps the etiology for the discomfort experienced by the patient 10 years ago. The patient understood the results of a thorough baseline dental examination, and she elected to undergo traditional therapy for advanced generalized chronic periodontitis, through interpretation and advice from her daughter. 3 figures. 14 references. •
Effect of Alcohol Consumption on Periodontal Disease Source: Journal of Periodontology. 72(2): 183-189. February 2001. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Alcohol consumption, like smoking, may be related to periodontal disease independently of oral hygiene status. This article reports on a study that assessed the relationship between alcohol consumption and severity of periodontal disease. The cross sectional study included 1,371 subjects ages 25 to 74, all from Erie County, New York. Alcohol intake was assessed by means of previously validated self reported questionnaires. Outcome variables were gingival (gum) bleeding, clinical attachment loss (a measure of periodontal disease), alveolar bone loss, and presence of subgingival (below the gum) microorganisms. Analyses adjusting for age, gender, race, education, income, smoking, diabetes mellitus, dental plaque, and presence of any of eight subgingival microorganisms showed that those consuming more than five drinks per week had an odds ratio (OR) of 1.65 of having higher gingival bleeding, and OR of 1.36 of having more severe clinical attachment loss, compared to those consuming less than five drinks per week. Those consuming more than 10 drinks per week had an OR of 1.62 of having higher gingival bleeding and OR of 1.44 of having more severe clinical attachment loss, compared to those consuming less than 10 drinks per week. Alcohol consumption was not significantly related to alveolar bone loss nor to any of the subgingival microorganisms. These results suggest that alcohol consumption is associated with moderately increased severity of periodontal disease. Longitudinal studies are needed to determine whether alcohol is a true risk factor for periodontal disease. 2 figures. 4 tables. 27 references.
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Potential Associations Between Chronic Respiratory Disease and Periodontal Disease: Analysis of National Health and Nutrition Examination Survey III Source: Journal of Periodontology. 72(1): 50-56. January 2001. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Associations between poor oral health and chronic lung disease have recently been reported. This article reports on a study that evaluated these potential associations by analyzing data from the National Health and Nutrition Examination Survey III (NHANES III), which documents the general health and nutritional status of randomly selected United States subjects from 1988 to 1994. This cross sectional, retrospective study of the NHANES III database included a study population of 13,792 subjects older than 20 years of age, with at least 6 natural teeth. A history of bronchitis or emphysema
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was recorded from the medical questionnaire, and a dichotomized variable combined those with either chronic bronchitis or emphysema, together considered as chronic obstructive pulmonary disease (COPD). Subject lung function and oral health status were assessed. Analyses adjusted for age, gender, race and ethnicity, education, income, frequency of dental visits, diabetes mellitus, smoking, and alcohol use. The mean age of all subjects was 44.4 years (plus or minus 17.8 years); the mean age of subjects with COPD was 51.2 years and subjects without COPD was 43.9 years. Subjects with a history of COPD had more periodontal attachment loss (a measure of periodontal disease) than subjects without COPD. A trend was noted in that lung function appeared to diminish with increasing periodontal attachment loss. The authors conclude that these findings support recently published reports that suggest an association between periodontal disease and COPD. 4 tables. 46 references. •
Fighting Gum Disease: How to Keep Your Teeth Source: FDA Consumer. 36(3): 16-22. May-June, 2002. Contact: Available from Food and Drug Administration (HFI-40). 5600 Fishers Lane, Rockville, MD 20857. Website: www.fda.gov/fdac/index/conindex.htm. Summary: Attention to every day oral hygiene (tooth brushing and flossing), coupled with professional cleanings twice a year, could be all that is needed to prevent gum disease, to actually reverse the early stage, and to help one keep teeth for a lifetime. This article familiarizes readers with recent research on gum disease and its prevention. The author first defines gum disease (periodontal disease) and its signs and symptoms. Other topics include diagnosis; treatment options, including curettage, flap surgery, bone grafts, soft tissue grafts, guided tissue regeneration, bone (osseous) surgery, and medications; and the use of antibiotics. A final section addresses the interplay between oral health and overall health. One chart summarizes FDA-approved products available to control infection and reduce inflammation in gum disease. One sidebar addresses other potential factors that contribute to gum disease, including tobacco use, hormonal changes, stress, medications, poor nutrition, illnesses, and clenching or grinding teeth. Three resource organizations are listed for readers who wish to obtain additional information. 5 figures. 1 table.
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Role of Cigarette Smoking in the Association Between Periodontal Disease and Coronary Heart Disease Source: Journal of Periodontology. 73(9): 988-994. September 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Cigarette smoking is a significant risk factor for both coronary heart disease and periodontal disease. This article reports on a study undertaken to better understand the role of smoking in the relationship between periodontal disease and heart attack history. The study population consisted of 5,285 participants in the Third National Health and Nutrition Examination Survey (NHANES) during 1988 to 1994 and who were age 40 years or older when examined. After adjustment for potential confounders, the authors only found significant associations between periodontal loss of attachment (LOA) and heart attack history for smokers. When the analysis was stratified by smoking status and age at heart attack, the statistically significant associations were limited to smokers who had a heart attack between the ages of 25 and 50 years. These results suggest that cigarette smoking is a necessary cofactor in the relationship between periodontal disease and coronary heart disease, and the increase in risk appears to be
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age dependent. However, the key role played by smoking in the etiology of both periodontal and heart diseases makes it difficult to determine how much of the observed association resulted from periodontal disease. 5 tables. 45 references. •
Tooth and Periodontal Disease: A Review for the Primary-Care Physician Source: Southern Medical Journal. 94(9): 925-932. September 2001. Contact: Available from Southern Medical Association. Journal Department, P.O. Box 190088, Birmingham, AL 35219-0088. (800) 423-4992. Fax (205) 945-1548. E-mail:
[email protected]. Website: www.sma.org/smj. Summary: Dental diseases are widespread and are often underrecognized and treated; this article reviews tooth and periodontal disease diagnosis and management for the primary care physician. Caries (cavities) and periodontal disease are common dental conditions that cause the majority of tooth loss. Although these conditions are preventable, many persons do not receive regular dental care and have acute problems when they are seen by their physician. Dental diseases frequently affect patients with multiple systemic disorders, including autoimmune disorders, diabetes, and human immunodeficiency virus (HIV) infection. The presence of dental disease may trigger inflammatory responses and have systemic consequences. Since dental disease affects almost all individuals, physicians should be able to recognize common conditions such as caries, periodontal disease, pulpitis, and dental abscess. In addition to initiating treatment and appropriate dental referrals, physicians should be familiar with the management of antibiotics and medications in the perioperative period. Another important role for physicians is to help reduce the societal and economic impact of these diseases through patient education and prevention. 4 figures. 1 table. 69 references.
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Protecting the Next Generation: The Dental Hygienist's Role in Managing Periodontal Disease as a Risk Factor for Low-Birth-Weight Babies Source: Dentistry Today. 21(5): 46-49. May 2002. Contact: Available from Dentistry Today Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: Dental researchers are finding greater amounts of evidence to support the theory of periodontal disease as a risk factor for systemic health problems, including poor pregnancy outcomes. This article reminds dental hygienists of their role in managing periodontal disease as a risk factor for low birth weight (LBW) babies. Topics include the concept of periodontal disease as an infectious disease process, the hygienist's role, and patient education. Hygienists can have an impact on two fronts: first, being very thorough and delivering outstanding customer service within their practices; second, helping to spread the word in their communities. The author concludes by reminding readers of the importance of educating themselves about changes in their field, and translating that new knowledge into patient education and health promotion. 11 references.
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Treatment of Periodontal Disease in a Patient with Ehlers-Danlos Syndrome: A Case Report and Literature Review Source: Journal of Periodontology. 73(5): 564-570. May 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225.
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Summary: Ehlers-Danlos syndrome (EDS) is the term used for a heterogeneous group of connective tissue disorders characterized by skin elasticity, tissue fragility, and chronic joint pain. Dental findings have been reported with some types of EDS. This case report describes the periodontal findings in a 48 year old Caucasian female patient with a previously undiagnosed EDS type VIII. Diagnostic aids utilized included microbial testing, histological examination, gingival crevicular fluid (GCF) analysis, and genetic counseling. Periodontal treatment consisted of mechanical debridement and adjunctive antibiotic therapy. Genetic counseling and clinical presentation confirmed the diagnosis of EDS type VIII. Periodontal treatment led to marked clinical improvements and GCF levels of the bone resorptive marker were significantly reduced. The patient and her siblings are currently pursuing appropriate medical care and genetic counseling. The authors conclude that periodontal involvement may lead to the diagnosis of an underlying systemic condition. Identification of suspected etiological factors of periodontal disease may prove critical for the general well-being of some patients. 6 figures. 48 references. •
Natural History of Periodontal Disease in Man. Risk Factors for Progression of Attachment Loss in Individuals Receiving No Oral Health Care Source: Journal of Periodontology. 72(8): 1006-1015. August 2001. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Few investigations have reported on the risk factors for periodontal attachment loss (PAL, a measurement of periodontal, or gum, health) over time in subjects with no home or professional dental care. This article identifies these potential risk factors for progression of periodontal attachment loss among male Sri Lankan tea laborers who participated in a 20 year investigation of the natural history of periodontal disease. Data were obtained from the 154 subjects who participated in the 1970 baseline and the final 1990 examinations and included data from their interim examinations, performed in 1971, 1973, 1977, 1982, and 1985. Oral health assessments included: attachment levels of all but third molar teeth; plaque index; gingival (gum) index; calculus index; caries (cavities) index, which was the DMFS or decayed, missing, or filled surfaces; and presence or absence of teeth. Other variables include age, history of smoking, and use of betel nut. The final adjusted model indicated that attachment loss increased significantly with age, gingival inflammation, calculus, and follow up time. Neither plaque index, history of smoking, or history of betel nut use were significantly associated with attachment loss over time. The authors caution that the study parameters, as designed more than 30 years ago, may have a significant impact on the findings. 3 figures. 3 tables. 57 references.
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Relationship of Oral Malodor in Patients With or Without Periodontal Disease Source: Journal of Periodontology. 73(11): 1338-1342. November 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Halitosis (bad breath) has been correlated with the concentration of volatile sulfur compounds (VSC) produced in the oral cavity by metabolic activity of bacteria colonizing the periodontal area and the dorsum of the tongue. This article reports on a study that investigated whether there is some relationship between the presence of BANA-positive species of bacteria Treponema denticola, Porphyromonas gingivalis, and Bacteroides forsythus and clinical and oral malodor parameters. The study included
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21 subjects (21 to 59 years old) with probing depths greater than 3.0 millimeters and 20 subjects (21 to 63 years old) with probing depths less than 3.0 millimeters. The quality of mouth air was assessed and a portable sulfide monitor was used to measure the concentration of VSC. The scores of the plaque index, gingival index, subgingival samples that tested positive for BANA hydrolyzing species, organoleptic ratings, and VSC values were significantly higher in the subjects with PD greater than 3.0 millimeters. The authors conclude that these results confirm that the BANA hydrolyzing bacteria in the subgingival plaque are an important source of malodor production in the oral cavity. 3 tables. 36 references. •
Nonsurgical Treatment of Patients with Periodontal Disease: Results After Five Years Source: JADA. Journal of the American Dental Association. 133(3): 311-320. March 2002. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2867. Website: www.ada.org. Summary: In a previous study involving patients seen at the dental clinic of the Detroit Receiving Hospital, the authors found that 87 percent of teeth initially recommended for surgery or extraction were spared those treatments by a combination of debridement and short term usage of antimicrobial agents. This article reports on a study undertaken to determine how long the surgery sparing benefits of less invasive treatment would persist. Ninety of the original patients were scheduled for maintenance therapy at three month intervals over a five year period. They were evaluated periodically for surgical needs by a clinician who was not aware of the nonsurgical periodontal treatment the patient had received. Results showed that the initial treatment benefits were sustained, as the number of teeth needing periodontal surgery or extraction was 0.06 teeth per patient after 1.1 year, 0.22 after 2.3 years, 0.51 after 3.6 years, and 0.86 after 5.1 years. The authors conclude that the noninvasive treatment regimen for an anaerobic infection in teeth seriously compromised by periodontal disease resulted in a reduced need for surgery or tooth extraction for at least five years after completion of the initial treatment. 4 tables. 29 references.
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Periodontal Disease and Cardiovascular Disease: Epidemiology and Possible Mechanisms Source: JADA. Journal of the American Dental Association. 133 (Supplement 6): 14S-22S. June 2002. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2867. Website: www.ada.org. Summary: Many early epidemiological studies reported an association between periodontal disease and cardiovascular disease. However, other studies found no association or nonsignificant trends. This article summarizes the evidence from epidemiological studies and studies that focused on potential contributing mechanisms to provide a more complete picture of the association between periodontal and heart disease. The authors summarize the longitudinal studies reported to date, because these studies represent the highest level of evidence available regarding the connection between periodontal disease and heart disease. The authors also review many of the case control and cross-sectional studies published, as well as findings from clinical, animal and basic laboratory studies. The evidence suggests a moderate association (not a causal relationship) between periodontal disease and heart disease. Results of some case-control studies indicate that subgingival periodontal pathogenic infection may be associated with myocardial infarction (heart attack). Basic laboratory studies point to the
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biological plausibility of this association, since oral bacteria have been found in carotid atheromas and some oral bacteria may be associated with platelet aggregation, an event important for thrombosis (clotting). Animal studies have shown that atheromas formation can be enhanced by exposure to periodontal pathogens. 1 figure. 2 tables. 50 references. •
Periodontal Disease and Diabetes Mellitus: The Role of Tumor Necrosis Factor-alpha in a 2-Way Relationship Source: Journal of Periodontology. 74(1): 97-102. January 2003. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Obesity is associated with many other multiple-risk factor syndromes such as hypertension (high blood pressure), hyperlipidemia (high levels of blood fats), type 2 diabetes mellitus, and periodontal disease. This article explores the role of tumor necrosis factor (TNF) alpha in the two conditions of periodontal disease and diabetes mellitus. The authors hypothesize that TNF-alpha produced by the adipose tissues of obese patients acts as a risk factor for periodontal inflammation; and TNF-alpha produced due to periodontal inflammation may be an important factor influencing insulin sensitivity in both obese and type 2 diabetes patients. The authors believe this interaction is a possible mechanism accounting for the two-way relationship between type 2 diabetes and periodontal disease. 3 figures. 3 tables. 26 references.
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Periodontal Disease Predicts and Possibly Contributes to Acute Myocardial Infarction Source: Dentistry Today. 20(4): 80-81. April 2001. Contact: Available from Dentistry Today Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: Patients experiencing an acute myocardial infarction (AMI, heart attack) are more likely to have periodontal disease than those free of coronary artery disease (CAD), according to a report read before the last annual session of the American Heart Association (AHA) in New Orleans (November 2000). This article summarizes that report, outlining the implications for dentists and periodontists. The researchers reported links between the presence of gum disease and coronary thrombosis, noting an amplification of the inflammation of the gums was correlated with the heart condition. The enhanced inflammatory response (as demonstrated by high C reactive protein, or CRP, levels in human blood serum) is predictive of recurrent events in both conditions. Therefore, there is reason to suspect a higher occurrence of CAD among people with periodontal disease compared with those free from periodontal disease. The author notes that treatment of periodontal disease may become a novel strategy for secondary prevention among patients with coronary artery disease or those surviving an AMI. The author also briefly reports on animal studies that support or explore the relationship between infection or inflammation and CAD.
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Relationship Between Diabetes and Periodontal Disease Source: Practical Diabetology. 16(3): 6-8, 10. September 1997. Summary: Patients with unsuspected, uncontrolled, or poorly controlled diabetes may present with a variety of symptoms and signs that involve the oral cavity. This article reviews the relationship between diabetes and periodontal disease. The authors focus on the signs and symptoms a physician should look for when performing a visual
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examination of the soft tissues in and around the mouth. Periodontal disease is a term that is used to describe a group of diseases that cause inflammation and destruction of the supporting tissues of the teeth, including the gigiva and alveolar bone. When performing a visual examination of the oral soft tissues of a patient with diabetes, physicians should look for certain signs and symptoms, including gingival inflammation, gingival bleeding, plaque, recession of the gingival margin, abscesses, and malodor. The authors conclude that patients with diabetes who are receiving periodontal treatment need to be under the care of both a physician and a periodontist, and both professionals need to work together to avoid any complications during or following treatment. Treatment of periodontal disease has the potential to reduce insulin requirements and improve glucose control. 9 figures. 1 table. 9 references. (AA-M). •
Maternal Periodontal Disease and Preterm Low Birthweight: Case-Control Study Source: Journal of Dental Research. 81(5): 313-318. May 2002. Contact: Available from International Association for Dental Research. Subscription Department, 1619 Duke Street, Alexandria, VA 22314. (703) 548-0066. Fax (703) 548-1883. Summary: Periodontal disease has been suggested to be an important risk factor for preterm low birthweight (PLBW) babies. This article reports on a case-control study of 236 cases (infants less than 37 weeks gestation and weighting less than 2499 grams) and a daily random sample of 507 controls (infants equal or greater than 38 weeks gestation and weighing equal or greater than 2500 grams). Clinical periodontal indices were measured on the labor wards. Associated risk factors for periodontal disease and PLBW were ascertained by means of a structured questionnaire and maternity notes. The risk for PLBW decreased with increasing pocket depth. After adjustment for maternal age, ethnicity, maternal education, smoking, alcohol consumption, infections, and hypertension (high blood pressure) during pregnancy, this decreased further. The authors found no evidence for an association between PLBW and periodontal disease. The authors conclude that their results do not support a specific drive to improve periodontal health of pregnant women as a means of improving pregnancy outcomes. 1 figure. 3 tables. 30 references.
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Advances in Dentistry: Using Host Response Modifiers in the Treatment of Periodontal Disease Source: Journal of Practical Hygiene. 11(6): 12 (1-15). November-December 2002. Contact: Available from Montage Media Corporation. 1000 Wyckoff Avenue, Mahwah, NJ 07430-3164. (201) 891-3200. Summary: Periodontal disease is the result of a complex interaction between microbial plaque, the host's inflammatory response to the plaque, and host modifying factors (e.g., smoking, diabetes, genetics) that may have an impact on the disease process. It is known that dental plaque initiates periodontal disease but that the host response is responsible for the destruction of periodontal tissues. This article describes why host response modifiers may be used to help control inflammation and tissue destruction as part of the initial phase of periodontal therapy in selected patient groups. Appended to the article is a posttest for continuing education units and a section of comments from clinicians in this field. 8 figures. 30 references.
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Periodontal Disease and Diabetes Mellitus: Bidirectional Relationship Source: Dentistry Today. 22(4): 107-113. April 2003.
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Contact: Available from Dentistry Today Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: Periodontal diseases are bacterial infections and can result in the destruction of tissues supporting the teeth. Diabetes mellitus results from an impaired ability to adequately utilize glucose and to regulate blood sugar levels. While these are considered separate medical conditions, they may mutually aggravate one another by means of biochemical mechanisms at the cellular and molecular levels. This article explores this bidirectional relationship between diabetes and periodontal diseases. The authors review the research evidence to support this relationship, and outline treatment options and strategies. The authors note that both diabetes and periodontitis can stimulate the chronic release of proinflammatory cytokines that have a deleterious effect on periodontal tissues. The chronic systemic elevation of proinflammatory cytokines caused by periodontitis may even predispose individuals to the development of type 2 diabetes. Periodontal procedures (such as mechanical scaling and root planing) designed to rid patients of periodontal pathogens also improve the management of diabetes. 4 figures. 1 table. 26 references. •
Exploring Interrelationships Between Diabetes and Periodontal Disease in African Americans Source: Compendium of Continuing Education in Dentistry. 22(3): 42-48. July 2001. Contact: Available from Dental Learning Systems. 241 Forsgate Drive, Jamesburg, NJ 08831. (800) 926-7636. Summary: Population based data on interrelationships between diabetes mellitus and periodontal diseases among African Americans are limited. This article offers an overview of the knowledge regarding the bidirectional relationship between diabetes and periodontal diseases and a descriptive analysis of data from the Third National Health and Nutrition Examination Survey (NHANES III). The author focuses on the diabetes-periodontal diseases interrelationship in African Americans. Results of the analysis are consistent with the current body of evidence supporting a bidirectional relationship between diabetes and periodontal diseases and indicate generally poorer periodontal health and glycemic control among African Americans. The results also indicate significantly lower dental care use in dentate (with teeth) African Americans with diabetes than in the U.S. non Hispanic white population with diabetes. The author concludes with a call for additional research and increased emphasis on targeting oral health promotion and advocacy efforts to increase access to and use of oral health care services among African Americans with diabetes as well as all dentate individuals with diabetes. 39 references.
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Association Between Hypercholesterolemia, Cardiovascular Disease and Severe Periodontal Disease Source: Journal of Clinical Periodontology. 28(9): 865-868. September 2001. Contact: Available from Munksgaard International Publishers Ltd. Commerce Place, 350 Main Street, Malden, MA 02148-5018. (781) 388-8273. Fax (781) 388-8274. Summary: Premature death in men is known to be significantly associated with coronary heart disease (CHD). More and more studies are pointing toward a possible association between periodontal disease and increased risk of cardiovascular disease. The association of poor oral hygiene and atherosclerosis (hardening of the arteries) can be explained by the effect of chronic inflammatory disease on blood rheology (altered
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flow and contents). This article reports on a study undertaken to assess the relationship between CHD and periodontal disease. The study population included 1094 Israeli army service men aged 26 to 53 years (mean 39 years plus or minus 5 years). The study group comprised 151 subjects classified as having CHD, i.e., myocardial infarction and or anginal syndrome with angiographic evidence of significant coronary disease, or suffer from atherosclerotic risk factors, i.e., diabetes (fasting glucose) and hypertension (high blood pressure) according to strict, well established criteria. Blood levels of cholesterol and triglycerides were also determined. The severity of periodontal disease was assessed by the aid of CPITN (community periodontal index of treatment need). Statistical analysis showed a significant association of CPITN score 4 with hypercholesterolemia (high levels of cholesterol in the blood) and a possible association with CHD. The authors conclude by proposing the generation of higher cholesterol blood levels as a possible link between chronic periodontal inflammation and atherosclerosis. 3 tables. 28 references. •
Periodontal Therapy May Reduce the Risk of Preterm Low Birth Weight in Women With Periodontal Disease: A Randomized Controlled Trial Source: Journal of Periodontology. 73(8): 911-924. August 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Recent studies have suggested that periodontal disease is a risk factor for preterm low birth weight (PLBW) babies. This article reports on a randomized controlled trial that was undertaken to help further evaluate the proposed association between periodontal disease and PLBW. The study included 400 pregnant women with periodontal disease, aged 18 to 35, who were enrolled while receiving prenatal care in Santiago, Chile. Women were randomly assigned to either an experimental group (n = 200) which received periodontal treatment before 28 weeks of gestation or to a control group (n = 200) which received periodontal treatment after delivery. Previous and current pregnancies and known risk factors were obtained from patient medical records and interviews. Of the 400 women enrolled, 49 were excluded from the analyses for different reasons. The incidence of PLBW in the treatment group was 1.84 percent (3 of 163 patients) and in the control group was 10.11 percent (19 of 188 patients), a statistically significant difference. Analyses showed that periodontal disease was the strongest factor related to PLBW. Other factors significantly associated with such deliveries were: previous PLBW, less than 6 prenatal visits, and maternal low weight gain. 2 figures. 9 tables. 58 references.
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Periodontal disease, Race, and Vascular Disease Source: Compendium of Continuing Education in Dentistry. 22(3): 34-41. July 2001. Contact: Available from Dental Learning Systems. 241 Forsgate Drive, Jamesburg, NJ 08831. (800) 926-7636. Summary: Recently, a number of studies have rekindled the possible hypothesis that oral health has repercussions beyond the oral cavity and is associated with systemic diseases. This represents a return to an old theory that chronic infections and inflammation played a crucial role in atherosclerosis (a cardiovascular disease, 'hardening of the arteries'). This larger theory was advocated by French physicians, among others, at the beginning of the 20th century. In this article, the author reviews the epidemiologic evidence pointing to a possible association between oral health and vascular diseases; the author also examines the role of race and ethnicity in the
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interpretation of this association. The author notes that, in summary, studies that have looked at stroke and coronary heart disease (CHD) together as outcomes have generally found a stronger association between periodontal diseases and stroke than with CHD. This association has been found in different populations. The authors conclude with a brief description of the Oral Infections and Vascular Disease Epidemiology Study (INVEST) which has been founded by the NIDCR (National Institute of Dental and Craniofacial Research) to investigate oral infections as risk factors for ischemic stroke and carotid atherosclerosis. Results from this study and others should significantly clarify the question of the potential contribution of oral infections to the incidence of atherosclerosis and vascular events, as well as explore racial differences in infectious load and inflammatory response. 71 references. •
Managing Risk Factors in Successful Nonsurgical Treatment of Periodontal Disease Source: Dentistry Today. 22(1): 64,66-69. January 2003. Contact: Available from Dentistry Today Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: Risk factors suggest that there is an increased chance for patients to develop periodontitis, yet the recognition of these risks and selective management of them can probably reduce the long term chances of developing periodontal disease. This article discusses how, with the advances in understanding the causes of periodontal disease, the opportunity to use combined therapies, systemic drugs to modify the hostdestructive pathway, plus locally delivered antimicrobial drugs, better oral hygiene products (such as power brushes) and the inclusion of risk-reduction treatment for the identified risk factors, dentists finally have the opportunity to predictably and successfully manage this chronic disease. The author discusses systemic risk factors, including smoking, diabetes mellitus, and osteoporosis or osteopenia (associated with estrogen deficiency). The author also considers the interrelationship of heart disease and stroke with periodontal diseases. 3 figures. 29 references.
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Prevalence and Severity of Periodontal Disease at Mandibular Molar Teeth in Smokers with Regular Oral Hygiene Habits Source: Journal of Periodontology. 73(7): 735-740. July 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Smoking appears to be detrimental to health because it has been associated with several diseases including cancer and cardiovascular diseases. Smoking also appears to be a major environmental factor associated with periodontal disease progression. This article reports on a study undertaken to evaluate the prevalence and severity of periodontal destruction as influenced by smoking in a Thai population. Gingival (gum) health and periodontal conditions at mandibular (lower jaw) molar furcation (division of the tooth root) sites in 120 Thai dental patients (60 smokers and 60 never smokers, age range 31 to 60 years) with generally high oral hygiene standards and regular dental care habits were evaluated. Smokers exhibited more frequent and severe mandibular molar periodontal destruction than never-smokers. The prevalence and severity of gingival recession, periodontal pocket formation, clinical attachment loss, furcation involvement, and tooth mobility were significantly increased in smokers compared to never-smokers. Seventy-three percent of the smokers exhibited furcation involvement in contrast to only 20 percent of the never-smokers. The authors conclude that smoking appears to be a major environmental factors associated with accelerated
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periodontal destruction in adult smokers with generally high oral hygiene standards and regular dental care habits in a Thai population. 6 tables. 43 references. •
Periodontal Diseases are Curable. (editorial) Source: Journal of Periodontology. 73(8): 950-953. August 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Some therapists believe that periodontal diseases are chronic diseases and are not curable, rather they are maintainable illnesses. However, this line of reasoning fails to recognize that most patients with periodontal diseases attain periodontal health after therapy at the vast majority of sites. Periodontal therapy usually eliminates the signs and symptoms, and either suppresses or eliminates the microflora associated with periodontal diseases. The need for maintenance post-treatment is an important aspect of optimizing long-term success, but recognition of this fact does not justify characterizing periodontal diseases as incurable. This editorial raises issues to support the idea that periodontal diseases should be considered curable, despite the recommendation that maintenance procedures ought to be continued after active therapy. 42 references.
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Periodontal Disease in Pregnancy Complicated by Type 1 Diabetes Mellitus Source: Journal of Periodontology. 72(11): 1485-1490. November 2001. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Systemic disease and hormonal changes have been implicated as complicating factors for periodontal disease. Diabetes has been identified as a risk factor for periodontal disease, and people with diabetes can experience periodontal destruction at an earlier age than nondiabetic individuals. Increased hormone levels during pregnancy can contribute to increased gingival inflammation. This article reports on a study undertaken to examine the association of type 1 diabetes mellitus (DM) on the periodontal status of pregnant women. The study included 33 subjects (13 with diabetes, 20 without), at 20 to 39 weeks gestation. The mean age of the subjects with diabetes was 28.5 years (plus or minus 7.1 years) and of the nondiabetics 27.0 years (plus or minus 7.3 years). The authors assessed plaque index (PI), gingival (gum) inflammation (GI), probing depth (PD), gingival margin (GM) location, and clinical attachment level (CAL). Subjects with diabetes had significantly higher PI and GI scores than nondiabetics. Mean PD for diabetics was significantly different from that of nondiabetics. Although mean GM location was coronal to the cemento-enamel junction (CEJ) in both groups, gingival margins were at a more apical position in the subjects with diabetes. Mean CAL values also varied significantly between people with diabetes and nondiabetics. Significant differences were seen for GI, GM location, and CAL when assessing the effect of diabetes and controlling for plaque. When assessing the effect of plaque and controlling for diabetes, the only significant difference was GI. The authors conclude that their results demonstrate that periodontal inflammation and destruction are increased in pregnant women with diabetes as compared to pregnant women who do not have the disease. These findings may have implications for diabetes control and, therefore, maternal and fetal outcomes. 3 tables. 34 references.
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Investigation of the Association Between Angiographically Defined Coronary Artery Disease and Periodontal Disease Source: Journal of Periodontology. 73(10): 1169-1176. October 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: The association between periodontal disease and coronary artery disease (CAD) has been investigated in numerous studies with inconsistent results. Resolving these differences is complicated by the use of varying definitions of CAD. This article reports on a study undertaken to investigate the association between angiographicallydefined CAD and periodontal disease. Non-smoking, non-diabetic patients over 40 years of age, with no history of a myocardial infarction (heart attack) in the previous 6 months and who had undergone cardiac catheterization within the previous 12 months were enrolled in the study. Patients were classified as CAD positive or CAD negative, depending on the stenosis (narrowing) of their epicardial arteries. The study included 100 patients (53 CAD positive; 47 CAD negative). CAD positive patients were more likely to be male and were older. Although all patients reported they were currently nonsmokers and had not smoked for at least 5 years, the fraction who were former smokers was greater for CAD positive patients and mean pack per year history of smoking was higher for CAD positive patients. After adjustment for age and previous smoking history, factors common to both diseases, the associations of CAD and periodontal disease were reduced and were not statistically significant. The authors conclude that further investigations into the relationship between periodontal disease and CAD should clearly separate chronic CAD and acute coronary events. 5 tables. 39 references.
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Periodontal Disease and Diabetes Source: Clinical Diabetes. 7(5): 1, 80-84. September-October 1989. Summary: The impact of periodontal disease on the diabetic patient and the special considerations when planning treatment are addressed. The types of periodontal disease and age groups primarily affected by each type are discussed along with evidence implicating bacterial activity as the primary cause of both gingivitis and various forms of periodontitis. Oral lesions can be a sign of diabetes; and studies are showing increased periodontal disease in people with diabetes. Other features of diabetes that predispose patients to periodontal disease include a decrease in the ability of white blood cells to destroy harmful bacteria, gingival vascular changes, and altered collagen metabolism. A table is provided which lists eight warning signs of periodontal disease. Dental treatments for diabetic patients are reviewed, including antibiotic treatment, root planing, scaling, and periodontal surgical procedures. Recommendations for proper follow-up treatment are presented. A list of suggested readings is included. 3 tables. 6 figures.
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Longitudinal Comparison of the Periodontal Status of Patients with Moderate to Severe Periodontal Disease Receiving No Treatment, Non-Surgical Treatment, and Surgical Treatment Utilizing Individual Source: Journal of Periodontology. 72(11): 1509-1519. November 2001. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225.
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Summary: The progression of periodontal disease without treatment and the response of existing periodontal disease to various types of treatment have been studied extensively. Many past studies have used the mean of the patient's probing depths or attachment levels to evaluate disease progression as opposed to following changes in patients' sites or teeth. This article reports on a study that evaluated the response of individual teeth to treatment or nontreatment. The records from a private periodontal practice were reviewed to find patients with complete periodontal examinations that were recorded at least 1 year apart. Patients who fit these criteria were divided into those who had none of the recommended treatment (untreated, n = 30); those who had only nonsurgical treatment (partially treated, n = 20); and a control group who had completed all recommended treatment (surgically treated, n = 41). The data for each tooth of each patient were placed in a database and analyzed. Teeth that received no treatment or nonsurgical treatment showed significant increases in probing depths, worsening of prognosis, worsening of furcation (where the tooth root divides) involvement, and increases in mobility when compared to surgically treated teeth. Teeth that received surgical treatment showed significant decreases in probing depths. No significant difference was noted between teeth that had no treatment and teeth that had nonsurgical treatment. The authors conclude that when individual teeth are used as the basis for analysis, teeth that receive no treatment or nonsurgical treatment show a significant worsening of probing depths, furcations, mobility, and prognosis when compared to teeth that receive surgical treatment, while surgically treated teeth show significant improvement in probing depths. 4 figures. 7 tables. 44 references. •
Diabetes: A Risk Factor for Periodontal Diseases Source: Journal of Practical Hygiene. 10(6): 11-16. November-December 2001. Contact: Available from Montage Media Corporation. 1000 Wyckoff Avenue, Mahwah, NJ 07430-3164. (201) 891-3200. Summary: The relationship between diabetes mellitus (DM) and periodontitis has been the subject of professional articles and clinical trials for many years. Early studies found a high prevalence of periodontal destruction in patients with severe diabetes, less severe periodontal problems in people with diabetes who keep their disease in good control, and a good response to periodontal therapy in young people with diabetes in good control. Today, the body of evidence regarding the relationship between periodontal diseases and DM is extensive. This article focuses on the current research relating to oral manifestations, the effect of DM on clinical parameters, and the patient's response to therapy. The author concludes that the patient with well controlled diabetes can be a candidate for complete periodontal therapy or prevention. The altered host response, however, helps explain the severity of periodontal conditions, especially in uncontrolled or poorly controlled DM patients. Patient education is imperative as many people with diabetes are not aware of the oral health complications of their disease. Dental hygienists have a unique opportunity to educate and promote good oral hygiene as a vital component of overall health. Appended to the article is a posttest with which dental hygienists can earn continuing education credit. 3 figures. 49 references.
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Type 1 Diabetes Mellitus and Oral Health: Assessment of Periodontal Disease Source: Journal of Periodontology. 70(4): 409-417. April 1999. Contact: Available from Journal of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225.
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Summary: This article describes a study that examined the periodontal status of a large population of adults with type 1 diabetes and evaluated the multiple demographic, behavioral, and medical factors that may be associated with extensive periodontal disease. During one of their regularly schedules medical examinations, a group of 320 adult dentate subjects received a periodontal examination as part of a comprehensive oral health assessment. The oral health assessment collected data regarding demographics, oral health behaviors, tooth loss, coronal and root caries, salivary functions, and soft tissue pathologies. For the periodontal assessments, three facial sites of the teeth in the right maxillary/left mandibular or left maxillary/right mandibular quadrants were evaluated for calculus, bleeding on probing (BOP), and loss of gingival attachment (LOA). The study found that attachment loss was significantly greater for older patients whereas BOP and calculus levels were relatively constant across age categories. Univariate analyses of factors possibly related to extensive periodontal disease indicate an association with older age, lower income and education, past and current cigarette smoking, infrequent visits to the dentist, tooth brushing less than once per day, older age of onset, longer duration of diabetes, and the diabetic complication of neuropathy. A multivariate regression model of all possibly significant factors found current cigarette use, type 1 diabetes onset after 8.4 years of age, and age greater than 32 years explained the majority of the extensive periodontal disease in this group of patients. The article concludes that the management and prevention of extensive periodontal disease for people with type 1 diabetes should include strong recommendations to discontinue cigarette smoking. 1 figure. 4 tables. 35 references. (AA-M). •
Periodontal Disease and Diabetes: Interdependent Conditions Source: Practical Diabetology. 19(4): 19, 22, 24-27. December 2000. Contact: Available from R.A. Rapaport Publishing, Inc. 150 West 22nd Street, New York, NY 10011. (800) 234-0923. Summary: This article discusses the association between diabetes and periodontal disease. Periodontitis is an inflammation of the supporting structures of the teeth. Periodontal disease is the result of a complex interaction between pathogenic microorganisms, host response mechanisms, and environmental factors. Approximately 15 bacterial species have been implicated in periodontal pathogenesis. Viruses may also have a role in the development of periodontal disease. The immune response of the host to these pathogens is an important determinant in the course of disease. Polymorphonuclear leukocyte function is also important in the pathogenesis of periodontal disease. Environmental factors, particularly smoking, influence susceptibility to periodontal disease. Diabetes and periodontal disease have a two way relationship. The person who has diabetes and active periodontal disease has been shown to have decreased glycemic control, with treatment of the periodontal disease improving glycemic control. Mechanisms linking diabetes and periodontal disease include advanced glycation endproduct related processes. Detection of periodontal disease involves asking patients with diabetes about their oral health and assessing their oral status through a thorough oral examination. The health professional should look for signs and symptoms that may indicate the presence of periodontitis. A positive intra oral finding or a positive response to questions about oral health indicate that the patient either has periodontal disease or is at risk for developing periodontal disease. Although several nonperiodontal oral conditions have been linked to diabetes, they are not as strongly linked to diabetes as periodontal disease. The article presents
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recommendations on when to refer patients for further care and offers considerations for dental care. 9 figures. 25 references. •
Diabetes Mellitus and Periodontal Disease: A Current Perspective Source: Compendium of Continuing Education in Dentistry. 15(2): 1018-1032. August 1994. Contact: Available from Dental Learning Systems Co., Inc. 9 Pheasant Run, Newtown, PA 18940-1818. (215) 860-9595. Summary: This article examines the relationship between diabetes mellitus and periodontal disease. The author reviews epidemiologic studies and possible physiologic mechanisms to clarify the possible role of diabetes as a risk factor for periodontitis. Although trends indicate that periodontal disease is more prevalent and severe among people with diabetes, multiple factors, including type, duration, and control, must be considered. Unfortunately, as the author points out, most studies neither differentiate between insulin-dependent diabetes (IDDM, or Type I) and noninsulin-dependent diabetes (NIDDM, or Type II) nor provide adequate statistical sampling methods and control groups. Other problems include a failure to assess age relationships in periodontal disease and the age of diabetes onset. Topics following discussion of various clinical studies include pathophysiology (vascular changes, impaired host response, oral microflora, and collagen metabolism) and treatment studies. The author notes that a dentist can play an important role in the individual's overall health care by recognizing and treating his or her periodontal needs. Appropriate management of the person's care requires an understanding of his or her metabolic control and potential and limitations for response to treatment with current periodontal therapy. 7 figures. 1 table. 70 references. (AA-M).
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Dental Plaque Attack: The Connection Between Periodontal Disease, Heart Disease, and Diabetes Mellitus Source: Compendium of Continuing Education in Dentistry. 22(1): 13-21. 2001. Contact: Available from Dental Learning Systems. 241 Forsgate Drive, Jamesburg, NJ 08831. (800) 926-7636. Summary: This article explores the connection between periodontal disease, heart disease, and diabetes mellitus. Identification of dental plaque as a bacterial biofilm has improved considerably the understanding of oral infections. The most significant consequence of biofilm formation on the tooth surface is the continuous release of bacteria cell surface components into the oral cavity and gingival sulcus. As such, subgingival biofilms constitute a significant continuous bacterial load on the host. These biofilms are self renewing reservoirs of endotoxin (lipopolysaccharide) and other bacterial toxins that can gain access not only into the surrounding periodontal tissues, but the general circulation as well. Chronic systemic challenge with subgingival biofilms induces upregulation of endothelial cell adhesion molecules, secretion of interleukin 1, and tumor necrosis factor (TNF) alpha, thromboxane, increased platelet aggregation, formation of lipid laden foam cells, and deposits of cholesterol. Dental plaque attack, the systemic seeding of oral infection, represents a significant factor complicating systemic conditions such as heart disease and diabetes mellitus. The author discusses the implications for specific treatment of peridontal infections as they apply to patients at high risk for systemic disease. The author outlines a comprehensive prevention strategy should be used in patients positive for a given risk factor but who have not yet exhibited clinical manifestations of subgingival (under the gums) infection. Treatment of
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periodontal infection is a first priority in achieving oral health and in promoting good general health. 7 figures. 2 tables. 33 references. •
Initial Outcome and Long-Term Effect of Surgical and Non-Surgical Treatment of Advanced Periodontal Disease Source: Journal of Clinical Periodontology. 28(9): 910-916. September 2001. Contact: Available from Munksgaard International Publishers Ltd. Commerce Place, 350 Main Street, Malden, MA 02148-5018. (781) 388-8273. Fax (781) 388-8274. Summary: This article reports on a clinical trial that was performed to determine the initial outcome of nonsurgical and surgical access treatment in subjects with advanced periodontal disease and the incidence of recurrent disease during 12 years of maintenance following active therapy. Each of the 64 subjects included in the trial showed signs of generalized gingival (gum) inflammation, had a minimum of 12 non molar teeth with deep pockets, and with greater than 6 millimeters alveolar bone loss. They were randomly assigned to 2 treatment groups; one surgical (SU) and one non surgical (SRP). Following a baseline examination, all patients were given a detailed case presentation which included oral hygiene instruction. The subjects in SU received surgical access therapy, while in SRP nonsurgical treatment was provided. After this basic therapy, all subjects were enrolled in a maintenance care program and were provided with meticulous supportive periodontal therapy (SPT) three to four times per year. The authors observe that surgical therapy (SU) was more effective than nonsurgical scaling and root planing (SRP) in reducing the overall mean probing pocket depth and in eliminating deep pockets; more SRP treated subjects exhibited signs of advanced disease progression in the 1 to 3 year period following active therapy than SU treated subjects. The authors stress that in subjects with advanced periodontal disease, surgical therapy provides better short and long term periodontal pocket reduction and may lead to fewer subjects requiring additional adjunctive therapy. 1 figure. 7 tables. 27 references.
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Prevalence and Severity of Periodontal Disease in Patients with Inflammatory Bowel Disease Source: Journal of Clinical Periodontology. 18(9): 690-697. October 1991. Contact: Available from Munksgaard. International Publishers Ltd., Three Cambridge Center, Suite 208, Cambridge, MA 02142. Summary: This article reports on a study in which the authors assessed the prevalence and severity of periodontal disease in patients with inflammatory bowel disease (IBD). Previous reports have demonstrated that oral mucosa and periodontal lesions occur in patients suffering from IBD (including Crohn's disease and ulcerative colitis). The periodontal status of 107 consecutive patients seeking treatment for IBD was assessed. Examination of the mid-and mesiobuccal aspects of one quadrant on one jaw and the contralateral quadrant of the opposite jaw revealed the 93.5 percent of the Crohn's disease patients and 95.1 percent of ulcerative colitis patients had at least one site with probing attachment loss of 2mm or greater. The authors note that, compared with the assessment of Oral Health of U.S. Adults, IBD patients revealed an 11.9 percent higher prevalence but 0.6mm lower severity of periodontal disease. The authors conclude that the magnitudes of these differences suggest no clinical implications for the management of periodontal disease in IBD subjects. 5 figures. 12 tables. 41 references. (AA-M).
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Chronic Renal Failure and Periodontal Disease Source: Renal Failure. 22(3): 307-318. 2000. Contact: Available from Marcel Dekker Journals. P.O. Box 5017, Monticello, NY 127015176. (212) 696-9000. Summary: This article reports on a study of 6 patients (4 male, 2 female) with chronic renal failure (CRF) who were on chronic hemodialysis for an average of 4.25 years (range 1 to 15 years). The study was undertaken to define the effects of CRF in the progress of gingival inflammation. Six healthy individuals, age and sex matched, were used as controls. The protocol comprised two periods: a 40 day duration period of preparation and a 28 day duration experimental period. During the preparation period, all subjects went through therapy of the chronic gingivitis and complete control of dental plaque by oral hygiene. During the experimental period, all subjects were advised to avoid, for at least 21 days, any mechanical or chemical media of oral hygiene and went through photographing, recording of gingival index (GI), recording of plaque index (PlI) and the collection and quantification of gingival crevicular fluid (GCF). On the 21st day, root planing and polishing were performed and subjects were advised to carry out oral hygiene. On the 28th day, all previous examinations were repeated. Results showed that, in both patients and controls, GI, PlI, and GCF were increased on the 7th, 14th, and 21st day, without significant differences between the groups and returned to normal (close to zero point) on the 28th day. The authors conclude that there are no significant differences between patients with CRF and normal controls in the evolution of experimental gingivitis. Therefore, chronic uremia has no effect on the defense of periodontal tissue against microbial plaque. 4 figures. 7 tables. 31 references.
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Periodontal Disease and NIDDM in Pima Indians Source: Diabetes Care. 13(8): 836-840. August 1990. Summary: This article reports on a study that attempted to determine the prevalence and incidence of periodontal disease and its relationship with noninsulin-dependent diabetes mellitus (NIDDM). Two thousand two hundred seventy-three Pima Indians (949 men, 1324 women) aged 15 years and older from the Gila River Indian Community in Arizona were examined between 1983 and 1989. Periodontal disease was diagnosed by tooth loss and by percentage of interproximal crestal alveolar bone loss ascertained from panoramic radiography. Subjects with little or no evidence of periodontal disease were classified as nondiseased. Although periodontal disease was common in nondiabetic Pima Indians, in whom most of the incident cases occurred, diabetes clearly conferred a substantially increased risk. The authors conclude that periodontal disease should be considered a nonspecific complication of NIDDM. 1 figure. 2 tables. 28 references. (AA-M).
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Relationship Between Periodontal Disease in Pregnant Women and the Nutritional Condition of Their Newborns Source: Journal of Periodontology. 73(10): 1177-1183. October 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: This article reports on a study undertaken to determine whether maternal periodontal disease (PD) could be associated with the nutritional condition of newborns. After controlling for traditional risk factors for premature childbirth and low birth weight (LBW), 69 mothers were selected: 13 were periodontally healthy and 56 had
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varying stages of PD. They and their newborns formed the study population. A decrease in the average newborn's weight and gestational age was observed as the mother's level of PD increased. Analyses demonstrated a highly significant clinical relationship between more severe PD and lower birth weight; a highly significant relationship was also clinically demonstrated between increasing PD severity and decreasing gestational age of the newborn babies. There were significant differences in the weight and gestations age of the newborns of mothers with PD. These data suggest that PD in pregnant women could be a clinically significant risk factor for preterm deliveries and low birth weight. There was considerable variability in the results, and these preliminary findings need to be confirmed in larger studies. 2 figures. 4 tables. 42 references. •
Epidemiology and Prevention of Periodontal Disease in Individuals with Diabetes Source: Diabetes Care. 14(5): 375-385. May 1991. Summary: This article reviews the epidemiological evidence of the relationship between diabetes and periodontal disease, possible physiological mechanisms for the association, and effects of interventions on the occurrence and severity of periodontal disease among individuals with diabetes. A comprehensive qualitative review of published literature in the area was performed. The authors found that much of the research in this area contained methodological problems, such as failing to specify the type of diabetes, small sample sizes, and inadequate control of covariates such as age or duration of diabetes. Trends indicate that periodontal disease is more prevalent and more severe among individuals with diabetes. People with diabetes who appear to be particularly susceptible to periodontal disease include those who do not maintain good oral hygiene or good metabolic control of their diabetes, those with diabetes of long duration or with other complications of diabetes, and teenagers and pregnant women. 3 figures. 5 tables. 82 references. (AA-M).
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Periodontal Disease Strikes All Adults, But May Create Extra Problems For Diabetics Source: Diabetes in the News. 10(5): 30-31. October 1991. Contact: Available from Ames Center for Diabetes Education. Ames Division, Miles Laboratories, P.O. Box 3115, Elkhart, IN 46515. (312) 664-9782 or (800) 348-8100. Summary: This article reviews the problem of periodontal disease in people with diabetes. The author reviews the causes of periodontal disease, how to prevent it, and the potential hazards caused by periodontal disease in people with diabetes. Also included is a list of signs and symptoms of this health problem. The author concludes with a brief review of treatment procedures used for periodontal disease, including laser surgery, transplants of bone or tissue, antibiotics, and antiplaque medications. One sidebar reviews the essentials of daily dental hygiene.
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Current Concepts and Future Trends for Periodontal Disease and Periodontal Therapy, Part 2: Classification, Diagnosis, and Nonsurgical and Surgical Therapy Source: Dentistry Today. 20(3): 86-91. March 2001. Contact: Available from Dentistry Today Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: This article, the second in a two part series on current approaches to periodontal disease, covers classification, diagnosis, and nonsurgical and surgical therapy. The author focuses on changes in the present recommendations for delivery of
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health care, as well as on future trends. The periodontal diseases are broadly defined as gingivitis (inflammation of the nonmineralized connective tissue and epithelium) and periodontitis (where the bone supporting the teeth is involved). The author covers a detailed classification system for the periodontal diseases, diagnostic tests, the development of microbiologial and biochemical or host response tests, the etiology of periodontal diseases, tests that identify specific microorganisms, host response to the pathogenesis of periodontal disease (primarily through the analysis of gingival crevicular fluid), the use of antibiotics (including local delivery of the drugs), antiinflammatory therapy for periodontal disease, and surgical techniques used to treat periodontal diseases (including bone grafts and tissue regeneration). The author believes that future assessment of patients will be more specific, and the development of risk profiles will allow identification of people who require greater or lesser amounts of care. Therapy can then be directed to the specific needs of each patient. Continuing education credit is available for this article. 2 tables. 22 references. •
Diabetes and Periodontal Disease Source: Oral Care Report. 12(1): 12. 2002. Contact: Available from Oral Care Report. Dr. Chester W. Douglas, Department of Oral Health Policy, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115. E-mail:
[email protected]. Website: www.colgate.com. Summary: This brief article familiarizes dentists with the interplay between diabetes mellitus and periodontal disease. The author reviews the clinical appearance of diabetes-related oral health problems, the general symptoms of diabetes itself, and implications for dental treatment. Both gingivitis and periodontitis have been linked to diabetes mellitus, if the disease is not under control. In more advanced stages of uncontrolled diabetes, the patient may develop periodontal abscesses and the rapid loss of periodontal attachment and supporting bone. For patients with diabetes, a key issue is that dental treatment plans, other than emergency care, should be delayed if the patient's diabetes is uncontrolled. These patients should be immediately referred for blood glucose testing and therapy under a physician's supervision. After the patient has received the appropriate medical care for their diabetes, the clinical appearance of the patient's gingivitis and or periodontitis may improve. Patients with controlled diabetes seem to be as receptive as non-diabetic patients to routine dental care procedures. 1 reference.
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Relationship Between Coronary Artery Disease and Periodontal Disease Source: Dentistry Today. 22(2): 100-105. February 2003. Contact: Available from Dentistry Today, Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: This continuing education article reviews the link between periodontal disease and coronary artery disease (CAD), with a discussion of the mechanisms involved and challenges for the future. The authors first review CAD, its causes, clinical manifestations, risk factors, and pathology. The authors then consider periodontal disease and CAD, notably the risk factors shared by both diseases (smoking, diabetes mellitus, low socioeconomic status), the role of bacterial infections, and other possible mechanisms for the link. A final section considers the dental implications of this relationship. The authors contend that it is fair to inform patients that evidence suggests a relationship between these conditions, and that periodontal therapy will help maintain the dentition in health and comfort, but it is premature to claim a cardiovascular-
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protective effect of treatment. A posttest with which readers can obtain continuing education credit is appended to the article. 2 figures. 3 tables. 58 references. •
Human Immunodeficiency Virus - Associated Periodontal Diseases: A Review Source: Journal of Dental Hygiene; Vol. 67, No. 4, May-June 1993. Contact: University of Illinois Chicago, 840 S Wood St, Rm7 C/C778, Chicago, IL, 60612, (312) 996-1226. Summary: This journal article reviews the classification, etiology, pathogenesis, clinical features, and treatment of periodontal diseases which are associated with HIV infection. It focuses on the clinically distinctive types of periodontal diseases associated with HIV infection. Concentrating on HIV-associated gingivitis, HIV-associated periodontis, necrotizing stomatitis, and necrotizing ulcerative gingivitis, the author identifies diagnostic criteria, discusses prevalence, and examines the microbiology of HIV-related periodontal diseases.
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Does Periodontal Disease Related to Pre-Term Low Birth Weight Babies? Source: Oral Care Report. 11(3): 1-3. 2001. Contact: Available from Oral Care Report. Dr. Chester W. Douglas, Department of Oral Health Policy, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115. E-mail:
[email protected]. Website: www.colgate.com. Summary: This newsletter article, from a summary journal of advances in dentistry and oral health care, considers the relationship between periodontal disease and preterm low birth weight (PLBW) babies. Even with widespread use of tocolytics (drugs that decrease uterine contractions), the incidence of LBW or preterm infants has not decreased in the past 20 years. In the hopes of improving the outcomes for PLBW babies, physicians and investigators have shifted their attention from symptomatic care to prevention of underlying causes. Oral infection, already associated with several systemic inflammatory conditions such as vasculitis, atherosclerosis, and thromboemoblic phenomena, is considered to be a risk factor for PLBW. It has been suggested that more than 18 percent of all PLBW cases are associated with periodontal disease. The article reviews recent studies, hypotheses regarding the biological pathway involved, and the role of dental care providers in prevention strategies. Due to the rising morbidity (related illness and complications) and mortality (death) associated with PLBW and its devastating financial and societal impact, finding ways to prevent this condition has become a priority. Based on the compelling findings to date, intervention studies have been launched to determine the safety and effectiveness of treatments for periodontal disease in pregnancy mothers. 1 figure. 1 table. 6 references.
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Diabetes and Periodontal Diseases: Position Paper Source: Journal of Periodontology. 70(8): 935-949. August 1999. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 787-5518. Fax (312) 573-3225. Website: www.perio.org. Summary: This position paper provides information on diabetes and periodontal disease. The paper first discusses the diagnosis and medical management of type 1 and type 2 diabetes, focusing on general signs and symptoms, complications, and management with diet and pharmacologic agents. The paper highlights the findings of
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the Diabetes Control and Complications Trial and the United Kingdom Prospective Diabetes Study with regard to the importance of glycemic control. Other issues addressed include the tests used to determine blood glucose levels. The paper then summarizes current knowledge on the relationship between periodontal diseases and diabetes. Research indicates that diabetes, especially poorly controlled diabetes, increases the risk of periodontal disease. Studies have found that attachment loss occurs more frequently and more extensively in people who have moderate and poorly controlled diabetes of both types than in those who have good control. Further research is needed to identify more precisely the pathways through which diabetes and periodontal disease interact. The paper continues by identifying the factors potentially contributing to the development of periodontal disease. Although the exact mechanisms have not been determined, alterations in host defenses and normal tissue homeostasis appear to have a major role. Glycemic control may also be altered by periodontal infection and periodontal treatment. In addition, the paper outlines special considerations associated with treatment of periodontal disease in people who have diabetes, such as the timing of treatment and the use of antibiotics, and discusses possible approaches to the management of diabetic emergencies in the dental office. Although intensive medical treatment with oral agents and insulin promises to decrease the long-term risks of major complications of diabetes, these treatments increase the risk of medical emergencies in the dental office, especially hypoglycemia. Familiarity with the various medications, monitoring equipment, and devices used by people who have diabetes allows provision of appropriate periodontal therapy while minimizing the risk of complications. 2 tables. 147 references. (AA-M). •
Periodontal Disease and Diabetes Mellitus Source: Diabetes Spectrum. 10(2): 112-118. 1997. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article outlines the interrelationship of periodontal disease (PD) and diabetes mellitus. People with diabetes are at increased risk for developing PD, including periodontitis. The authors briefly describe the etiology and progression of periodontitis, particularly in patients with diabetes. They present a comprehensive model in which the interaction of personal factors with the social environment provides the potential for the initiation of generalized periodontitis. In this model, diabetes is considered under systemic risk factors for PD. The authors stress that this identification of risk factors for PD may permit health care workers to predict those at risk. In addition, early identification can increase patient education in the prevention and treatment of PD. 4 figures. 1 table. 68 references. (AA-M).
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Century of Progress in Understanding Periodontal Disease Source: Compendium of Continuing Education in Dentistry. 23(5 Supplement): 3-10. May 2002. Contact: Available from Dental Learning Systems. 241 Forsgate Drive, Jamesburg, NJ 08831. (800) 926-7636. Summary: Throughout the 20th century, investigators and clinicians sought to discover the causes and trace the natural history of periodontal disease. This article outlines the noteworthy progress that has been made on several fronts. It was once believed that oral hygiene and age accounted predominantly for variances in the prevalence and severity of periodontal disease; now, a number of innate, acquired, and environmental risk
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factors have been identified. There have been advances in the understanding of the roles in periodontal disease pathogenesis (development) of both specific bacteria and bacterial complexes and host immunoinflammatory responses. Insight into periodontal wound healing has fostered promising approaches to promoting regeneration of damaged periodontal structures. Finally, although theories of 'focal infection' as a primary cause of systemic disease have been discredited, recent studies have confirmed the existence of an intimate connection between oral and systemic health. The progress made in understanding the nature of periodontal disease has been complemented by equally noteworthy therapeutic advances. The author concludes that the coupling of surgical and medical approaches to treatment ushers in a new era in the management of periodontal disease. 4 figures. 1 table. 60 references. •
Periodontal Disease and Atherosclerosis Source: RDH. 23(1): 52,54,56,58,60,62,64,66. January 2003. Contact: Available from Penwell Corporation. 1421 South Sheridan, Tulsa, OK 74112. Website: www.rdhmag.com. Summary: Total health promotion includes education on reducing the risk factors for periodontal disease, as well as reducing the major controllable risk factors associated with cardiovascular diseases (CVD). Early prevention and intervention can significantly delay the onset of atherosclerosis ('hardening of the arteries') and cardiovascular disease which may result in disability and death from heart attack and stroke. This article brings dental hygienists up to date on the connections between periodontal disease and atherosclerosis. Topics include epidemiology and statistics about CVD and periodontal disease, definitions of atherosclerosis and how it develops, how periodontitis becomes a factor, blood cholesterol, physical inactivity, obesity, lifestyle and lifestyle modification, and the role of dental care providers, including dental hygienists. Dental hygienists can provide enough education so that patients can make informed decisions based on the risk factors identified during their medical history taking. Hygienists can also assist their patients in identifying the major controllable risk factors associated with CVD to establish risk of atherosclerosis and cardiovascular disease and offer suggestions regarding the necessary lifestyle changes to reduce those risks. One figure offers a risk assessment tool for CVD. One sidebar lists recommended Web sites for further information. 1 figure.
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Update on HIV and Periodontal Disease Source: Journal of Periodontology. 73(9): 1071-1078. September 2002. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: With the advent of newer pharmacological approaches to the treatment of human immunodeficiency virus (HIV) infection, the incidence and progression of both atypical and conventional periodontal diseases are changing. This article offers readers an update on HIV and periodontal disease. The incidence of necrotizing periodontitis and gingival diseases of fungal origin appears to be on the decline as a result of these therapies that have led to increased life spans for HIV patients. However, in cases where these therapies lose their effectiveness and HIV patients relapse into an immunosuppressed state, these conditions may recur. Recent evidence has shown that HIV patients with more conventional periodontal diseases such as chronic periodontitis may have increased attachment loss and gingival (gum) recession when compared to their HIV-negative counterparts. This pattern of loss of periodontal support may be due
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in part to a diffuse invasion of opportunistic bacterial infections, viruses, and fungi into the gingival tissue, leading to a more elevated and more diffuse destructive inflammatory response in the periodontal soft and hard tissues. While the accepted approaches to treating the spectrum of periodontal diseases in HIV patients remain essentially unchanged over the past 15 years, the impact of newer systemic therapies on patient immunocompetence may influence treatment decisions. 83 references.
Federally Funded Research on Periodontal Disease The U.S. Government supports a variety of research studies relating to periodontal disease. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to periodontal disease. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore periodontal disease. The following is typical of the type of information found when searching the CRISP database for periodontal disease: •
Project Title: ACTINOBACILLUS ACTINOMYCETEMCOMITANS VIRULENCE Principal Investigator & Institution: Dirienzo, Joseph M.; Professor; Microbiology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-MAY-2003 Summary: (adapted from the Investigator's abstract): The gram-negative bacterium, Actinobacillus actinomycetemcomitans, has been the subject of intensive study because it is considered to be a major pathogen of periodontal diseases. Some of the hallmarks of the pathogenic potential of this species are the ability of select strains to invade gingival tissues and to produce relatively high levels of leukotoxin. A number of lesscharacterized virulence potentials include a variety of cytostatic and cytotoxic factors. The focus of this application is a novel toxin, known as cytolethal distending toxin (CDT), which the Principal Investigator has recently discovered in A. actinomycetemcomitans. In preliminary experiments, the cdt locus was cloned in a nonenteropathogenic strain of Escherichia coli and the complete nucleotide sequence obtained. Extracts of the recombinant cells caused morphological changes in Chinese hamster ovary (CHO) cells, human epithelial cell-like lines and periodontal ligament fibroblasts characteristic of CDT. The major objective of this study is to initiate an investigation towards the complete genetic and biochemical characterization of the CDT of A. actinomycetemcomitans. Three specific aims are proposed. Aim 1 is to identify and characterize the genes and gene products of the putative cdt locus. Aim 2 is to determine the kinetics of cytostatic and cytolytic effects of CDT on cultured cells, and Aim 3 is to
2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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examine the genetic organization of the cdt locus. Frame shift mutants will be constructed and employed to examine the contribution of each of the cdt genes to distension and killing activities. The kinetics of cell distension and cytotoxicity will be characterized using CHO cells as a model system. Northern blotting and primer extension will be used to determine if the three genes that comprise the cdt locus are organized into a polycistronic operon. The CDT represents a previously unknown potential virulence factor for A. actinomycetemcomitans. The expression of this novel toxin may have important implications in the development of localized juvenile periodontitis (LJP), as well as in other types of bacterial disease, because it extends the repertoire of virulence potentials of the bacterium. Significant advances have been made in the identification and description of this toxin locus and it is now important to extend our understanding of its expression and biological activities. The availability of the cloned and sequenced cdt genes provides an advantage in the development of tools for the study of the role of this toxin in the pathogenicity of oral disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ACUTE PHASE CARDIOVASCULAR DISEASE
REACTANTS
IN
PERIODONTITIS
AND
Principal Investigator & Institution: Slade, Gary D.; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2002 Summary: The purpose of this molecular epidemiological study is to elucidate, with representative populations of US adults, mechanisms of systemic inflammatory response that are associated with elevated risk of cardiovascular disease (CVD) observed among persons with periodontal disease. This nested cross-sectional study will select subjects from the existing Atherosclerosis Risk in Communities (ARIC) study, an ongoing longitudinal cohort study of a random sample of 16,000 people aged 45-64 years in four states. Existing records of clinical periodontal status from the ARIC study will be used to study equal number of subjects across categories of probing pocket depth (PPD) extent scores. Stored serum samples will be analyzed by ELISA for C-reactive protein (CRP- a non-specific acute phase-reactant) and for lipopolysaccharide binding protein (LBP- an endogenous carrier molecule that binds LPS to the CD14 receptor of polymorphonuclear leukocytes, enhancing the release of inflammatory mediators). Those data will be linked to existing ultrasound measurements of intimal wall thickness of the carotid and popliteal arteries, physician diagnoses of acute CVD events, and other risk factors collected in the ARIC study. In addition, data currently are being collected (with no cost to this project) from assays of inflammatory mediators (IL-6, IL-10 and TNFalpha) in gingival crevicular fluid (GCF) and serum in the same subjects. Statistical analyses will evaluate key components of our hypothesized model of periodontal-CVD etiology. Relationships between extent of PPD and GCF inflammatory mediators will be evaluated using least squares regression models that control for other intra-oral conditions and socio-demographic variables. Severity (mean levels) and prevalence (thresholds of clinically meaningful elevation) of serum inflammatory mediators (CRP, IL-6, IL-10 and TNFalpha) will be compared between PPD groups controlling for other mediators (CRP, IL-6, IL-10 and TNFalpha) will be compared between PPD groups controlling for other systemic diseases. Finally, the multivariate models will assess hypothesized synergistic effects between periodontal disease and serum LBP on systemic inflammatory mediators and prevalent CVD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: AGING: EFFECTS ON INFECTION, INFLAMMATION AND DISEASE Principal Investigator & Institution: Novak, M. John.; Professor and Associate Director; Ctr for Oral Health Research; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant): This proposal is a collaborative submission from the University of Kentucky, the University of Maryland, and the Nutritional and Molecular Physiology Unit of the Laboratory of Neurosciences of the National Institute on Aging. The proposed studies will build on existing data obtained from Rhesus monkeys being maintained on calorie restricted and normal diets by the NIA, and will provide a biologic basis for our preliminary observations of altered inflammatory responses in calorie restricted animals. This proposal focuses on utilizing the oral cavity as a model system to examine the impact of aging on host-bacterial interactions as they relate to microbial colonization of mucosal surfaces, the induction and regulation of inflammatory/immune responses, and the pathologic destruction of host tissues that may result from these interactions. The aims of this study will test the following contrasting scientific hypotheses: (a) that caloric restriction (CR) reduces clinical inflammation by affecting the pathogenicity of microbial plaque, and that these changes are due to shifts in the proportions and/or clonal type of the constituent pathogenic and non-pathogenic microorganisms; (b) that CR alters the clinical manifestation of inflammation through an effect on innate immune mechanisms through increased proinflammatory molecule release; and/or (c) that CR alters the clinical manifestation of inflammation through an effect on innate immune mechanisms by regulating the release of anti-inflammatory molecules. Aim 1 is a cross-sectional retrospective study to determine the effects of a long-term calorie restricted diet on the progression of naturally occurring inflammatory periodontal disease in CR and non-CR Rhesus monkeys. The effects of CR on clinical inflammation, microbial colonization of mucosal surfaces, and pro-inflammatory and anti-inflammatory mechanisms will be evaluated. Aim 2 is a longitudinal prospective study to determine the effects of a calorie-restricted diet on the clinical, microbiological, and host responses observed during experimental ligature-induced periodontitis in the same CR and non-CR Rhesus monkeys. These studies will provide information on the effects of CR on the kinetics of clinical, microbiologic, and inflammatory changes at mucosal sites. The significance of these studies lies in our capability to use nonhuman primates and the oral cavity to evaluate the efficacy of CR as a means to regulate infection, inflammation, and inflammatory disease. The long-term implications are that diet control may be considered as an effective public healthcare measure for improving the oral and general health and welfare of the population as a whole. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ALVEOLAR BONE REGENERATION BY TRANSCRIPTIONAL CONTROL Principal Investigator & Institution: Hollinger, Jeffrey O.; Professor and Director; Bone Tissue Engineering Ctr; Carnegie-Mellon University 5000 Forbes Ave Pittsburgh, Pa 15213 Timing: Fiscal Year 2003; Project Start 08-AUG-2003; Project End 31-MAY-2007 Summary: (provided by applicant): The aftermath of periodontal disease frequently includes alveolar bone loss. Contemporary periodontal therapy has not been effective for regenerating alveolar bone. Therefore, the long term goal of the applicants is to
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design and develop a tissue engineered bone regenerating therapy. The applicants reason that transcriptional control of osteoblast differentiation offers an innovative and powerful new treatment approach for controlled bone regeneration. To accomplish the goal, we will focus on a plasmid (p) encoding for the nuclear transcription factor Osterix (Osx) that will be delivered to bone using an injectable, biodegradable, biocompatible hydrogel of hyaluronate (HA) and polylysine (PL). The overall hypothesis for this application is that controlled, predictable delivery ofp.Osx with HA/PL will promote osteoblast differentiation and bone formation. Testing the hypothesis will be accomplished by four specific aims. Specific aim 1. Will Osx encoded by a plasmid (p.Osx) up regulate osteoblast-like gene expression in a designated cell line? Specific aim 2. Will p.Osx delivered in HA/PL enhance transfection efficiency of p.Osx and therefore increase oseoblast-like gene expression? Specific aim 3. Will the optimized p.Osx/HA_L assessed in vitro promote bone formation in a critical-sized defect (CSD)? We reason a non-dental CSD model is less stringent than the periodontal model. The CSD model will enable a level of control of therapy design and optimization not available in the periodontal model and the CSD is a logical antecedent to aim 4. Specific aim 4. Will the optimized formulation work either as effectively as a contemporary periodontal therapy of demineralized freeze-dried bone allograft in an alveolar bone model in the dog? Data will be analyzed by analysis of variance and post hoc multiple comparison analyses with p less than or equal too 0.05. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANALYSIS INNATE IMMUNE RESPONSES TO ORAL PATHOGENS Principal Investigator & Institution: Mcinerney, Marcia F.; Medicinal & Biological Chemistry; University of Toledo 2801 W Bancroft St Toledo, Oh 43606 Timing: Fiscal Year 2002; Project Start 05-AUG-2002; Project End 31-JUL-2004 Summary: (provided by applicant): Diabetes is a risk factor for severe periodontal disease. Major pathogens associated with periodontitis are Porphyromonas gingivalis (P. gingivalis), Bacteroides forsythus (B. forsythus) and Treponema denticola (T. denticola), all Gram-negative anaerobes. Previous studies suggest that both innate and adaptive immunity are involved in protection against periodontal infection. Innate immune responses are the first line of defense against an infection. Innate immune system cells, such as macrophages, react to common microbial surface molecules through newly discovered receptors on the macrophage cell surface called Toll-like receptors (TLRs). Preliminary studies have found that lipopolysaccharide (LPS) derived from Gram-negative bacteria regulate the expression of several different TLRs in macrophages and trigger cytokine production and expression of co-stimulatory molecules in macrophages. These events are essential for macrophage activation and initiation of specific adaptive immune responses for generation of antigen specific cells. The purpose of this project is to study innate immunity in type 1 diabetes, in particular, the role of TLR in the initiation of host immune responses against oral pathogens in periodontal infection, using the well established non-obese diabetic (NOD) mouse model of type I diabetes. NOD macrophage responses to live bacteria and LPS isolated from P. gingivalis, B. forsythus and T. denticola in terms of cytokine production, costimulatory molecule expression, TLR mRNA levels and TLR signal transduction will be compared to NOR mice, a diabetes resistant control strain. Our hypothesis is that a defect in innate immunity in type 1 diabetes contributes to the susceptibility to periodontal infection since it should be the interaction between the TLR and the oral pathogen that initiates immune responses. These experiments will generate novel information on innate immune responses to oral pathogens in type 1 diabetes and may
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lead to development of therapeutic interventions to alleviate severe periodontitis in diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: B FORSYTHUS PROTEASE AND SIALIDASE--GENES AND SUBSTRATES Principal Investigator & Institution: Maiden, Mark F.; Forsyth Institute Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-FEB-1999; Project End 31-JAN-2004 Summary: The long term objective of this proposal is to determine the molecular mechanisms of periodontal disease pathogenesis by Bacteroides forsythus. Although B. forsythus has been implicated as an important periodontal pathogen, especially in the early stages of disease, very little is known about its virulence factors. B. forsythus possesses two enzyme activities which are known to be virulence factors in other pathogens; a "trypsin-like" protease and a sialidase. New data is presented characterizing the protease as a 79 kDa cell envelope-associated arginine-X cleaving serine protease. The protease has been partially purified and peptide fragments for sequencing have been generated. Additional new data shows that B. forsythus has a gene homologous to a probe derived from the sialidase gene of Bacteroides fragilis. The studies proposed will address the hypothesis that the trypsin-like serine protease and sialidase activities of B. forsythus are virulence factors, possibly targeted at host cellsurface glycoproteins. The experimental design will be to first isolate clones of the two genes by screening a B. forsythus genomic library (Specific Aims 1 and 3). The cloned genes will be sequences and expressed in E. coli. The substrates specificities of the enzymes will be tested with a range of natural proteins and glycoproteins to determine their potential host targets (Specific Aims 2 and 4). Inactivated mutants of the two genes will be constructed in vitro and introduced into B. forsythus recipients using IncP plasmid-based suicide vectors to produce protease-negative and sialidase-negative single, isogenic mutants by allelic exchanges (Specific Aim 5). The mutants will permit the testing in animal models of the hypothesis that the protease and sialidase are important virulence factors of B. forsythus. The genetic methods developed will be important in future studies of other B. forsythus virulence factors, and their role in pathogenesis. The results of this study will contribute to improvements in oral health by increasing our knowledge and understanding of the mechanisms of periodontal disease pathogenesis. Understanding these mechanisms will be vital for developing improved preventative and therapeutic treatments for periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: B.FORSYTHUS BSPA PROTEIN: ROLE IN VIRULENCE Principal Investigator & Institution: Sharma, Ashu; Oral Biology; State University of New York at Buffalo Suite 211 Ub Commons Amherst, Ny 14228 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-DEC-2006 Summary: Bacteroides forsythus is a Gram-negative oral anaerobe implicated in the development of periodontal disease pathogenesis. Although, very little is known about the virulence factors of this organism, based on our recent in vitro and in vivo studies, a surface-associated 98-kDa protein (BspA) has been suggested as a virulence factor. The BspA protein contains homologous sequences belonging to the leucine-rich repeat motif family (LRR), and to motifs belonging to the immunoglobulin superfamily (Ig-SF). In vitro, the BspA protein binds to extracellular matrix components fibronectin and fibrinogen, and to epithelial cells, and induces release of proinflammtory cytokines from
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monocytic cells. Further, a mutant of B. forsythus defective in BspA expression constructed in our laboratory has been found to be significantly attenuated in its ability to bind to fibronectin, fibrinogen, and epithelial cells. The studies proposed here will address the hypotheses that LRRs and IgSF domains are critical for host cell interactions via binding to specific cellular receptors, and that the BspA protein plays important roles in pathogenesis via mediating bacterial colonization and triggering of host cellular responses, such as release of cytokines and other mediators. The experimental design will include: 1) studies to determine the specific BspA-domains involved in host cell (epithelial and monocytic cells) interactions (Specific Aim 1a), and investigate intracellular signaling events resulting from BspA binding (Aim 1b); 2) biochemical characterization of epithelial (Aim 2a) and monocyte receptors (Aim 2b) that bind BspA protein; and 3) assessment of the in vivo role of BspA protein as judged by studies in a mouse model of periodontal disease (Aim 3a), and by evaluating the host immune response against the BspA protein in patients with a history of periodontitis (Aim 3b). The findings will be important in determining the roles of BspA protein, and the underlying contribution of its domains in bacterial pathogenesis. The studies will also be critical from a proteomic standpoint in defining the roles of LRR and Ig-like signatures found in other bacterial proteins in general. In the long term, understanding the basic mechanisms of the BspA-mediated pathogenesis of B. forsythus will be vital in developing intervention strategies against periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BACTERIA-HOST CELL INTERACTIONS IN PERIODONTAL DISEASE Principal Investigator & Institution: Diamond, Gill; Associate Professor; Biochem and Molecular Biology; Univ of Med/Dent Nj Newark Newark, Nj 07103 Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 31-MAR-2006 Summary: Localized juvenile periodontitis (LJP) is a periodontal disease which primarily affects peripubertal children of African descent. Over 95 percent of the LJP patient population is colonized with the facultative Gram negative rod Actinobacillus actinomycetmcomitans (Aa). In LJP, virulent strains of Aa invade the epithelial cells, and colonize the oral mucosa, and induce a hyperinflammatory response. A bacterial virulence factor which encodes a secreted leukotoxin inhibits bactericidal activity by the PMNs, allowing colonization. For the initial colonization and subsequent invasion, however, the bacteria must first evade the initial line of host defense in the oral cavity. This primary part of oral innate immunity is based in the response of the epithelial cells by the production of antimicrobial agents and inflammatory mediators. Little is known about how the periodontal epithelium responds to the presence of bacteria in general, and Aa in particular. Furthermore, while LJP is a disease with a large genetic component which only manifests with localized periodontal infections, the deficiencies in the host defense capabilities of this epithelium have not been examined. Thus, a more complete analysis of the innate immune response of the gingival epithelium to Aa will allow for a better understanding of the etiology of this disease. The long-range goal of our research is to better understand the dynamic host defense systems in the mucosal epithelium. The objective of these studies is to determine how a pathogenic bacterium evades the innate immune response in individuals which are predisposed to this infection. Our central hypothesis is that the gingival epithelium provides an active host defense tissue. A combination of deficiencies in this host defense and bacterial virulence factors can lead to severe infection. By characterizing the response of the epithelial cells to the pathogen, and identifying differences in cells from diseased versus normal individuals,
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we will be able to better address the issues of early detection and treatment. This would include strategies to modulate the endogenous antimicrobial peptide expression to prevent serious bacterial infections. To achieve this we propose to: 1. Characterize the specific pattern recognition receptors to Aa in the gingival epithelium. 2. Define the host defense gene expression of the cultured gingival epithelium in response to Aa. 3. Determine innate immune gene expression in the oral epithelium from healthy and LJP patients. For this study we will focus on the role of pattern recognition receptors such as CD14 and Toll- like receptors, antimicrobial peptide and production of proinflammatory cytokines. Our approach, which includes studying the interactions of the epithelium with live bacteria and the use of microarrays, will provide a detailed picture of the host defense capabilities of the oral cavity. Characterization of variability in the expression of specific natural antibiotics such as beta-defensins or stimulants of neutrophil antibacterial function such as chemotactic and proinflammatory cytokines, which may prevent colonization of periodontal tissues by this persistent bacterium, may allow for early identification of the susceptible individuals or provide an alternative treatment approach for this patient category. The result from this study will allow us to develop novel strategies to prevent attachment and colonization of disease-causing bacteria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BONE MINERAL DENSITY AS A PREDICTOR OF PERIODONTITIS Principal Investigator & Institution: Wactawski-Wende, Jean; Assistant Professor; Social and Preventive Medicine; State University of New York at Buffalo Suite 211 Ub Commons Amherst, Ny 14228 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2006 Summary: (provided by applicant): The overall purpose of this study is to determine the role of oral and systemic bone mineral density (BMD) in the development of new and progressive periodontal disease in postmenopausal women. We hypothesize that low BMD will be associated with both new and progressive periodontitis over time by increasing susceptibility to destructive periodontitis. We propose a longitudinal assessment of BMD and its role in establishment of periodontal disease in postmenopausal women with systematic studies using sensitive and accurate measures of skeletal and oral BMD, and periodontal disease. As part of the BMD assessment, we will further validate the methodology for oral BMD. In concert with these, assessment of a variety of potential co-risk factors for both low BMD and periodontitis will allow us to determine their contribution to this association. The systemic covariates include age, body mass index, smoking, alcohol, hormone use, socioeconomic and psychosocial factors, medications, medical and reproductive history, and diet. Local covariates include plaque, gingivitis, probing depth, previous dental care, and dental care habits. Study subjects will be recruited from an established cohort of postmenopausal women with baseline assessments of BMD and periodontitis as part of an ongoing crosssectional study. We propose a 3-vear follow-up examination in 1000 postmenopausal women already enrolled in the NIH Women's Health Initiative study. To date, studies have not characterized the specific role of BMD either skeletal or mandibular on periodontal disease incidence and progression in a large cohort of postmenopausal women. Our preliminary cross-sectional studies have determined that skeletal BMD is associated with alveolar crestal height, tooth loss and clinical attachment loss. The proposed longitudinal study will have sufficient sample size and statistical power to assess the temporal relationship between BMD and periodontitis and the effects of a large set of co-risk factors and potential confounding factors affecting osteopenia, periodontal disease or both. This study provides a unique opportunity to define this
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relationship in a cost effective manner in a cohort of postmenopausal women under study as part of the Women's Health Initiative and has great practical significance. Low BMD is likely of considerable importance in the onset and progression of periodontitis. Hence once the relationship is established, modalities effective in the prevention and treatment of osteoporosis may prove useful for prevention and treatment of periodontitis and subsequent tooth loss. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: C1Q-INDUCED HETEROGENEITY
CA2+
RESPONSES
IN
FIBROBLAST
Principal Investigator & Institution: Bordin, Sandra F.; Associate Professor; Periodontics; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 30-SEP-1995; Project End 31-MAR-2003 Summary: In periodontitis, the consecutive tissues supporting the teeth are systematically destroyed by long term infections. Treatment, if successful, usually leads to repair by scarring as a result of the replacement of normal fibroblasts with granulation cells. Periodontal repair is not as advantageous to the patient as regeneration of a fully functional periodontium. In order to facilitate clinical regenerative therapies, we studied molecular and cellular mechanisms that control proliferation of distinct populations of normal and granulation fibroblasts cultured from human gingiva. These studies led us to scrutinize how the anti-microbial complement component C1q, which occurs in high quantities in normal and inflamed tissues, inhibits the growth of the host's cells. C1q acts as a stress activator. While normal fibroblasts respond to C1q by activating intracellular stress proteins associated with delays in cell select growth of granulation fibroblasts over normal fibroblasts, thus hampering periodontal regeneration. Verification of this hypotheses could provide a basis for more effective prevention and treatment of human periodontal disease through pharmacological and genetic manipulations of the affected tissues to enhance normal fibroblast function and regeneration of the periodontal apparatus. Specific goals are: Aim I: To assess whether C1q modifies the growth response of the fibroblast populations by a block in cell cycle progression (cytostasis) or programmed cell death (apoptosis). Whereas cytostasis is reversible, apoptosis is irreversible. This information will provide a more predictable basis for evaluating the outcome of the disease on cellular composition, and therefore functionality, on the periodontium. Aim II: To identify the molecular events that protect the granulation cells from C1q- induced stress, and use this information for future clinical applications aimed at improving the survival of normal fibroblast populations. Our strategy consists of characterizing C1q-induced stress pathways of normal fibr9oblast for identification of the biochemical steps activated by high levels of protein kinase A and by translocation of protein kinase C, which occurs in granulation cells only, in response to C1q. The methods for achieving these goals apply established pharmacological bioassays, histology, and flow cytometry techniques. This information will provide insights for the design of drugs that neutralize the detrimental effect of C1q upon the growth of normal fibroblasts, while retaining the beneficial antimicrobial activity of the complement cascade. While this work focuses on periodontitis, its results should be applicable to a variety of inflammatory diseases as well as wound healing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Periodontal Disease
Project Title: CELL/CELL JUNCTION, STRUCTURE AND DYNAMICS IN ORAL EPITHELIUM Principal Investigator & Institution: Green, Kathleen J.; Professor; Northwestern University Office of Sponsored Programs Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-MAY-2002 Summary: The reversible modulation of both cell-cell and cell-substrate adhesive contacts if thought to play an important role during epithelial tissue remodeling. During the migratory phase of remodeling, a dramatic reduction in the number of cell-cell junctions known as desmosomes has been reported. However, the mechanisms governing desmosome disappearance or reassembly during this process are unknown. One example of remodeling that contributes to the progression of periodontal disease, which is a major health problem in the U.S., is the inward migration of junctional epithelium along the tooth surface that occurs following dissolution of gingival connective tissue. In order to understand how modulation of desmosomes may impact on oral epithelial cell migration, the molecular mechanisms that regulate desmosome assembly and dissolution must be elucidated using well-defined in vitro and cell culture models. In this project we will continue our efforts to define protein-protein interactions in the desmosome and t investigate how adhesive junctions are modulated in oral epithelial cell cultures. The specific aims are: 1) To determine the protein-protein interactions involved in establishing the structure of the desmosomal plaque and ensuring segregation of desmosomal and adherens junction components into distinct membrane domains, 2) To investigate intercellular junction dynamics and the role of the associated cytoskeleton and underlying extracellular matrix during migration of oral epithelial cells, using a combination of live cell observations and molecular genetic manipulation of oral epithelial ells, 3) To examine the contribution of proteinases present in the gingival microenvironment to junction dissolution and to define whether specific desmosomal cadherins are substrates for these proteinases. These studies will interface extensively with other project leaders who will provide reagents (i.e., IFAP300 from Dr. Goldman and laminin-5 peptides from Drs. Jones and Stack) and expertise (generation of fluorescently labeled probes for living cell observations, Dr. Goldman; zymographic analysis, Dr. Stack). This work will provide important insights into mechanisms by which cell-cell adhesive junctions are assembled and modulated in migrating oral epithelial cells, and will provide a basis for the design of therapeutic approached to curb the progression of periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: CELLULAR BASIS OF CRANIOFACIAL BONE DISORDERS Principal Investigator & Institution: Osdoby, Philip A.; Professor; Biology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-JUL-2003 Summary: Normal bone development and remodeling require complex humoral, cellcell, and cell-matrix interactions. The integration of humoral and local signals is necessary to permit proper development, maintain mineral homeostasis, insure mechanical strength, and support haematopoeisis. There is now good evidence that osteoblasts can orchestrate osteoclast development and modulate osteoclast activity via paracrine signals. Information is just beginning to emerge that osteoclasts themselves synthesize and release factors that may influence bone remodeling. We therefore hypothesize that osteoclast-derived signals may function as autocrine effectors of osteoclast development and activity and therefore influence normal and pathological
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osteoclastogenesis and osteoclast-mediated bone resorption. We have shown that osteoclasts produce small proinflammatory molecules known as chemokines, such as IL8 and GRO alpha and that such molecules can act to modulate osteoclast precursor recruitment, development, and activity. Therefore, to further investigate and define osteoclast autocrine regulation we propose the following specific aims: 1) Identify a profile of chemokines produced by human and mouse OC and determine which exhibit autocrine effects on OC function (bone resorption, motility, free radical production, TRAP, cathepsin K, and carbonic anhydrase II expression). The regulation of this subset of chemokines by select known modulators of OC function will be analyzed. Included here will be studies employing selective chemokine and chemokine receptor antagonists, chemokine neutralizing antibodies, and mouse OC-like cells formed in vitro from bone marrow obtained from IL-8 receptor knockout mice. 2) Identify and characterize the profile of chemokine receptors expressed on OC as a function of OC physiology, and pathophysiology. As part of this aim we will begin to elucidate the intracellular signal transduction pathways involved in chemokine modulation of OC activity. 3) Examine the potential role of chemokines in OC precursor recruitment and differentiation in vitro, in vivo, and in ovo. 4. Examine spatial and temporal aspects of chemokine and chemokine receptor expression in normal and pathological bone tissue by in situ hybridization and immunohistochemistry. Included here are mouse IL-8 receptor knockout studies. All of the above studies will use a combination of in vivo and in vitro approaches, and model systems including the mouse calvarial injection model for histomorphometric studies, human tissue sections for in situ hybridization and immunohistochemical analysis, isolated human and avian Ocs, human Oc-like cells, the mouse Oc-like cell developmental model, and cells obtained from an IL-8 receptor knockout mouse. Oc- chemokine production, mRNA steady state levels and regulation will be assessed by RT-PCP, RNAse protection assay, chemokine ELISA, and in situ hybridization techniques. Osteoclast development and activity will be evaluated based on functional, biochemical and molecular markers of the osteoclast phenotype, including bone resorption, osteoclast antigen expression tartarate-resistant acid phosphatase activity, and calcitonin receptor levels. Such studies are anticipated to reveal new aspects of normal bone remodeling mechanisms such as tooth eruption and have potential to lend insight into skeletal pathologies such as periodontal disease, implant loosening, osteoarthritis, other inflammatory skeletal disorders, and osteoporosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHRONIC DENTAL DISEASE AND CARDIOVASCULAR DISEASE Principal Investigator & Institution: Joshipura, Kaumudi J.; Assistant Professor; Oral Health Policy & Epidem; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-JUL-2003 Summary: Several recent reports have found significant associations between periodontal disease, tooth loss and increased coronary heart disease (CHD). Possible associations between dental caries and CHD and between dental disease and stroke have also been reported. Recent literature also supports the possible role of other chronic bacterial and viral infection, fibrinogen and other inflammatory mediators in increasing CHD risk. We propose to study the relation between periodontal disease, caries and tooth loss, and risk of incidence of coronary heart disease and stroke and to assess if these associations are independent of common risk factors including behavioral factors. Additionally, we propose to evaluate two possible explanations for these
36
Periodontal Disease
associations: (1) tooth loss leads to reduced masticatory efficiency, which could lead to reduced intake of dietary antioxidant and fiber, which in turn has been associated with increased risk for cardiovascular disease; and (2) chronic dental disease could lead to hyperfibrinogenemia which is strongly and probably causally associated with increased risk of CHD. We will also evaluate C-reactive protein, von Willebrand factor, tissue plasminogen activator, and Factor VII as additional mediators. Participants include 51,529 men enrolled in the Health Professionals Follow-Up Study since 1986 and 90,000 females enrolled in the Nurses Health Study since 1976 who reported their dental status in 1992. The follow-up in these cohorts is excellent and has been consistently over 90 percent. The outcome measures will include incident cases of CHD and stroke in 15 years of follow-up among men and 9 years of follow-up among women free of cardiovascular disease and cancer at baseline. Over 4500 incident cases of CHD and stroke are anticipated. Biomarker assays will be performed for a sub-population consisting of new CHD cases incident after the time of initial blood collection, and one matched control per case. Blood samples were provided by 32,000 nurses in 1989-90 and by 18,100 male health professionals in 1993-94, allowing for sufficient follow-up to include an estimated 600 incident cases among males and 600 cases among females for the biomarker analyses. The high prevalence of dental infection makes its potential association with inflammatory and dietary mediators, and ultimately increased risk of CHD and stroke very important with implications for millions of Americans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CLONAL DIVERSITY OF ORAL PATHOGENS Principal Investigator & Institution: Chen, Casey C.; Associate Professor and Chair; Periodontics; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2001; Project Start 01-JAN-1999; Project End 31-DEC-2003 Summary: Actinobacillus actinomycetemcomitans and Eikenella corrodens are suspected pathogens in periodontitis but both also occur in healthy individuals. This research plan will (1) examine the variabilities of clonal diversity and stability of these organisms within the host, (2) evaluate the synergism between these organisms in localized juvenile periodontitis, and (3) identify pathogenic clones within species. The degrees of clonal diversity of these organisms within the host vary among subjects. Juvenile periodontitis patients harbor greater numbers of distinct E. corrodens clones than healthy subjects; the differences may result from increased susceptibilities of the patients to repeated infections by exogenous clones. Repeated colonization/infection may result in a reduced clonal stability due to replacement of the resident clones by exogenous clones. Colonization/infection by one organism may predispose the host to colonization/infection by the other organism; the relationship is recognized as synergism between the organisms. Within A. actinomycetemcomitans and E. corrodens, strains associated with health may be relatively harmless while others recovered from infections may be more pathogenic. The objectives of this research plan are to: (1) Compare the degrees of clonal diversity, by AP-PCR, of subgingival A. actinomycetemcomitans and E. corrodens in periodontally healthy subjects and localized juvenile periodontitis patients. (2) Examine the clonal stability of subgingival A. actinomycetemcomitans and E. corrodens. Subjects will be sampled again in 9 and 18 months. A quantitative method will be used to assess and compare the clonal stabilities between subject groups. (3) Determine the correlations in the proportional levels or the degrees of clonal diversity between subgingival A. actinomycetemcomitans and E. corrodens. (4) Examine the genetic distinctions between A. actinomycetemcomitans and
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E. corrodens clones recovered from health and disease by serotyping, AP-PCR genotyping and mutilocus enzyme typing. The study subjects will be limited to AsianAmericans to avoid variations arising from using subjects with different ethnicities, and to examine an ethnic group which is under-represented in previous periodontal disease research. This research plan will provide crucial information regarding the significance of clonal diversity and stability of A. actinomycetemcomitans and E. corrodens in periodontal disease and the synergism between these two organisms, and identify virulent clonal types within these species. The information will be important for the (1) future studies of bacterial virulence factors and (2) prevention and treatment of periodontitis associated with these organisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMMUNITY COMPOSITION AND PHYSIOLOGY OF ORAL BIOFILMS Principal Investigator & Institution: White, David C.; Distiguished Scientist; None; University of Tennessee Knoxville Knoxville, Tn 37996 Timing: Fiscal Year 2001; Project Start 20-SEP-1999; Project End 31-JUL-2003 Summary: Long-term goals of the proposed research are development of simple, quantitative measures of oral microbial (saliva and plaque biofilm) community composition and physiology, examination of temporal and spatial variations in structure/function relationships in oral communities, and characterization of nutrientand environment-dependent shifts in community composition and physiology. These goals seek to elucidate the shifts natural to the progression of plaque biofilms, especially pathogen communities of periodontal disease. The present proposal seeks to define a species-composition measurement using phospholipid-bound fatty-acid (PLFA) profiles of whole-community biomass, and will validate that measurement by correlation with checkerboard hybridization and cultivable flora methods. Analysis of biofilm architecture will be performed using electron microscopy and laser confocal microscopy, and correlation of that data with compositional and physiological data will be performed. Community physiology measures will be established and applied to in vitro biofilm microcosms and defined-species consortia. "Functional blocks" will be defined by characterizing enzymatic activities (proteases, mucin-specific exoglycosidases, urease) as indicators of nutrient-protein catabolism, mucin catabolism, and urea hydrolysis; the rate of glucose fermentation and of acid production as indicators of saccharolytic fermentation and ammonia release as an indicator of amino acid metabolism. Whole-community metabolic profiles will be performed using BiologTM and API-ZymTM technologies. The effects of shifts in nutrient composition and environmental pH will be examined by monitoring community physiology, community composition, and architecture. Hypotheses for the proposed work are: 1) that application of PLFA analysis principles proven effective in community taxonomy of natural samples to oral biofilms will yield rapid and significant information on community composition. PLFA analysis will permit simple, frequent, and informationrich patient monitoring and thus improve our understanding of microbial communitycomposition shifts that underlie the progression of periodontal disease and dental caries. 2) that bacterial community composition and community physiology respond in a understandable manner to shifts in nutrient composition and environmental pH. Composition and physiology are related though not necessarily directly linked. Ecologically induced shifts are presumed to be key factors in the progression of periodontal disease; knowledge of the controls over normal and pathogen communities
38
Periodontal Disease
in plaque will enhance our understanding of cause-and-effect in periodontal disease and caries as well as underpinning development of new intervention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMPREHENSIVE ORAL HEALTH RESEARCH CENTER FOR DISCOVERY Principal Investigator & Institution: Derouen, Timothy A.; Professor and Chairman; Dental Public Health Sciences; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2004 Summary: We propose to establish a comprehensive Oral Health Research Center of Discovery that has its central theme "The basis of oral and craniofacial health and susceptibility to disease: a focus on the child as a key to lifelong oral health." Thus, this Center is designed to address the oral/craniofacial health of children, an approach that has great potential to produce life-long oral health, in a population recently cited by Congress as a priority for NIH. Seven specific aims are delineated which progress from basic research to provide new insight into origins of disease susceptibility in children; to translation of basic knowledge into new diagnostics, tretments, and preventive interventions; to evaluation of the efficacy and effectiveness of the new interventions when applied to populations; to outreach designed to communicate the findings and educate professionals to conduct more research. The Center proposal consists of five cores (administrative, outreach, biometry, basic science, and clinical) and fourteen ongoing funded projects. are affiliated with the Center, which leverages the NIDR investment of $7.96 million direct costs into a Center with budgets exceeding $30.9 million. The projects are organized into four clusters around the topics of innate host defense and mucosal health, periodontal disease, craniofacial disorders, and cries, with cluster coordinators who will organize meetings and ensure communication and collaboration. Quarterly Center-wide meetings with scientific presentations by investigators will encourage inter-cluster collaboration. The Center involves three health science schools (Medicine, Dentistry, and Public Health); Children's hospital and Regional Medical Center, insurance carrier Washington Dental Services; Departments of Health of Washington and Micronesia; and collaboration with four foreign universities. The Center capitalizes on established strengths and activities in basic biological, clinical, behavioral and health services research and brings them to bear on understanding and addressing susceptibility to oral and craniofacial diseases and disorders in children. Highlights include new investigations into basic cellular responses to oral bacterial biofilms, expanding community demonstration research to increase access to preventive dental care for children, enhancing an established unique short-term research training institute for faculty, and follow-up on a Center-sponsored outreach symposium "Children Our Future: Ethics, Health Policy, Medical/DENTAL Care for Children" which has garnered national attention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--DEMONSTRATION Principal Investigator & Institution: Stahl, Gregory L.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: Studies in the area of periodontal disease have defined the crucial factors involved in the inflammatory process including; 1) the role of neutrophils; 2) the role of lipid mediators; 3) identification of bacterial processes in amplifying the inflammatory
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condition; and 4) the role of the hosts innate and humoral immune systems. In support of projects 1-4, and to optimize, centralize and facilitate the discovery of novel, topically active anti- inflammatory and anti-PMN analogues of naturally occurring lipid mediators; this Core will provide and apply established in vivo animal, cellular and organ models, as well as carry out in vitro assays to: a) assist in the discovery of structure/function relationships of novel, topically occurring anti-PMN and antiinflammatory compounds generated in Projects 1-4 and establish their actions in vivo in wild type and genetically altered rabbits. b) provide flow cytometric analysis of cells from Project 1-4. c) provide PMN functional assays in vitro and in vivo. d) provide and develop animal and cellular models/assays for the evaluation of novel therapeutics in periodontitis. Providing a centralized location of these routine tasks to this Core will eliminate costly duplication of these assays/models within the other projects. This Core will optimize productive interactions and resource utilization and provide the other projects with efficient and timely access to novel. Prioritization of the provide the other projects with efficient and timely access to novel cell and in vivo assays. Prioritization of the assays/models will be accomplished through individual meetings between Core D's principal investigators and the Program Project principal investigators and during monthly meetings of the Program Project team. Centralization of these models and assays will facilitate the demonstration and the effectiveness of these novel therapeutics in periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CYTOSKELETAL CELL SURFACE INTERACTION IN ORAL EPITHELIAL CELLS Principal Investigator & Institution: Goldman, Robert; Northwestern University Office of Sponsored Programs Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-MAY-2002 Summary: The objectives of this research are to determine the basic mechanisms that regulate the interactions between cytoskeletal keratin intermediate filaments and the cell surface associated adhesion junctions, desmosomes and hemidesmosomes, of gingival epithelia cells. The long term goal of the proposed studies is to gain insights into the molecular bases of the epithelial cell migration that represents a hallmark of periodontal disease. The specific aims include determining how the intermediate filament associated protein, IFAP300, connects desmosomes and hemidesmosomes to intermediate filaments. To this end, IFAP300 will be cloned and sequenced. Once the complete cDNA sequence is available, transient transfection will be used to determine the physiological functions of this important cross-bridging protein. Other aims are to determine in vitro the molecular interactions among keratins, IFAP300 and the major cytoplasmic plaque proteins of the desmosome (desmoplakin) and the hemidesmosome (BP230). In vivo studies will be targeted at determining the dynamic properties of keratin-intermediate filaments in living cells using microscopic imaging techniques. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DEFENSIN-INDUCED ADAPTIVE IMMUNITY TO HAGB Principal Investigator & Institution: Brogden, Kim A.; U.S. National Animal Disease Center Box 70, Dayton Rd Ames, Ia 50010 Timing: Fiscal Year 2003; Project Start 15-JUL-2003; Project End 31-MAY-2008 Summary: The severity of periodontal disease is dependent on a combination of host, microbial agent, and environmental factors. One strong correlate related to periodontal
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Periodontal Disease
disease pathogenesis is the immune status of the host. Our approach to improve the immune status is to use human neutrophil peptide (HNP) defensins or human betadefensins (HBD), elements of innate host defense, to initiate and regulate the adaptive immune response to foreign antigens. In this Plan, we posit that HNP or HBD, coadministered with Porphyromonas gingivalis antigens to oronasal mucosal surfaces, regulates the adaptive immune response resulting in class switching of antibodies to high avidity isotypes. Results from this work will not only provide fundamental information on the regulating role of defensins in generating adaptive immune responses to various bacterial antigens in the oral cavity but specific preliminary evidence on ways to direct an adaptive immune response to select P. gingivalis antigens that would likely hinder the pathogenesis of periodontal disease and lessen associated inflammation and tissue damage caused by this organism. The following Aims are proposed: 1) to determine if defensins induce an adaptive immune response to bacterial antigens. Preliminary studies suggest that defensins, co-administered intranasally with ovalbumin, induced different antibody isotype, interferon-gamma, and interleukin profiles that were unique to the individual defensin used. We will use hemagglutinin B of P. gingivalis, one of the leading etiologic agents of periodontal disease, as the antigen to assess the ability of defensins to induce a similar response. 2) to assess the nature of the defensin-antigen interaction and the conditions necessary for induced adaptive immunity. We will also use the capsular polysaccharide and fimbrial antigen of P. gingivalis to determine if the nature of the antigen influences the ability of defensins to induce an adaptive immune response. 3) To determine the defensin domain necessary for dendritic cell chemotaxis and activation. HBD2 is chemotactic for immature dendritic cells and may initiate the mechanism for defensin-induced adaptive immunity to microbial antigens. Preliminary studies suggest that HBDs can chemoattract murine dendritic cells, and we will use this assay to determine the chemotactic domain of HBDs and the conditions of HBD-hemagglutinin B interaction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DETROIT DISPARITIES
CENTER
FOR
RESEARCH
ON
ORAL
HEALTH
Principal Investigator & Institution: Ismail, Amid I.; Professor; Cariology/Restor Sci/Endod; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-JUL-2008 Summary: (Provided by the applicant) - The Detroit Center for Research on Oral Health Disparities aims to promote oral health and reduce disparities within the community of low-income African American children (0-5 years) and their main caregivers (14 + years) living in the City of Detroit. The driving theme of the center's research program is to identify determinants and design interventions to answer the following question: why do some low-income African American children and their main caregivers have better oral health than others who live in the same community? The proposed center will focus on studying intra-group disparities in oral health. The community based partners, the City of Detroit Department of Health (DDH) and the Voices of Detroit Initiative (VODI) have strongly supported this theme. The Center will include 3 support cores, 5 research core projects and 1 pilot study. The Center's Methodology Core will select a multistage random sample of African American families living in the poorest 39 Census Tracts in the City of Detroit. A total of 1,529 families will be sampled and interviewed in their homes. It is estimated that 994 families will be examined at community centers in year 2 (2002) funding. Based on extensive data collected by the investigative team (R01
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MH58299) in Detroit, the investigators predict that 760 families will be retained by the third examination phase in year 6 (2006). The research teams will investigate the social characteristics of parents, families, and neighborhoods, that are associated with disparities in oral health (dental caries and periodontal diseases) of children and their caregivers; lead levels in saliva of children and saliva and blood (finger prick) of the main caregivers; dietary intake; and genetic, behavioral, social and bacteriologic risk factors of periodontal disease in adults. Using information from 3 core research projects, the investigators propose to develop a tailored multi-media educational intervention (Project #3), based on the transtheoretical model of behavioral change, which will be administered using a randomized controlled design in year 4 of funding, just prior to the second examination phase. Additionally, the center will evaluate the impact on access to dental care of the state-funded experiment on utilization where Medicaid children are managed like privately insured patients (Project #4). The center will support health professionals from the DDH and VODI and the University of Detroit Mercy to receive research training. Doctoral students in three programs targeting minorities in the Schools of Public health and Social Work will be offered stipends to conduct research on health disparities. All families will have access to dental care in a DDH dental clinic (funded by DDH, HRSA, Delta Dental of Michigan and VODI). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENT AND CHARACTERIZATION OF CD14 DEFICIENT MICE Principal Investigator & Institution: Freeman, Mason W.; Chief; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2001; Project Start 15-FEB-2001; Project End 31-JAN-2006 Summary: (Adapted from the applicant's abstract): CD14 is a 55 kDa glycosyl phosphatidylinositol-linked protein that is also present in a soluble form in serum. CD14 binds lipopolysaccharides (LPSs) derived from the outermost layer of Gram-negative bacteria and activates a signaling cascade that results in the production of inflammatory cytokines that include tumor necrosis factor alpha, interleukin-6, and interleukin-1. This response has been shown to be important in the pathogenesis of septic shock following Gram- negative septicemia. Recent data have also suggested that a similar response may play a role in accelerating atherosclerotic plaque development and in enhancing the formation of the macrophage foam cell, the histologic hallmark of the early atheroma. Several lines of evidence also implicate this pathway in the pathogenesis of PID, a leading cause of infertility in the developed world, and in the phagocytosis of apoptotic cells, an essential event in tissue remodeling and development. Investigators working on inflammatory bowel disease, periodontal disease, and a variety of inflammatory pulmonary disorders have also postulated an important role for CD14 in these conditions. Given the widespread interest in understanding the contributions of CD14 to normal physiology and pathologic conditions, the applicant's laboratory has generated homologous recombinant mice lacking this protein. This grant application proposes to generate a breeding colony of these animals and to distribute these mice to the many investigators that have requested them. These investigators, working on diseases supported by a diverse group of NIH Institutes, can then utilize these animals in experiments that explore the biological processes in which CD14 activity has been implicated. In addition to developing the breeding colony of CD14 deficient mice, this application proposes to characterize the utility of these animals as models for diseases that represent major human health problems in which the principal investigators of the grant have established research efforts. Thus, the CD14 deficient animals will be bred
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Periodontal Disease
into mouse strains that are susceptible to atherosclerosis in order to explore the role of Chlamydial infections in the pathogenesis of cardiovascular disease. In addition, CD14null mice will also be used to explore the role of the endotoxin signaling pathway in mouse models of PID. This work is intended to broaden the applicability of CD14 deficient mice to research involving acute and chronic inflammatory disease and to make a critical animal resource available to the investigative community at large. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENT OF AN HA2 DOMAIN BASED PERIODONTITIS VACCINE Principal Investigator & Institution: Decarlo, Arthur A.; President and Chief Science Officer; Agenta Biotechnologies, Inc. Box 531032 Birmingham, Al 35253 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2002 Summary: ( Applicant's Abstract) Periodontal disease can be diagnosed in >50 percent of adults and may contribute to poor health through oral and systemic infection. The disease process is induced by bacteria and the severity of the disease seems due in large part to the immune response of the host. Over the past decades certain microorganisms have become highly implicated in the pathogenesis of periodontal disease including the gram negative Porphyromonas gingivalis (P. gingivalis). We have recently described and patented a small protein domain from P. gingivalis (HA2) that may be essential for the acquisition of iron and the porphyrin molecule, and, therefore, essential for survival of P. gingivalis in the periodontal pocket. Data indicated that the HA2 domain was detectable in clinical plaque samples and its detection was associated with hemoglobin binding activity within the plaque as well as with periodontal disease severity. Further, data indicated that an IgG humoral antibody response against the HA2 domain was stimulated with periodontal therapy and that this serum IgG could functionally inhibit hemoglobin-binding of the gingipains. These data implicate the HA2 domain of P. gingivalis as a good candidate for vaccine development to inhibit periodontal disease initiation and progression. PROPOSED COMMERCIAL APPLICATION: An effective vaccine against periodontal disease could be applicable to the entire population for the prevention of abatement of bone loss around the teeth that is often accompanied by acute abscess formation and loss of teeth. Notwithstanding malnourishment that accompanies partial or complete edentulism, periodontitis has significant untoward systemic effects so the value of this vaccine in terms of overall medical cost savings is enormous. Current treatment and prevention of periodontitis is ineffective or timeconsuming and expensive. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EARLY ONSET PERIODONTITIS Principal Investigator & Institution: Critchlow, Cathy W.; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2002 Summary: Early onset periodontitis (EOP) encompasses a number of periodontal diseases in children and adolescents that result in rapid destruction of the periodontal attachment apparatus leading to pronounced tooth loss. The prevalence of EOP was estimated to be 0% among African-American, 5% among Hispanic, and 1.3? among white adolescents in a national survey among U.S. school children between the ages of 13-17, and 2.1% among the same age group studied as part of NHANES III. Although risk factors for EOP were investigated, relationships between EOP and the
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microbiological and clinical characteristics of the moth, and effects of the primary dentition and systemic health of children are unknown. Moreover, the occurrence of EOP in systematically compromised children, such as those with human immunodeficiency virus (HIV infection), remain unexplored. We propose a 3 year crosssectional study to assess the correlates of, and specific risk factors for EOP, and to investigate the clinical features, microbial patterns of transmission, and risk to oral and systemic health associated with EOP in Senegal, a site where we currently have ongoing studies among women who have on average 5 children between the ages of 4 and 17, in order to evaluate the following specific aims: (1) Determine specific risk factors for EOP in a Senegalese pediatric population by evaluating demographic factors, health history of both the child and mother, and findings from comprehensive oral examinations including measurements of gingival inflammation and decayed, missing and filled teeth; and (2) Compare the prevalence of specific periodontal bacterial pathogens, and the immune responsiveness to those pathogens among children with and without EOP. Furthermore, we propose to assess whether children of moths with specific periodontal bacteria have comparable microbial patterns, and compare children with and without EOP with respect to humoral immune response to specific periodontal pathogens. We will examine 1,100 Senegalese children of mothers currently being followed in ongoing studies. Presence of EOP will be assessed by probe measurements of all teeth, exclusive of the third molars. Mothers will undergo a standardized interview, and children will undergo oral examination and have paperpoint and blood samples collected. Bitewing radiographs (among children greater than 3 years of age with EOP) will be taken to assess the degree of bone loss. The proposed study will contribute important information which may be useful in designing strategies to prevent periodontitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFECT OF LAMININ-5 PROCESSING ON ORAL EPITHELIAL CELLS Principal Investigator & Institution: Stack, Mary S.; Associate Professor; Northwestern University Office of Sponsored Programs Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-MAY-2002 Summary: Periodontal disease is characterized by degradation of the basement membrane between the junctional epithelium and the tooth, resulting in detachment of the epithelium from the tooth surface followed by apical migration and proliferation of epithelial cells. Formation of this long junctional epithelium precludes attachment of periodontal ligament cells to the root surface, thereby preventing successful healing. Stable attachment of epithelia cells to the internal basal lamina prevents this ling junctional epithelium formation and facilitates repair of damaged periodontal tissue. Ultrastructural data indicate that hemidesmosomes are present at the dento-epithelial junction and contribute to maintenance of normal tissue architecture. A newly described laminin isoform, laminin-5, is involved in an unique integrin-mediated interaction with epithelial cells which can induce hemidesmosome assembly, resulting in the formation of a stable cell:matrix attachment and loss of migratory capacity. However, laminin-5 has also been associated with migrating cells, suggesting a role in mediating cellular motility. To address the differential role of laminin-5 in promoting both gingival epithelial cell adhesion and migration, it is the working hypothesis of this proposal that proteolytic processing of laminin-5 by enzymes present in the gingival microenvironment alters laminin-5 structure and thereby modulates its function. To address this hypothesis, experiments are proposed to analyze the normal processing of laminin-5 which accompanies incorporation into the insoluble extracellular matrix; to
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Periodontal Disease
identify the subunit and site of cleavage of laminin-5 by a variety of proteinases, and to analyze the effect of these proteolytic modifications on cellular functions related to adhesion and migration. A more detailed understanding of the factors which regulate gingival epithelial cell migration may lead to the development of novel therapeutic approaches by which the formation of long junctional epithelium may be inhibited. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFECTS OF PERIODONTAL THERAPY ON PRETERM BIRTH Principal Investigator & Institution: Michalowicz, Bryan S.; Polymer Science & Engineering; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2005 Summary: (provided by applicant): The goal of this proposed multi-center randomized clinical trial is to determine if non-surgical therapy for pregnant women with [periodontitis] reduces the incidence of preterm birth. As noted in the year 2000 Surgeon General's Report on Oral Health, preterm birth and low birth weight are the leading prenatal problems in the U.S. and it has been estimated that the annual costs associated with preterm birth total $5.4 billion. Despite significant efforts to prevent preterm birth, it remains a major cause of neonatal morbidity and mortality. Moreover, preterm birth is more likely to affect minority women who have disparities in health care. Human, animal, and bacteriologic studies have linked periodontal disease with preterm delivery and low birth weight and there are preliminary data indicating that periodontal therapy may reduce the incidence of preterm birth. After obtaining informed consent, this clinical trial will enroll [816 women] who are 13 to 16 weeks pregnant. Volunteers will be recruited from four populations in Minnesota, Mississippi, [Kentucky, and New York City (Harlem)] with high numbers of minorities and high rates of preterm birth. They will be randomly assigned to either a Test [n=408] or a Control [n=408] Group. Test Group subjects will receive non-surgical mechanical periodontal therapy. Control Group subjects will have periodontal therapy delayed until after delivery. All subjects will be monitored and treated as soon as possible if there is evidence of progressive periodontitis and all will receive essential dental care to restore caries and treat abscessed teeth. Maternal risk factors for preterm birth and/or intrauterine growth restriction will be used as covariates in the data analysis. Both Groups will be followed until delivery and the primary birth outcome variable will be gestational age at birth. [We will also document the effect of periodontal therapy on immune response, systemic markers of inflammation, periodontal infection and clinical periodontal measures.] If this study demonstrates that periodontal therapy has a positive effect in reducing preterm birth, it will have enormous public health implications in terms of neonatal mortality, morbidity and cost savings. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EXPRESSION OF PKC ISOFORMS IN HUMAN OSTEOBLASTS Principal Investigator & Institution: Lampasso, Judith D.; Oral Biology; State University of New York at Buffalo Suite 211 Ub Commons Amherst, Ny 14228 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2004 Summary: Twelve isoforms have been identified in the PKC family of serine/threonine protein kinases, which are encoded by different genes. The PKC isoforms are classified as a result of enzymatic and molecular analysis into three major classes. It is known that the isoforms of PKC are major intracellular mediators that control cell proliferation and
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differentiation in a variety of cell systems. The expression and function of the isoforms appear to be tissue specific, and the various isoforms appear to be involved in specific physiological processes. In primary human osteoblasts, the role and expression of PKC isoforms remains to be investigated. We hypothesize that the proliferative process in human osteoblast involves specific isoforms of PKC. The aim of this proposal is to investigate PKC isoforms that are expressed by human osteoblasts and to examine the role that specific isoforms play in osteoblastic cell proliferation. Specific aims are: 1) to determine which PKC isoforms is involved in the proliferative process of human osteoblastic cells. First, known activators of human osteoblastic cell proliferation will be used as tools to determine the isoforms involved in proliferation (PDGF, S1P, serum enriched vs serum deprived human osteoblastic cell cultures will be used). The proliferative responses will be monitored by [3H]-thymidine incorporation and the effects on PKC isoform expression and activation will be determined using Western blotting. Second, to better define the role of specific isoforms in proliferation, antisense oligonucleotides to individual PKC isoforms will be used to inhibit the expression of the isoforms and proliferation will be monitored. 2) To investigate the mechanism by which specific PKC isoforms affect osteoblastic cell proliferation. It will be determined if the effects of PKC isoforms are mediated through Gi and MAP kinase dependent pathways by making use of PTX. The information obtained through these studies should elucidate factors regulating proliferation of human osteoblast and aid in the development of rationale therapeutic to control systemic and local bone loss as in osteoporosis and periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FUNCTION OF B-DEFENSINS IN COMMON ORAL INFECTIONS Principal Investigator & Institution: Guthmiller, Janet M.; Dows Inst for Dental Research; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-MAY-2003 Summary: (adapted from the Investigator's abstract): The most prevalent infections in the oral cavity are represented by periodontal diseases and candidal infections. Both result in an immune response represented, in part, by innate mechanisms. Antibiotic peptides are considered a key component of innate immunity. The beta-defensins are recently discovered antimicrobial peptides produced by epithelial cells whose role in protection against oral infections is as yet unknown. The hypothesis underlying the planned research is that beta-defensins function as antimicrobial agents in periodontal diseases and Candida infections. In this application, the Principal Investigator proposes studies of human beta-defensins 1 and 2 (HBD1 and 2) which they and others have recently found to be expressed in oral epithelia. The following specific aims are proposed for these studies. Aim 1 is to determine the cell-specific localization and expression of HBD-1 and HBD-2 in the oral cavity in health and disease. This aim will be addressed using both in situ hybridization and immunohistochemistry to reveal localization, and ribonuclease protection assays and RT-PCR to indicate expression. Secretion of the peptides will be assessed using Western blots. Aim 2 is to determine what the antimicrobial properties of the human beta-defensins are against periodontal bacteria and Candida. Using recombinant peptides in established antimicrobial assays, the spectrum of antimicrobial activity of the beta-defensins against oral organisms will be determined. Aim 3 is to determine what factors regulate the expression and secretion of beta-defensins in oral epithelia. To understand how beta-defensin gene expression and secretion may be regulated, cultured oral keratinocytes will be treated with candidate regulatory factors including periodontal bacteria, Candida organisms, pro-
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and anti-inflammatory cytokines and glucocorticoids. Expression of mRNA and peptide levels will be examined through the use of ribonuclease protection assays and Western blots, respectively. From these studies the Principal Investigator hopes to increase current understanding of the role beta-defensins play in the innate immunity of periodontal and Candida infections so as to be able to develop new therapeutic modalities against a group of prevalent oral diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC ANALYSIS OF ORAL STREPTOCOCCAL BIOFILM FORMATION Principal Investigator & Institution: Ganeshkumar, Nadarajah; Associate Professor; Molecular and Cell Biology; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: Initial colonization of tooth surfaces by oral viridans streptococci, including Streptococcus gordonii, leads to the eventual formation of biofilms called dental plaque. The most common disease of man, caries and periodontal disease, result from imbalances in the oral microflora, which allow pathogenic species to dominate. Initial plaque formation is characterized by the adhesion of planktonic cells of bacteria such as streptococci to tooth surfaces via specific salivary proteins of the acquired pellicle. Subsequent growth of these initial colonizers and other bacteria on the abiotic surface leads to the formation of dental plaque. Studies have extensively characterized of the initial binding of the planktonic bacteria to saliva-coated/hydroxyapatite surfaces, but the prerequisite signals that trigger the transition from a planktonic to a sessile mode of life and the subsequent accumulation of dental biofilms are poorly understood. It is hypothesized that novel genes are required for initial dental biofilm formation, and identification of such genes and characterization of their expression will be crucial for the development of novel methods of dental plaque control. A simple, but effective method of microbial accumulation on polystyrene surfaces will be used in this study to characterize isolation of biofilm-defective mutants of S. gordonii using Tn916 transposan mutagenesis, (2) characterization of biofilm-defective mutants, and (3) cloning and genetic analyses of biofilm genes. These studies of biofilm formation in streptococci will provide valuable information on the initial stages of dental plaque formation. Understanding the mechanisms involved in biofilm formation will be crucial for the development of novel therapeutic strategies to modify the composition of dental biofilm flora towards that found in health. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC SYSTEMS FOR FUSOBACTERIUM NUCLEATUM Principal Investigator & Institution: Haake, Susan K.; Assistant Professor; Periodontics; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-JUN-1998; Project End 31-MAY-2003 Summary: (Adapted from investigator's Abstract): Fusobacterium nucleatum is an important pathogen that is commonly involved in periodontal disease and other common human infections. Little is known about the virulence mechanisms of this pathogen and investigation has been hampered by a lack of systems for genetic manipulation. The importance of F. nucleatum in oral and systemic diseases has led to interest in genomic sequencing within the next few years. Systems for molecular
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analysis will be required to effectively utilize sequence data in the study of virulence properties. The Principal Investigator's laboratory has recently isolated and characterized a F. nucleatum plasmid, pFN1. In this proposal, the hypothesis to be tested is that pFN1 can be used to develop a system of gene transfer as well as a host vector system for the application of molecular techniques in F. nucleatum. In Specific Aim 1 a gene transfer system for F. nucleatum will be developed using electroporation with pFN1-based plasmids that encode a tetracycline selectable marker. Transformation studies will identify a "first generation" shuttle plasmid, a F. nucleatum strain with high transformation efficiency, and additional antibiotic resistance determinants that confer a selectable phenotype in F. nucleatum. The gene transfer system will be optimized in Specific Aim 2 through refinement of both the shuttle plasmid and the transformation procedures. Characterization of the pFN1-based plasmids will include confirmation of the theta mechanisms of replication, and determination of segregational and structural stability, the pFN1 minimal replicon, and the plasmid copy number. A "second generation" plasmid will be developed by eliminating nonessential regions of the pFN1 DNA. The efficiency of transformation will be optimized with the second generation shuttle plasmid and evaluated in representative F. nucleatum strains. A chromosomal integration plasmid for F. nucleatum, which lacks a F. nucleatum replicon but contains F. nucleatum genomic DNA sequences and a tetM determinant, will be developed in Specific Aim 3. The genomic organization of transformants will be evaluated by Southern and PCR analyses to confirm the chromosomal integration, and to characterize the site and mechanism of integration. The results of these studies will create the foundation for genetic analysis in F. nucleatum by developing molecular techniques of mutagenesis and complementation. Because systems of gene transfer are not currently available for F. nucleatum, these results will have significant impact on our understanding of F. nucleatum virulence and potentially in the prevention of human infectious diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETICS OF BACTERIALLY-INDUCED ALVEOLAR BONE LOSS Principal Investigator & Institution: Baker, Pamela J.; Associate Professor; Biology; Bates College Lewiston, Me 04240 Timing: Fiscal Year 2001; Project Start 01-MAY-1994; Project End 31-MAR-2003 Summary: (adapted from the Investigator's abstract): Periodontal disease among adult humans is a significant public health burden. It is strongly associated with the gramnegative bacterium, Porphyromonas gingivalis, yet bacteria alone do not explain population variance in the disease. There is a notable genetic component to both disease incidence and severity. Mouse models have proven extremely valuable in dissecting the pathobiology of various diseases. Modern molecular genetics, including quantitative trait locus (QTL) analysis, is a powerful tool for unraveling the genetic polymorphisms underlying various diseases in the mouse, including susceptibility and resistance to infectious diseases. Large portions of the murine genome are shared with the human genome, so that identification and localization of murine loci have facilitated discovery of their human counterparts. During the current support period, the Principal Investigator has developed a mouse model in which alveolar bone loss is reliably induced in mice by oral infection with P. gingivalis. In collaboration with Dr. Derry Roopenian of The Jackson Laboratory, knockout mice with various discrete immunodeficiencies have been used to identify several factors that contribute to bone loss. The Principal Investigator has also found that different strains of immunocompetent mice differ in their susceptibility to bone loss after oral infection.
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Through F1 crosses and backcross of these mice, we have initial evidence that susceptibility and resistance to P. gingivalis- induced alveolar bone loss are heritable traits. It is proposed to study the genetic basis for this susceptibility and resistance. First, the pathophysiological processes that coincide with bone loss in this mouse model will be further characterized and other phenotypic biomarkers will be developed that correlate with bone loss. Second, QTL analysis will then be used to identify chromosomal regions associated with susceptibility and resistance. Together these aims will provide a fuller description of the pathobiology of P. gingivalis-induced alveolar bone loss and will allow the Principal Investigator to map loci and alleles involved in susceptibility and resistance. Mouse strains developed in this investigation will be available for others to study. Knowledge of the genetics gained here has a high likelihood of contributing to the identification of candidate genes in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GOLDENSEAL(HYDRASTIS CANADENSIS)REMEDY FOR ORAL DISEASES Principal Investigator & Institution: Wu, Christine D.; Associate Professor; Periodontics; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2001; Project Start 15-APR-2001; Project End 31-MAR-2003 Summary: (APPLICANT'S ABSTRACT): Complementary and alternative medicine (CAM) has recently gained popularity with the American public. Research validating CAM has focused mainly on the treatment and prevention of systemic medical diseases while less attention has been paid to oral diseases. Oral diseases including dental caries and periodontal disease, are a major cause of loss of work and school days. Chemical and mechanical means have been used to control dental plaque bacteria, the etiologic agent of caries and periodontal disease. However, none of the available agents is ideal and frequently cause adverse effects. This justifies further search and development of alternative agents from natural sources that are safe and effective. The North American plant, Hydrastis canadensis L. (Ranunculaceae), known commercially as "Goldenseal," has been used for centuries as an antiseptic to treat skin disorders and as an antidiarrheal, antiseptic, astringent, hemostatic, and vasoconstrictor agent. Goldenseal is one of the major phytomedicines ("herbal remedies") sold in health food stores and pharmacies in the U.S. Several mouthrinses and toothpastes containing Goldenseal are available on the market. Although claims have been made by the manufactures regarding its ability to fight gum diseases and prevent caries, no scientific data is available to substantiate these claims. The goal of the proposed research is to evaluate the potential of Goldenseal as a remedy in prevention and treatment of oral diseases and to maintain oral health. It is hypothesized that antimicrobial compounds that are safe for humans can be identified from H. canadensis. These compounds may have potential as dental prophylactic/therapeutic agents and may also serve as lead compounds for the subsequent design and synthesis of new agents that are even more effective than the existing ones. The Specific Aims of this study are: SA1: To isolate and identify active antimicrobial compounds from H. canadensis by activity-guided fractionation and characterization; SA2: To determine antimicrobial activity of the purified compounds against cariogenic and periodontal pathogens; SA3: To investigate mixtures of purified antimicrobial compounds from H. canadensis for synergistic antimicrobial activities; SA4: To correlate bioactivity of various commercially available Goldenseal-containing oral hygiene products with levels of active alkaloids identified in SA2. The proposed research is innovative in that it represents collaboration between an oral microbiologist and a natural product chemist that will assure the speedy discovery of novel or known
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active compounds from Goldenseal and will provide scientific explanation as to the remedy's efficacy. It will also serve as a model system for the evaluation of existing herbal remedies for their oral health related claims. This application of CAM research will help to achieve better oral health and oral disease prevention, one of the to priority areas of focus specified b the U.S. Public Health Service in "Health People 2000." Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GORDON CONFERENCE--BIOLOGY OF THE SPIROCHETES Principal Investigator & Institution: Weis, Janis J.; Professor; Gordon Research Conferences Box 984, 512 Liberty Ln West Kingston, Ri 02892 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2002 Summary: The fifth Gordon Research Conference on the Biology of Spirochetes will be held in January 2002 in Ventura, California. The Biology of Spirochetes Conference is unique. This is the only ongoing international meeting devoted to discussions on basic research of all medically important and biologically relevant spirochetes, a unique group of Eubacteria. Many spirochetes are pathogens and cause a variety of diseases, including syphilis, Lyme disease, relapsing fever, leptospirosis, periodontal disease, digital dermatitis of cattle, and swine and human dysentery. Historically, spirochetes have been difficult to study. These bacteria often have fastidious nutritional requirements and some have yet to be successfully cultured in vitro. Methods for genetic manipulation and mutational analysis of several spirochete species do not exist. The opportunity for exchange of ideas among groups working on different spirochetes has been one of the greatest benefits of past conferences, particularly in the area of new techniques for genetic manipulation. The application of genetic advancements and the availability of genomic sequences of Borrelia burgdorferi, Treponema pallidum, T. denticola, and new sequencing projects in Leptospira spp, are proving a wealth of new information. Combined, these data are being integrated into ongoing studies on the physiology, structure, pathogenesis, and immunobiology of these bacteria. Each of the previous Biology of Spirochetes conferences have been highly successful, receiving high praise by attendees, forging new collaborations, providing a forum for presenting stateof-the-art research on these bacteria, and helping to set new research directions. As in previous conferences, we expect attendance at the 2002 conference to reach the maximum of 150 faculty, graduate students, postdoctoral fellows, and industrial scientists. A broad spectrum of scientists representing different research interests, geographic locations, and seniority will be invited to attend. Special efforts will be made to insure strong attendance of young investigators (graduate students, post-docs and junior faculty), and achieve a balance in gender and ethnicity of attendees. The oral and poster-presentations are organized to provide many opportunities for discussion, the exchange of ideas, and development of collaborations. Funding from the National Institutes of Health is requested to partially offset the travel and registration expenses of the participating graduate students, fellows, and junior faculty members. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GUIDED POCKET RECOLONIZATION (GPR) IN PERIODONTITIS Principal Investigator & Institution: Quirynen, Marc; Catholic University of Louvain Naamsestraat 22 Louvain, Timing: Fiscal Year 2003; Project Start 04-APR-2003; Project End 31-MAR-2005 Summary: (provided by applicant): Periodontitis is an infectious disease resulting in an often-painless destruction of tooth supporting tissues (the periodontium) and enhances
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the risk for various systemic diseases including atherosclerosis, coronary heart disease, stroke and infants with low birth weight. Active periodontitis occurs in a susceptible host and in the presence of pathogenic species in combination with low concentrations of so-called "beneficial bacteria". The success of periodontal therapy primarily depends upon dealing with the negative environmental/behavioral factors and the reduction/elimination of periodontopathogens in combination with the reestablishment of a more suitable environment (less anaerobic) for a beneficial microbiota. Even after therapy, the presence of pathogenic species in subclinical levels is often encountered so that there remains a continuous threat for further periodontal destruction and disease. Therefore, this project aims to improve treatment outcome by guiding the periodontal pocket recolonization after periodontal therapy by local administration of beneficial bacteria (probiosis). An optimal mixture of known beneficial periodontal bacteria will be determined in vitro by investigating the adhesion of these bacteria to dentine- and enamel surfaces and epithelial cells in relation to their probiotic effect using flow cell microscopy and fluorescence microscopy. The in vivo effects of the therapy will be evaluated using a split mouth study design in a beagle dog model for periodontitis. After lesion induction and establishment of severe periodontitis in 8 beagle dogs (20 lesions/dog), 8 lesions do not receive treatment (reservoir for pathogenic recolonization of the treated lesions), 4 lesions receive mechanical debridement (classic strategy), 4 lesions receive mechanical debridement followed by a single subgingival application of the probiotic mixture (experimental treatment 1) and 4 lesions receive mechanical debridement followed by a repeated subgingival application (week 1, 2 and 4) of the probiotic mixture (experimental treatment 2) in each dog. Plaque samples will be obtained from all pockets after 2, 4, 6, 8, and 12 weeks and evaluated via standard culture techniques and checkerboard DNA-DNA hybridization. Clinical data will be collected after 2, 4, 6, 8 and 12 weeks. The results should indicate the possible role for commensal organisms in periodontal disease and subgingival biofilm formation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HIV AND NEUTROPHIL FUNCTION IN ORAL DISEASE Principal Investigator & Institution: Thomas, Larry L.; Associate Professor; RushPresbyterian-St Lukes Medical Ctr Chicago, Il 60612 Timing: Fiscal Year 2002; Project Start 03-SEP-2002; Project End 31-AUG-2004 Summary: (provided by applicant): Neutrophils play a key and essential role in the innate immune response against candida infection, which is the most frequent oral manifestation of HIV infection. Results obtained with neutrophils isolated from blood of HIV-infected individuals have variously demonstrated that neutrophils of HIV-infected individuals display increased apoptosis, constitutive activation, and diminished responsiveness to inflammatory stimuli. It is not known, however, how HIV infection influences the functional status of neutrophils within the oral cavity. It is postulated that an alteration in neutrophil function contributes to the increased incidence of candidiasis and periodontal disease in HIV-infected individuals. Moreover, a second role for neutrophils in HIV infection is suggested by the findings that neutrophils bind HIV-1 and increase infection of T lymphocytes as well as increase viral replication in HIVinfected PBMC. Consistent with this postulated role, increased shedding of HIV-1 is observed with gingival linear erythema, which is frequently associated with candida infection and, thus, also an influx of neutrophils into the oral cavity. The relationship between the neutrophil functional status and the capacity of neutrophils to enhance HIV infection and replication, however, is not known. This relationship may be directly
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relevant to the vertical transmission of HIV infection to infants via breast-feeding by HIV+ mothers, which remains an important route of infant HIV infection in underdeveloped countries. Indeed, oral candidiasis in infants is a risk factor for the vertical transmission of HIV infection via breast milk by HIV+ mothers. Accordingly, this proposal has two specific aims. (1) Does dysregulation of neutrophil function contribute to the increased incidence of oral candidiasis and periodontal disease in HIV-infected patients? (2) Does activation or apoptosis alter the capacity of neutrophils to bind HIV and/or to enhance HIV infection and replication of macrophages or lymphocytes? It is proposed that the results of this study will provide important insight into the essential role of neutrophils in innate immunity within the oral cavity of HIVinfected patients and also into a possible role of neutrophils in the vertical transmission of HIV infection. As such, the results may provide an additional target to enhance innate immunity within the oral cavity and also to decrease the vertical transmission of HIV in breast milk. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IDENTIFY PERIODONTITIS
ANTIGENIC
DETERMINANTS
OF
HUMAN
Principal Investigator & Institution: Teng, Yen-Tung A.; Associate Professor; University of Western Ontario 1151 Richmond St N London, Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2002 Summary: Human periodontal diseases (e.g., periodontitis) are heterogeneous and result from specific bacteria-host immune interactions. Periodontitis is the major cause of tooth loss in adults and has been recognised as a significant risk factor associated with coronary heart disease, stroke and bacterial pneumonia. The long-term objective of this research program is to identify bacterial antigens important for immune and inflammatory responses in human periodontitis. Engraftment of immunodeficient NOD/SCID mice with human peripheral blood leukocytes (HuPBL) provides an excellent model for studying immune responses to inoculated pathogens. The applicant proposes to use this unique system and a well characterized clinical entity, Actinobacillus actinomycetemcomitans:Aa-associated localized juvenile periodontitis (LJP), to study the immune basis of human periodontitis, for which no animal model exists and which, for ethical and practical reasons, cannot be directly studied in humans. The applicant has shown that oral inoculation of live Aa into NOD/SCID mice carrying high levels of (up to 60 percent) HuPBL from periodontitis patients can be achieved. Further, engrafted human leukocytes present in mouse periodontal tissues can functionally respond to Aa challenge. Therefore, microbial antigen-specific immune responses of LJP can be studied in this model. The specific aims of this proposal are: 1) to identify Aa-antigens involved in LJP using a genetic screening approach, and 2) to assess the periodontal immune responsiveness elicited by the identified Aa-antigens in the current animal model. Identification of Aa-antigens will be achieved by screening an Aa genomic-DNA library in transformed E. coli. This would allow the expressed Aaantigens to be captured by patient's antigen-presenting cells which will present and activate the same host's periodontal CD4+T-cells carrying an activation marker for visual identification as probes. The Aa antigens identified will be assess by in vitro T-cell activation (by IL-2) and B-cell IgG antibody (by ELISA) assays for specificity and correlation analyses in LJP and LJP-free subjects. The new information obtained from the proposed studies will provide rationales and hypotheses to investigate the clinical correlates and significance for important bacterial antigens involved in Aa- associated LJP. Further, it will increase our knowledge of host immune-parasite interactions and
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could eventually lead to the development of new protocols (e.g., Mabs or vaccines) for the treatment of human periodontal diseases. Therefore, the patient's periodontal health will be improved, thereby their complications and health-care costs will be reduced. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IGA1-REGULATION OF COMPLEMENT IN PERIODONTAL DISEASE Principal Investigator & Institution: Boackle, Robert J.; Professor; Stomatology; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-MAY-2003 Summary: (abstract verbatim) Uncontrolled complement activation plays a fundamental role in collateral host tissue damage during chronic inflammatory periodontal disease. Our preliminary evidence suggests that specific serum IgA1 antibodies (e.g., produced within the inflamed submucosal periodontal tissues), normally work in conjunction with serum C1-inhibitor (the rate-limiting component of the classical complement pathway) to be one of the main factors in properly regulating complement and limiting the subsequent immunopathological tissue damage. We hypothesize that to function properly, these IgA1 antibodies must escape digestion by bacterial IgA1 proteases. In preliminary studies, specific human IgA1 antibodies, when bound to immobilized dansylated-BSA (DNS-BSA) antigen, displayed a tightly controlled ability to activate the classical complement pathway. The tightly controlled C1 mediated C4b deposition was best detected after short incubation times with neat fresh human serum. We hypothesize that deposition of C4b on the alpha-1 tailpiece carbohydrate is important because of the subsequent weakened IgA1-C1 avidity resulting in enhancement of C1-inhibitor mediated irreversible elimination of C1 function. Genetically engineered human IgA1 mutant antibodies, deficient in carbohydrate in the CH2 region, exhibited C1 activating properties approaching human IgG1-DNS-BSA. Therefore, the tightly-controlled complement activation by specific IgA1 appears to be directly related to the position of the Fc-carbohydrate. We propose that IgA1 tightly regulates complement's role in submucosal immunity and inflammation and we are beginning to define a new role for IgA1 antibodies in controlling complement-mediated periodontal tissue damage. IgA1 function is especially necessary at the earliest stages of inflammatory periodontal disease, before local C1-inhibitor levels become partially depleted by neutrophil elastase. Genetically engineered human IgA1 antibodies (to dansyl), which have sitespecific carbohydrate deficiencies on the CH2 and/or CH3/tailpiece will be used to accomplish the following objectives: 1) To ascertain a new function for IgA1 antibodies in regulating C1 via the enhancement of C1-inhibitor especially as a consequence of C4b and C3b deposition on the Fc-carbohydrate and to determine the overall affect on C1 and C1-inhibitor when IgA1 antibodies are co-deposited with IgG1 antibodies; and 2) To ascertain the relative potential of Fc alpha-1 fragments (released by specific bacterial IgA1 proteases) to bind C1q, activate C1 and/or to competitively block IgG1 immune complex and IgA1-immune complex interactions with C1. The results of these studies will provide needed information about the mechanisms that defeat proper complementmediated host responses during inflammatory periodontal disease and will allow the systematic development of treatment strategies to prevent these harmful effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IMMUNODOMINANT STRESS PROTEINS OF P. GINGIVALIS Principal Investigator & Institution: Lopatin, Dennis E.; Professor; Biologic & Materials Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-APR-1996; Project End 31-MAY-2006 Summary: Studies performed in our laboratory implicate the Porphyromonas gingivalis HtpG stress protein, the prokaryotic homologue of Hsp90, in the etiology of periodontal disease. We have reported that elevated levels of anti-Hsp90 antibodies, concomitant with P. gingivalis colonization, are associated with periodontal health. Transcription of HtpG message was also found to be upregulated 7-10-fold in P. gingivalis obtained from diseased subgingival plaque. There is a precedence for Hsp90 homologues contributing to pathogenicity of other microorganisms. Immunity to a single Hsp90 epitope of Candida albicans has been demonstrated to confer protection against systemic candidiasis. Studies performed by our laboratory have revealed that P. gingivalis HtpG has a significant degree of homology with human Hsp90, but remains clearly distinct from other HtpG proteins due to its unique C-terminal region. We have found that HtpG is localized to P. gingivalis membranes and extracellular vesicles, and that it crossreacts with other prokaryotic and eukaryotic Hsp90 homologues. Our findings suggest that HtpG is readily accessible to participate in host cellular invasion processes, as well as to interfere with normal host cell functions one P. gingivalis enters the host cytoplasmic compartment. Transfection of KB cells with the P. gingivalis htpG gene stimulates IL-8 production by these cells. This application proposes to extend our investigations into the role that molecular mimicry by HtpG plays in the pathogenicity of P. gingivalis. Previous studies of other pathogenic microorganisms which appear to use the Hsp90 homologue as a virulence factor have been purely descriptive. Our application is unique in that while will propose to evaluate the role of HtpG in adherence and invasion mechanisms, we also propose to elucidate novel pathogenic mechanism(s) by which microorganisms such as P. gingivalis utilize molecular mimicry to disrupt normal eukaryotic cell function(s). Since the most clearly defined eukaryotic Hsp90-mediated mechanisms involved signal transduction pathways, these will be the primary foci of our investigations. The hypothesis to be tested in this study is: 1) HtpG plays a role in adherence and invasion of host cells; and 2) once internalized, signal transduction mechanisms mediated by Hsp90/TRAP1 within eukaryotic cells are disrupted by the HtpG of P. gingivalis through molecular mimicry. This leads to disruption of normal inflammatory cytokine responses to microbial invasion by P. gingivalis and other oral microorganisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INNATE HOST DEFENSE AND ORAL EPITHELIAL CELL FATE Principal Investigator & Institution: Clark, Edward A.; Professor; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2004 Summary: The tumor necrosis factor (TNF) and TNF receptor (TNFR) families play essential roles in regulating the role of cells during development and inflammatory processes, yet relatively little is known about how they regulate inflammatory responses and wound healing in the oral cavity. We will examine how CD40, CD95 and other TNFR members regulate the fate of gingival epithelial cells (GECs). Very little is known about why children by-in-large re resistant to periodontal disease and what resistance mechanisms break down in individuals who develop early onset periodontitis and the
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Periodontal Disease
associated tissue destruction in the oral cavity. This project will investigate not only how the fate of GECs is normally regulated but also how oral bacteria influence the growth or death of GECs. These studies will contribute to the understanding of the molecular basis of resistance or susceptibility to initial invasion by oral cavity pathogens. Our specific Aims are: 1) To test the hypothesis that CD40 or CD95 regulate the expression of TNFR family members on GECs, thereby making them susceptible to apoptosis. The ability of Fas mAB, CD40 mAb, soluble TNF- alpha or TRAIL to induce apoptosis of activated GECs will be evaluated. We will test if GECs express CD40L, FasL, TRAIL and TNF-alpha and in particular if Fas ligation may influence death or inflammatory responses in the gingival mucosa; 2) To test the hypothesis that death pathwayassociated genes are regulated by CD40 and Fas receptors in GECs. The set of death pathway-associated genes induced in GECs by CD40 will be evaluated in depth for possible roles in regulating epithelial cell fate; 3) To tet the hypothesis that oral bacteria regulate gingival epithelial cell fate and dendritic cell fate. GECs or CD1+ DCs will be exposed to planktonic bacteria or biofilms of periodontopathic Porphyromonas gingivalis (Pg), and an early plaque bacterium. Streptococcus gordonii (Sg). Induction by planktonic Pg or Sg or biofilms of chemokine receptor, TNF/TNFR family members and cell fate genes will be compared. Further understanding of cell death processes in epithelial and dendritic cells could also lead to new insights into how bone formation, regeneration and wound healing in the periodontium are regulated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INNATE IMMUNITY AND PERIODONTAL DISEASE IN MICE Principal Investigator & Institution: Stashenko, Philip P.; Senior Member of the Staff and Head; Forsyth Institute Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 15-APR-2001; Project End 31-JAN-2005 Summary: This is a revised application to study the role of elements of innate immunity in the pathogenesis of periodontal disease. Specifically, a novel model of P- and Eselectin deficient mice (P/E(-/-)) will be utilized to investigate the role of innate immunity, specifically, Toll-like receptors (TLR), in periodontal disease. Previous studies have shown that P/E(-/-) mice develop a progressive periodontitis that is initiated shortly after tooth eruption, and is characterized by an oral flora that is increased in mass and pathogenicity, gingival inflammation, increased expression of the bone resorptive cytokine IL-1, and extensive bone loss. Moreover, antibiotic treatment completely prevents bone loss. It is suggested that this model offers advantages over other systems, including the naturally occurring nature of the disease, the rapidity of periodontal destruction, the ability to control and manipulate the oral flora and the host immune response, and the availability of a vast array of reagents and geneticallyengineered strains. The investigators will test the hypothesis that periodontal destruction can be ameliorated by modulating TLRs, their signaling pathways, and the cytokines that they induce. The proposed study is divided into four Specific Aims: 1) to identify the periodontal pathogens that are responsible for disease in P/E(-/-) mice; these studies will utilize 16S rRNA sequencing to characterize the oral flora in P/E(-/-), P/E(+/+) , and antibiotic treated mice; 2) to determine the immune mechanisms activated by pathogens in P/E(-/-) mice. Cell infiltrates, cytokines and Toll-like receptors (TLRs) will be characterized in vivo and in vitro; 3) to determine the function of TLRs in cytokine and co-stimulatory molecule expression in response to pathogens. Dominant negative constructs of TLR signal transducing molecules will be used to inhibit TLR responses and the effect on pathogen-induced cytokine responses determined. Also, the role of TLRs in skewing the immune response towards a Th1 and
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Th2 profile will be assessed; 4) to determine the roles of TLRs and cytokines in periodontal bone destruction. Knockout mice and modulation of IL-1, IL-6 and IL-10 will be used to establish the role of these factors in periodontal bone loss. The long-term goal of these studies is to determine the role of innate immunity in periodontitis and to apply this information to the development of immune modulators that ameliorate disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INTERGENERIC SIGNALING MOLECULE OF STREPTOCOCCUS CRISTATUS Principal Investigator & Institution: Xie, Hua; Meharry Medical College 1005-D B Todd Blvd Nashville, Tn 37208 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: Dental plaque (biofilm) has been implicated as a primary causative agent of adult periodontal disease. The key event leading to initiation of the disease is the transition from commensal dental biofilm to pathogenic biofilm. It is well known that the process of the transition is involved in the colonization of several specific periodontal pathogens such as Porphyromonas gingivalis. Our long-range goal is to understand events and factors leading to the transformation of healthy plaque to pathogenic plaque and to change the course of development of periodonpathogenic biofilm by preventing attachment of P. gingivalis. In our ongoing studies, we have identified several environmental factors that can influence expression of fimA gene, a virulence gene encoding a major protein unit (fimbrillin) of fimbriea. One of the striking findings is that the presence of Streptococcus cristatus molecule(s) could significantly repress fimA expression in P. gingivalis at the transcriptional level. As a result, S. cristatus could inhibit the formation of P. gingivalis biofilm in vitro. In this grant proposal, we will put our focus on characterization of S. ctristatus signaling molecule, biochemically and genetically. The hypothesis for this proposal is that S. cristatus plays an important role in impeding P. gingivalis' colonization on dental biofilm through intergenric signaling systems. To test this hypothesis, we will start with identification and purification the signaling molecule(s) of S. cristatus. The signaling molecule will be characterized in the terms of functional and genetic structures. We will also attempt to understand regulation of the signaling gene expression in oral biofilm. Therefore, the signaling gene of S. cristatus will be cloned. The promoter region of the gene will be fused with the reporter gene such as chloramphenical acetyltransferase gene, and level of the gene expression will be determined by measuring enzymatic activity. Finally the role of this molecule in the formation of pathogenic oral biofiim will be investigated. Studies will be initiated to determine the distribution of the signaling molecule in the dental plaques from healthy subjects and pedodontitis patients. Our ultimate goal is to convert the knowledge gained from these laboratory studies to practical technology that may be used to reprogram development of the dental biofilm and to reduce the incidence of adult periodontitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: JUNCTIONS CYTOSKELETON AND MATRIX OF THE ORAL EPITHELIUM Principal Investigator & Institution: Jones, Jonathan C.; Professor; Cell and Molecular Biology; Northwestern University Office of Sponsored Programs Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-MAY-2002
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Summary: During the development of periodontal disease, the junctional epithelium undergoes an aberrant migration over the tooth surface. In addition, a pocket is formed between the tooth and epithelium which can harbor bacteria. A combination of bacterial infection and inflammation results in epithelial and connective tissue destruction, leading to loosening of a tooth and eventual tooth loss. We propose that the migration of epithelial cells which is part of the pathology of periodontal disease involves modulation in those elements of the cytoskeleton, cell-cell and cell-matrix adhesive machinery which contribute to epithelial tissue homeostasis. To this end, in this application, we intend to study the dynamics and functions of the keratin elements of the cytoskeleton, desmosomal and hemidesmosomal cell junctions and a laminin component of the extracellular matrix. The proposal details a multidisciplinary, interdependent series of studies from four investigators at Northwestern University Medical School. Project 1, "Laminin-5 and hemidesmosomes in oral epithelial cells" will involve identification of the functional domains of laminin-5 and its role in nucleation of assembly of hemidesmosomes which tether oral epithelial cells to the tooth surface and to the gingival connective tissue. In addition, the nature of laminin-5-cell surface interactions will be evaluated. In Project 2, "Effect of laminin-5 processing on oral epithelial cells", normal processing of laminin-5 as well as its degradation via proteinases present in the oral cavity will be studied. Analyses of the function of laminin-5 fragments that result from matrix degradation will be evaluated at the cell biological level. Project 3, "Cytoskeletal-cell surface interactions in oral epithelia cells" will investigate the dynamic aspects of keratin networks in oral epithelial cells and the molecular mechanisms underlying keratin- cell surface associations. In Project 4, "Cellcell junction structure and dynamics in oral epithelia", molecular genetic approaches will be used to investigate protein-protein interactions in desmosomes which link oral epithelial cells together into sheets. In addition, growth factor and proteinase regulation of junction structure will be studies. These studies are expected to provide new insights into the role of cytoskeletal, junctional and matrix proteins in the maintenance of oral epithelial tissue integrity and their potential contribution to the development of periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MATERNAL PERIODONTITIS AND ADVERSE PREGNANCY OUTCOMES Principal Investigator & Institution: Pitiphat, Waranuch; Postdoctoral Fellow; Oral Health Policy & Epidem; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2003 Summary: (provided by applicant) We propose to evaluate whether periodontitis is a risk factor for adverse pregnancy outcomes. The published studies evaluating these associations are few, small, mostly retrospective and show inconsistent results; although relative risks as high as 7.5 have been reported. We plan to add an oral component to the ongoing Project Viva, a prospective study of 6,000 pregnant women, to evaluate this association. Maternal infection during pregnancy has been demonstrated to play an important role in etiology of preterm delivery. Periodontal infection can serve as a reservoir of gram negative anaerobic organisms and their products, and proinflammatory mediators which could target the placental membranes via systemic circulation thus leading to preterm delivery or fetal growth restriction. The primary aim of this study is to examine the effect of maternal periodontitis on length of gestation and fetal growth. The secondary aim is to explore the association between periodontitis and
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serum levels of TNF-alpha. The proposed prospective nested case-control study will request pre-existing radiographs from Viva participants. Cases will be mothers who give birth to a preterm infant and mothers who give birth to a restricted fetal growth infant. Controls will be mothers with normal pregnancy outcome. We will enroll all cases and a random sample of controls in a 1:3 ratio, frequency matched by race, age and smoking status. Periodontal bone loss as a result of chronic periodontitis will be evaluated from the pre-existing radiographs. Viva participants who report having x-rays taken within last 5 years will be requested on the supplemental questionnaire after delivery to provide their existing dental radiographs or the name and address of the dentist who has these. We will then request the participants' dentists to provide existing bitewing radiographs. The radiographs will be interpreted by one well-calibrated dentist by using a visual categorization method. We will employ multivariate analyses to adjust for potential confounders. In addition, we will perform the analysis of TNFalpha using blood samples that were pre-collected at first prenatal visit in Project Viva's pilot study (Pregval Study) to evaluate one potential pathway relating periodontitis and adverse pregnancy outcomes. The proposed study will help us clarify the relationships between periodontal disease and adverse pregnancy outcomes. Since periodontal disease is a highly prevalent condition that can be controlled, understanding these relationships is of significant importance, both for individuals and for public health policy aiming to improve the well-being of mothers and infants. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MATRIX METALLOPROTEINASES AND DIABETIC NEPHROPATHY Principal Investigator & Institution: Thrailkill, Kathryn M.; Arkansas Children's Hospital Res Inst Research Institute Little Rock, Ar 72202 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Matrix metalloproteinases (MMPs) are a family of zinc-dependent proteinases that are involved in the breakdown and remodeling of extracellular matrix (ECM). Dysregulation of MMP activity has been implicated in many pathologic processes characterized by degradation of connective tissue matrices, including rheumatoid arthritis, periodontal disease and metastatic cancer. Recent studies both in vitro and in animal models of diabetes suggest that hyperglycemiamediated alterations in MMP secretion, activation or action may also contribute to the development of diabetes-related complications including diabetic retinopathy and nephropathy. Based on these findings one can hypothesize that the mesangial accumulation and renal hypertrophy characteristic of diabetic nephropathy may result from reduced matrix degradation caused by a hyperglycemia-mediated suppression of renal MMP activity. In fact, preliminary clinical data from our laboratory confirm that in children with type 1 DM, serum MMP-2 concentrations are suppressed in the face of uncontrolled hyperglycemia, yet normalize with near-normalization of blood glucose levels. In the present study, we propose to investigate the hypothesis that MMPs are involved in the pathogenesis of diabetic nephropathy by measuring concentrations of specific MMPs (MMP-2, -8 and -9), concentrations of the naturally occurring inhibitors of MMPs (Tissue Inhibitor of Matrix Metalloproteinases, TIMP-1 and -2), and concentrations of the MMP-activated growth factor, insulin-like growth factor-I (IGF-I) in the serum and urine of patients with type 1 DM. We will examine levels of MMPs, TIMPs, and IGF-I in these biologic fluids among diabetic patient subgroups, ages 14-40 years, chosen to represent various time points in the natural history of d abet c nephropathy. Moreover, we will examine the correlation between observed differences in MMPFl'lMP/IGFconcentrations and differences in glycemic control at the time of
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study, as indicated by HbA1 c measurements and concurrent (72 hour) Continuous Subcutaneous Glucose Monitoring (CGMS). We anticipate that this study will provide preliminary evidence to establish a link between dysregulation of MMP activity and the pathogenesis of nephropathy in type 1 DM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF PERIODONTAL DESTRUCTION Principal Investigator & Institution: Graves, Dana T.; Professor; Oral Biology; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 08-SEP-1999; Project End 31-JUL-2003 Summary: Periodontal tissue destruction involves the elicitation of a host-response by oral pathogens capable of invading the connective tissue. A prominent bacterium in periodontal infections is P. gingivalis, which produces two well defined virulence factors, LPS and fimbriae. Individuals with diabetes are at a higher risk for periodontal disease than non-diabetics. The goal of this project is to investigate mechanisms which might contribute to an enhanced risk of periodontal infection in non- insulin-dependent diabetics (NIDDM). NIDDM is a polygenic disorder that involves resistance to insulin action and occurs most frequently in conjunction with obesity. Individuals with NIDDM and murine models of NIDDM exhibit alterations in cytokine expression, particularly over-expression of TNF-alpha. A breakthrough in understanding the mechanisms leading to NIDDM occurred with the discovery that obese mice which develop NIDDM have mutations in the gene encoding leptin (ob/ob mice). These mice over-express the cytokine TNF and have defects in insulin receptor signaling. Humans with NIDDM also exhibit similar defects in TNF expression and insulin receptor signaling. The goal of this project is to determine whether dysregulation of TNF in NIDDM alters the hostresponse rendering these individuals more susceptible to periodontal pathogens. We will examine the response of ob/ob diabetic mice to P. gingivalis LPS and P. gingivalis fimbriae and directly test the impact of TNF hyper- expression in ob/ob mice by inhibiting TNF activity and measuring the consequences. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OSTEOCLASTOGENSIS
OF
TNF
RECEPTOR
MEDIATED
Principal Investigator & Institution: Abu-Amer, Yousef; Associate Professor; Orthopaedic Surgery; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 01-SEP-1999; Project End 31-AUG-2004 Summary: (adapted from the Investigator's abstract): Tumor necrosis factor alpha (TNFalpha) is an inflammatory cytokine with osteoclastogenic and osteolytic activities that contribute to pathogenesis of bone disorders such as periodontal disease, postmenopausal osteoporosis, and arthritis. This proposal will investigate mechanisms underlying TNF-alpha stimulation of osteoclast formation from mouse bone marrow macrophages (BMM). Proposed studies are based on the premise that two TNF-alpha receptors transduce TNF-alpha signals in osteoclast precursors with opposing effects on osteoclast formation. The p55 receptor (p55r) is proposed to mediate positive effects of TNF-alpha (mainly soluble TNF-alpha) on osteoclast formation through activation of csrc kinase, subsequent phosphorylation and inactivation of the NFkB inhibitor IkBalpha, and activation of NFkB. The p75 receptor (p75r) is proposed to mediate inhibitory effects of TNF-alpha (mainly membrane TNF-alpha) on osteoclast formation. This hypothesis is
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supported by previous studies and preliminary data. The specific aims of the proposal are (1) to determine the mechanisms by which p55r promotes osteoclastogenesis, and (2) to determine the mechanisms by which p75r suppresses osteoclastogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MICROARRAY INFECTION/AUTOIMMUNTY
ANALYSIS-INTRACELLULAR
Principal Investigator & Institution: Humphreys-Beher, Michael G.; Professor; Oral Biology; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-JUL-2002 Summary: The salivary glands are a major source of several factors, which play important roles in both oral and systemic organ homeostasis and wound healing. The roles of these factors, which include IGF-I, IGF-II, NGF, TGF alpha and beta, and EGF, has been well-studied. However, the fact that the salivary glands appear to be a major source of these growth factors present a interesting question both in the primary route of reentry into the system and the relative importance of these salivary- derived proteins systemically. In diabetic patients both (Type I and II) a major disease complication is diminished capacity of wound healing and in the oral cavity increased periodontal disease. A similar picture occurs in animal models of diabetes in there is also a progressive loss of growth factors from saliva in accordance with diabetes onset. Therefore, the investigators propose to look for the potential loss of salivary-derived growth factors associated with the observed decrease in wound healing capacity in diabetic patients. To accomplish this goal, they first plan to use the diabetic patient base of the University of Florida to investigate the changes in growth factor levels in patient saliva and serum after surgical procedures, as compared to healthy non-diabetic individuals undergoing similar procedures. Second, they intend to determine the influence of changes in growth factor levels in saliva on wound healing in the NOD mouse model for IDDM. With this, they intend to establish the NOD mouse as a viable model for this aspect of the disease and then to be able to employ this model to more thoroughly investigate the impact of decreased levels of salivary growth factors on experimentally introduced soft and hard tissue injuries. The results of these studies should elucidate the importance of salivary-derived growth factors on systemic homeostasis and wound repair and potentially provide insight into the viability of replacement strategies to combat several complications of human diabetes which may involve an underlying deficiency in wound repair mechanisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MICROBIAL ECOLOGY OF PERIODONTAL DISEASES Principal Investigator & Institution: Socransky, Sigmund S.; Forsyth Institute Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-JUN-1999; Project End 31-MAY-2004 Summary: The long-term objectives of this Project are to define the microbial complexes that are most compatible with periodontal health leading to therapeutic and/or preventive strategies to produce the desired plaque composition Specific Aim 1 will examine periodontally health subjects in order to determine the composition of their subgingival plaque and the associations among species within the plaque samples. The data will be used to seek differences in bacterial profiles among health subjects and examine differences between periodontally healthy subjects and subjects who have periodontitis and who are on periodontal maintenance. In this cross- sectional study, 100
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periodontally healthy subjects will be assessed clinically at 6 periodontal sites per tooth. Subgingival plaque samples will be take separately from the mesial aspect of each tooth and evaluated individually for their content on 40 bacterial species using checkerboard DNA-DNA hybridization. The dissemination of species from host to host is important for their intraoral survival. Specific Aim 2 will determine if family members of index subjects colonized by low levels and prevalence than family members of high-redcomplex colonized index subjects. 30 high and 30 low red complex index subjects will be chosen and their spouses, siblings, parents or children examined clinically and for subgingival plaque composition (as described for SA1). Data will be used to determine if colonization by low or high levels of red complex species is a trait within families. Specific Aim 3 will determine if strains of B. forsythus, P. gingivalis and T. denticola in families show identical DNA base sequences for selected genes, suggesting transmission within the family. The method will involve PCR amplification of the chosen gene directly from plaque samples, followed by sequencing of the product. The proposed studies will clarify the composition of subgingival plaque in periodontally healthy subjects, determine if one or more healthy profiles exist, compare healthy profiles to profiles of diseases subjects before and after therapy, provide a data base for examining important bacterial associations in plaque, determine if colonization by high or low levels of the presumed pathogenic red complex is a trait exhibited within families and determine how frequently transmission occurs within families. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MMP-2 IN PERIODONTAL DISEASE AND ORAL CANCER Principal Investigator & Institution: Steffensen, Bjorn; Associate Professor; Periodontics; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-MAY-2006 Summary: MMP-2 is a member of the family of matrix metalloproteinases (MMPs), which together cleave a broad range of tissue components. While this property of the MMPs is a beneficial feature of normal development and tissue adaptation, uncontrolled MMP-2 activity has been strongly associated with inflammatory diseases, such as periodontal disease and arthritis, and tumor expansion and metastasis. This application is designed to develop compounds, which specifically inhibit MMP-2 activity. Since cleavage of molecules by MMP-2 occurs only if there is binding between the enzyme and substrate molecules, the specific mechanism by which MMP-2 binds its main collagen substrates will be investigated. In a collaborative effort, molecular biology and protein structural analysis methods will be applied to first identify specific MMP-2 binding sites on collagen by screening a random peptide library and mapping the functional peptide sequences on collagen. To identify the precise collagen binding site residues on MMP-2, nuclear magnetic resonance studies will be used to analyze the MMP-2 collagen binding domain (CBD) complexed with synthetic peptides, which mimic the CBD binding sites on collagen. The specificity of the identified sites and amino acids will be tested in competitive ligand binding assays and by analyzing the effects of site-specific mutations in the CBD. Once the precise binding sites on both collagen and MMP-2 are defined, small molecules will be developed that can inhibit the full-length native MMP-2 activity by competing for substrate binding and by substituting binding site residues on the CBD. This will be accomplished in both MMP-2 ligand binding and activity assays, and in experiments with MMP-2 expressing cells. The proposed studies should define the specific binding site interactions between MMP2 and its main collagen substrate and explore a new strategy to inhibit MMP-2 in inflammatory diseases and cancer based on competition for substrate binding.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MODULATION MOLECULAR PATHOGENESIS IN SYSTEMIC DISEASES Principal Investigator & Institution: Genco, Caroline A.; Professor; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: The major focus of this application is to define the molecular mechanisms of host-parasite interactions as it relates to secondary systemic complications of periodontal disease. We propose to examine the response of defined host cells to the periodontal pathogen Porphyromonas gingivalis. The sequelae associated with periodontal disease have received considerable attention over the past few years. However, little is known about the specific interactions of P. gingivalis with host cells as it relates to cardiovascular disease and diabetes. The goal of this program project is to begin to define the response of host cells to specific P. gingivalis components at the molecular level with particular emphasis on these processes in the context of diabetes, cardiovascular disease, and periodontal disease. Project 1 will examine the molecular mechanisms of P. gingivalis interactions with human endothelial cells by defining the endothelial cell receptor for fimbriae and the signal transduction events concurrent with P. gingivalis infection. Project 2 will examine the role of P. gingivalis fimbriae and LPS in leukocyte recruitment, expression of inflammatory mediators and host-derived proteolytic enzymes, the destruction of hard and soft tissue, and the proliferation of P. gingivalis in vivo. These will be examine din the context of diabetes using 2 well defined animal models. Project 3 will examine the role of the macrophage response to P. gingivalis LPS. The goal of this project will characterize the LPS receptor and Co receptor in normal cells. There are gaps in our knowledge regarding specific details of the interactions between host cells and P. gingivalis particularly in diabetes and cardiovascular disease. This study will use novel approaches to increase our understanding of the molecular mechanisms of host parasite interactions and the modulation of these processes in systemic diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR ANALYSIS OF T. DENTICOLA-HOST INTERACTIONS Principal Investigator & Institution: Fenno, J Christopher.; Assistant Professor; Biologic & Materials Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 15-APR-2001; Project End 31-JAN-2005 Summary: The predominance of spirochetes in subgingival plaque associated with severe periodontal lesions suggests an important role in periodontal pathogenesis. The goal of this research is to characterize interactions of Treponema denticola with subgingival tissues at the molecular level. By focusing on analysis of surface-expressed proteins that directly affect host cells, insights will be gained into mechanisms of periodontal cytopathology. The major outer membrane protein (Msp) of T. denticola binds to cells and ECM components, and has pore-forming cytotoxic activity. Msp is genetically conserved in many oral spirochetes, yet shows considerable inter-strain heterogeneity, suggesting that it is an important immunogen. The overall hypothesis is that Msp is a significant virulence determinant in periodontal disease, and is a key component of an outer membrane protein complex mediating interactions of the spirochete with subgingival tissue. Specific Aims of the proposed research, and the
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individual hypotheses to be tested are: 1) to characterize T. denticola proteins associated with Msp expression. Outer membrane components other than Msp are required for native Msp expression and assembly of the native outer membrane complex. Isogenic mutants and recombinant expression systems will be used to characterize these processes. 2) to identify immunodominant and functional domains of Msp. Antigenic heterogeneity of Msp is a factor in host antibody recognition of oral spirochetes. Archived serum samples will be screened for reactivity with specific Msps. Genes encoding novel Msps will be identified in patient plaque samples. 3) to characterize the role of Msp in cytopathic cellular responses to T. denticola. The ability of parent and msp mutant strains to bind host cells, ECM and serum components, and to activate proinflammatory cellular responses will be assayed. A putative Msp receptor identified on epithelial cell surfaces will be characterized. These studies, which involve both genetic and biochemical analyses, are intended to contribute significantly to the understanding of microbe-host interactions in the etiology of periodontal diseases, and to basic knowledge of the molecular biology of pathogenic spirochetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR BIOLOGY OF VIRULENCE IN PERIODONTAL DISEASE Principal Investigator & Institution: Lally, Edward T.; Professor; Pathology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 01-JUL-1990; Project End 31-MAR-2006 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR MECHANISMS IN LEUKOCYTE-MEDIATED TISSUE INJURY Principal Investigator & Institution: Serhan, Charles N.; Professor and Director; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: The basic molecular and cellular mechanisms involved in the regulation of neutrophil (PMN)-mediated inflammation in periodontal disease have yet to be clearly defined. The mission of this program project is to investigate the molecular mechanisms and pathways that regulate production of inflammatory mediators by human neutrophils that contribute to periodontal disease. This program project and its structure was developed in recognition of the interdependence of the elements that initiate and can regulate PMN-derived mediators can serve as templates for design of novel typically active anti-inflammatory agents. A general hypothesis that emerges from our recent experiments and shall be addressed in each project is as follows: In individuals without periodontal disease, down-regulatory bioactive lipids of the host serve as "natural anti-inflammatory local mediators" to prevent harmful PMN responses, thus protecting the periodontal disease. To this end, projects are linked in thematic content and via highly complementary expertise of the investigators. Project #1 (Principal Investigator Charles N. Serhan) will focus on novel lipid mediators generated by PMN. Proposed experiments will highlight receptors and novel signaling molecules that regulate PMN function in vitro and in vivo. Project #2 (Project Leaders T. Van Dyke & J. Badwey) focuses on the role of novel lipid mediators and their stable analogs in regulating the generation of reactive oxygen species by PMN. This project addresses intracellular mechanisms and targets involved in this new pathway. In Project #3, Sean
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Colgan (Project Leader) will establish the key determinants involved in PMN cross talk pathways with oral epithelial cells and determine their functions in oral epithelial cells. Project #4 (Project Leader N.A. Petasis) will pursue the total synthesis and design of new stable analogs of lipid mediators isolated in this program to establish their structure-function and bioimpact. Conformational studies and new approaches to facilitate syntheses will be evaluate. Studies will utilize patient acquisition, synthesis and demonstration cores to rapidly translate structure to bioimpact. Conformational studies and new approaches to facilitate syntheses will be evaluated. Studies will utilize patient acquisition, synthesis and demonstration cores to rapidly translate structure to bioimpact. Our long-term goals are to elucidate endogenous counter-regulatory mechanisms in inflammation and to provide new therapeutic approaches to periodontal diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOTOR-MATERNAL ORAL THERAPY TO REDUCE OBSTETRIC RISK Principal Investigator & Institution: Offenbacher, Steven; Professor of Periodontology; Dental Research Center; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 05-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Recent studies have confirmed that there is an association between maternal periodontal disease and pregnancy complications that result in premature delivery [e.g. gestational age (GA)<37 weeks: adjusted odds ratio 2.1(CI95%:1.12, 4.09)and OR=4.2 for GA<28 weeks (CI95%: 1.42,12.6)] and decreased fetal weight [e.g. among mothers with births of GA between 35-37 weeks, those with periodontal disease (4+ sites with 5+mm PD and 2+mm AL) have neonates that are 13.8% smaller (p=0.004). The deleterious effect of maternal periodontal infection on pregnancy is particularly pronounced among African Americans and may, in part, account for some of the disparities in the prevalence of these unfortunate complications. Not only does the presence of periodontal disease early in pregnancy confer risk, but the worsening of periodontal disease during pregnancy - a relatively frequent event (35.5% of 814 deliveries) appears to independently enhance the risk of fetal exposure to periodontal pathogens (as evidenced by fetal cord blood IgM antibody to maternal oral pathogens) and preterm birth (OR=5.0, CI95%:2.22,11.3). These data suggest that periodontal disease and its progression may represent an infectious and inflammatory exposure that could have serious deleterious effects during pregnancy. Scientifically, to determine whether periodontal disease is causally related to preterm delivery and confers any modifiable risk, it will be critical to demonstrate that treating periodontal disease in pregnant mothers results in a decreased incidence of preterm birth and growth restriction. It is our central hypothesis that mothers with periodontitis that receive periodontal treatment during the second trimester of pregnancy will experience a lower rate of preterm delivery and a higher mean birth weight of the premature infants. We propose to conduct a 5-year randomized, 2-armed, clinical trial completing 1800 mothers at 3 medical/dental centers (UNC/Duke, UAB & UTHSCSA) that combine both periodontal and Obstetrics/Gynecology clinical trial expertise. We propose to randomly assign 1800 pregnant mothers with periodontal disease to one of two treatment arms 1) scaling and root planning during the second trimester or 2) scaling and root planning post-partum. Biological samples will be collected and archived during the conduct of the study to enable future investigations that will seek to further elucidate the role of maternal oral and vaginal infections on pregnancy. We
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hypothesize that periodontal treatment during pregnancy will significantly reduce the incidence of preterm deliveries of GA<35 weeks and also enhance the mean weight of those of GA<37 weeks. The impetus for this study is further supported by results from a pilot study conducted at UAB that demonstrated that scaling and root planning reduced the rate of GA<35 weeks from 6.4% in the untreated group to 0.81%. This application entitled MOTOR (Maternal Oral Therapy to Reduce Obstetric Risk) includes 5 separate components: an administrative oversight project (UNC Dental School), 3 clinical trial performance sites (UNC Dental/Duke Medical, UAB Dental & Medical and UTHSCSA Dental & Medical) and a clinical trials data and statistical coordinating center (UNC Collaborative Studies Coordinating Center, School of Public Health). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: N-3 FATTY ACID & HOST RESPONSES TO ORAL INFECTION Principal Investigator & Institution: Lakshmyya, Kesavalu N.; Research Associate Professor; Ctr for Oral Health Research; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-AUG-2004 Summary: (provided by applicant): The major objectives of this R21 application are to explore the potential role of dietary n-3 polyunsaturated fatty acid (PUFA) regulation on molecular host responses to oral infection with Pg in vivo in an animal model. It is clear that host pro-inflammatory mediators provide a significant contribution to tissue destruction in chronic inflammation. Dietary n-3 fatty acid has been shown to modulate inflammatory responses via regulating lymphocyte proliferation, cytokine production, signal transduction, and gene expression in humans and rodents; providing a benefit by reducing inflammatory disorders, cardiovascular diseases, increasing anti tumorigenic effects on breast cancer, colon cancer, pancreatic neoplasms, and improving bacterial and autoimmune responses. Thus, we will initially focus on n-3 PUFA, which is the primary dietary lipid in "fish oil." We will determine its capability to modify host responses, affecting Pg pathogenesis, as a prototype periodontal pathogen. The experiments will utilize an in vivo rodent model of infection and alveolar bone resorption. Substantial evidence has established the contribution of host derived inflammatory cytokines in periodontal inflammation and disease that can lead to the alveolar bone loss and subsequent tooth loss, characteristic of periodontitis. To5knowledge, there are no in vivo investigations evaluating how n-3 PUFA regulates specific host-bacterial interactions in gingival tissues and alveolar bone resorption in periodontal disease. Two Specific Aims designed to test this hypothesis: 1) To examine the effect of dietary n-3 PUFA on gingival tissue expression of proinflammatory (TNFa, IL-1b,IL-6, lipid per oxidation, TBARS), anti-inflammatory (IL-10, TGF-b1, antioxidants) biomolecules, and T cell phenotypes (Th1, Th2) induced by Pg infection, and 2) To determine the effects of dietary n-3 fatty acid on Pg colonization and alveolar bone resorption. The long-range goal of this nutrition and oral infection project is to contribute to understanding the cellular and molecular mechanisms that enable dietary n-3 fatty acid to ameliorate tissue destructive aspects of periodontal pathogenesis. Positive findings could enable improved dietary strategies as adjuncts in the prevention of periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NEUTROPHIL/ORAL EPITHELIAL INTERACTIONS Principal Investigator & Institution: Colgan, Sean P.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115
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Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: The pathological hallmark of many periodontal diseases is the accumulation of large numbers of neutrophils within oral mucosal tissue, and in particular, at the level of the epithelium. At present, little is known about the molecular events and regulatory pathways associated with neutrophil (PMN) recruitment to, and transmigration across, oral epithelia. As work in progress, we have defined a model to analyze potential regulatory sites in PMN-oral epithelial interactions in vitro. Results from these studies suggest that PMN utilize a previously undescribed pathway to traverse oral epithelial monolayers, and that this pathway is regulated by metabolically stable eicosanoids derived from transcellular biosynthesis of arachidonic acid (lipoxins). Further studies indicate that oral epithelial-PMN interactions are modulated by paracrine factors endogenous to the inflamed oral mucosa. The overall goal of this proposal is to examine protein and lipid mediators of PMN-oral epithelial interactions and to define potential targets for development of novel small molecule therapeutics. Three specific aims are proposed to accomplish this overall goal: As a first specific aim, we will dissect lipoxin interaction pathways during PMN-oral epithelial adhesion and transmigration, and establish the role of epithelial chemokine generation during these modeled inflammatory events. Specific aim two will define the existence of novel PMN adhesion molecules expressed on oral epithelia and elucidate molecular determinants for these molecules. In specific aim three, we will define the impact of paracrine mediators on oral epithelial function and PMN- epithelial interactions. Results at each juncture will be integrated with other programmatic projects to address the more global goal of defining novel targets for the development of experimental therapeutics to heal oral mucosal inflammatory disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NF-KB ATHEROGENESIS
ACTIVATION
AND
ORAL
INFLAMMATION
IN
Principal Investigator & Institution: Nichols, Timothy C.; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2004 Summary: Atherosclerosis, the major cause of death and disability in the United States, is a chronic disease with inflammatory components. Our overall objective is to use molecular, cellular and animal models to study how activation of NF-kappaB contributes to atherosclerosis. This nuclear transcription factor controls the expression of many genes linked to atherogenesis, including those involved with inflammation. We hypothesize that one unifying mechanisms in this complex disease is the activation of NF-kappaB. The mechanism(s) that activates NF-kappaB in atherogenesis is unknown and the effect of inhibiting NF-kappaB atherogenesis is untested in animal models. In Aim 1, we focus on shear stress and oxidized LDL-induced activation of NF-kappaB in cultured porcine endothelium and smooth muscle cells as models for determining the mechanism(s) of activation of NF-kappaB in atherogenesis. The role of phosphorylation and degradation of IkapaB and the operative kinases and signal transduction pathways will be identified. In Aim 2, we will develop and test a series of reagents that inhibit NFkappaB activation in response to shear stress and oxidized LDL. The most promising inhibitors will be tested in Aim 3 where we will use our pigs with shear and dietinduced atherosclerosis to determine the effect of inhibiting activation of NF-kappaB. Periodontal disease has now been established as a risk factor for atherosclerosis and its thrombotic complications. It is unknown if periodontal disease contributes to the initiation or progression of atherosclerosis. NF-kappaB likely plays an essential role in
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bone loss due to periodontitis since IL-1beta and TNFalpha are key mediators in humans and animal models of the disease and strong activators of NF-kappaB. We hypothesize that the chronic and intense inflammatory response accompanying periodontal disease produces an excess burden of circulating mediators of inflammation that initiate or exacerbate the inflammatory components of atherosclerosis. To test this hypothesis, we will adapt a model of ligature-induced periodontitis to our pig models of atherogenesis. Our goal in Aim 4 will be to determine if the presence of periodontal inflammation contributes to the initiation and/or progression of atherosclerosis. If so, then we will determine whether or not activated NF-kappaB is present in cells in the atherosclerotic lesion that is modulated by oral inflammation. Our data on the mechanisms involved in the critical role of NF-kappaB in atherosclerosis could lead to important therapeutic applications especially as it relates to the impact of periodontitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GINGIVALIS
NITRIC
OXIDE
DEFENSE
AGAINST
PORPHYROMONAS
Principal Investigator & Institution: Gyurko, Robert; Periodontology & Oral Biology; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2006 Summary: (provided by applicant): Periodontal disease, the leading cause of tooth loss in the adult population, is an inflammatory disease which is triggered by bacteria, but it is thought that periodontal tissue damage is primarily inflicted by the host's own defense reaction. Nitric oxide (NO) is a multifunctional molecule present in periodontal tissues, which can be toxic to bacteria as well as to cells of the periodontal tissue. NO is released in response to Porphyromonas gingivalis (P. gingivalis) infection, a bacterium which is clinically and experimentally associated with periodontal disease. We propose experiments to elucidate the role of NO in the defense against P. gingivalis infection. In preliminary studies we have compared P. gingivalis-induced periodontal bone loss in normal mice and in mutant mice which do not produce NO in response to bacteria (iNOS KO mice). We found that iNOS KO mice are resistant to P. gingivalis induced bone loss. To investigate the mechanisms by which NO participates in antimicrobial defense, the role of NO in inflammatory reaction is evaluated in an implant chamber model of P. gingivalis infection. We study the interaction of NO with other antibacterial molecules, such as superoxide, by testing mutant mice deficient in NO, superoxide, or both NO and superoxide. To assess the importance of NO in regulating bone destruction, isolated bone tissue from normal and iNOS KO mice is tested for a series of signaling molecules which are known to cause bone loss. The role of NO in bone development at various ages of normal and iNOS KO mice is also tested. Robert Gyurko, DDS, PhD is currently conducting research on the role of NO in cardiovascular diseases at the Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA. He is applying for the NIDCR Scholar Development and Faculty Transition Award to pursue scientific career as an independent investigator at Boston University School of Dental Medicine. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NON ANTIBIOTIC PROPERTIES OF TETRACYCLINE Principal Investigator & Institution: Lokeshwar, Balakrishna L.; Associate Professor; Gordon Research Conferences Box 984, 512 Liberty Ln West Kingston, Ri 02892
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Timing: Fiscal Year 2001; Project Start 19-JUN-2001; Project End 31-MAY-2002 Summary: This application is a request for supplemental support for a multidisciplinary conference entitled "Non-Antibiotic Properties of Tetracyclines and Other Antibiotics" to be held at Colby Sawyer College, New London, CT during the week of July 1-6, 2001. This meeting held under the auspices of the Gordon Research Conference Society will be the second of its kind on a unique and exciting topic, covering both basic and clinical applications of a class of tetracycline derived compounds and other antibiotics. Since first reported in1983 by Golub et al., the non-antibiotic properties of tetracyclines (TCs) and chemically modified non-antimicrobial tetracyclines (CMTs) have found applications in diverse areas of biomedical research. These include: activity as an inducer of tet-on and tet-off gene constructs for in vivo and in vitro gene expression studies, treatment of periodontal disease (Periostat FDA approved 1998), a potential treatment for cancer, arthritis, acute respiratory distress syndrome (ARDS), Sjogrens syndrome and other dry eye diseases, and as an early treatment for stroke. All these applications are based on the anti-metalloproteinase (MMP) and anti-inflammatory properties of TCs. Previous meetings on this novel topic have generated in the biomedical community such immense interest that an overwhelming 80% of the previous attendees have responded with their desire to attend the upcoming meeting. A roster of scientists from the US and Europe, both established workers and those new to the field, have agreed to present and share their recent work on the non-antibiotic properties of TCs and other antibiotics and their application to the treatment of disease. The conference will focus on the exchange of new information regarding promising biological models of TC investigation, the molecular mechanism of action and the pharmacology of TCs with an emphasis on cancer, in 8 intensive talk and discussion sessions plus five after session gatherings. The conference is expected to have a significant impact on this rapidly emerging field by fostering collaborations and establishing a forum for discussion regarding the direction of future research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NON-INVASIVE SYSTEM FOR AND ARREST OF PERIODONTITIS Principal Investigator & Institution: Bogomolova, Anastassia; Fractal Systems, Inc. 200 9Th Ave N, Ste 100 Safety Harbor, Fl 34695 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-MAR-2002 Summary: The goal of this application is to create a system for the prevention and treatment of the early stages of periodontal disease. This will be accomplished by developing an adhesive, biodegradable hydrogel that will form inside the periodontal pocket following ionotropic gelation of mixed liquid components. The gel will adhere to existing bacterial plaque and inhibit the growth, adherence and penetration of bacteria. The application proposes to develop a chitosan hydrogel with three different polyanions: collagen, heparin and polylactic acid. The optimal gel composition with regard to physical stability in orally relevant conditions, gelation time, biodegradation, oxygen permeability and attachment to oral surfaces will be determined. The ability of the most appropriate gel to inhibit the growth and adhesion of oral bacterial will be assessed. PROPOSED COMMERCIAL APPLICATION: Development of a non-invasive system for prevention and treatment of early periodontitis will allow to create a product for home application. The use of this product will result in avoiding advanced periodontal disease. The product will become an affordable alternative to expensive periodontal surgical treatment and will result in better dental health of the world population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NON-TOXIC ANTIMICROBIAL RINSE FOR GINGIVITIS Principal Investigator & Institution: Bhatt, Bakul M.; Biomedical Development Corporation 500 Sandau, Ste 200 San Antonio, Tx 78216 Timing: Fiscal Year 2003; Project Start 01-SEP-2000; Project End 31-AUG-2005 Summary: (provided by applicant): The overall goal of this proposal is to develop Iocide(r), a unique non-toxic, non-staining mouthrinse to treat gingivitis. Antimicrobial mouthrinses are valuable supplements to normal oral hygiene procedures and have demonstrated their ability to control plaque formation and prevent the onset of early periodontal disease. However, currently available antimicrobial rinses are either indicated only for short term use or demonstrate ineffective microbicidal activity. Chlorhexidine is the most effective antimicrobial mouthrinse available, but due to its side effects can only be used in acute settings. Other available animicrobial mouthrinses can be used over longer periods of time but are less effective than chlorhexidine in reducing oral bacteria. The Specific Aims of this grant are to 1) Optimize the Iocide(r) oral rinse formulation for use in the oral cavity, 2) Evaluate the safety profile in animals, and 3) Demonstrate its safety and efficacy in human clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NORTHWEST/ALASKA CENTER TO REDUCE ORAL HEALTH DISPARITY Principal Investigator & Institution: Milgrom, Peter M.; Professor of Dental Public Health Scienc; Dental Public Health Sciences; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-JUL-2008 Summary: This proposal is in response to RFD DE-99-003 to establish the Northwest and Alaska Center for Oral Health Disparity for research to reduce oral health disparities in the Pacific Northwest and Alaska. It is proposed that the Center develop basic and applied knowledge that addresses the needs of poor, minority, and rural children and their caretakers, utilizing approaches that go beyond the traditional strategies from dental public health that have not found success in these populations. While the research in the proposed center may involve traditional dental personnel, it also stresses the roles of pediatricians, mothers as well as children; and preventive agents beyond fluorides. Participants include Alaska Natives, Native Americans from the Yakima Indian Nation, Hispanics from the agricultural areas of Washington, African Americans and Hispanics from the local military reservations, Hispanics and Pacific Islanders served by urban hospitals as well as rural and low-income Whites. We propose to accomplish this goal through five specific aims: (1) To address the needs of the Pacific Northwest and Alaska by conducting clinical research to evaluate the efficacy of nontraditional interventions to prevent and treat oral disease in children and their caretakers; (2) To develop community-based research that translates existing knowledge and new information regarding children and their caretakers into new technologies and interventions that hold promise for reducing disparities in these high risk populations; (3) To expand health science education and research training opportunities for minority populations in the Pacific Northwest and Alaska by collaborations with key minority educational and health serving institutions in the region; (4) To conduct basic research to further understand the role of host defenses and genetic bases for caries and periodontal disease affect underserved populations as well as to probe the biologic basis for antibacterial that change disease susceptibility; and (5) To increase the impact of the center beyond the projects included in this proposal by recruiting investigators
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and students from minority institutions in the Pacific Northwest and Alaska and prioritizing and encouraging pilot and center-affiliated studies in which they are involved. The collaborating institutions and partners are Heritage College (Hispanic and Native American-serving institution sited on the Yakima Indian Nation), Alaska Native Tribal Health Consortium/Yukon-Kuskokwim Native Health Corporation, Yakima Valley Farm Workers Clinic, Northwest Portland Area Indian Health Board/Northwest Tribal Epidemiology Center, Washington Dental Service an Foundation (major private dental insurer); and Medical Assistance Administration (Medicaid agency for Washington State). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL ANTI-INFLAMATORY LIPID MEDIATORS Principal Investigator & Institution: Petasis, Nicos A.; Professor of Chemistry; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: The long-term goal of this project is the development of novel regulators of leukocyte function to serve as anti-inflammatory molecules based on the modulation of the mode of action of some new types of lipid-derived mediators (LM). Our recent collaborative work with Dr. Serhan (Project 1) has led to the identification and biological investigation of several new LM that have novel and promising activities, including several biostable analogues of the lipoxins (LX), the aspirin-triggered (ATL) and presqualene disphosphate (PSDP). A typical feature of the above LM is that they are topically active and that they have multi-faceted biological activity, which involves a number of other cell-signaling molecules related to inflammation. Following recent studies that suggested the potential involvement of these LM in periodontal diseases, this project seeks to develop a series of new molecules that would elucidate their role. Thus, this project will pursue the design and synthesis of: (1) new structural analogues of LX and ATL, and (2) new structural analogues of PSDP. In addition to synthetic and conformational studies of these molecules, this project will pursue several new synthetic approaches that may facilitate their synthesis. The synthetic molecules will be used in bioassays in Projects 1-3 of this program and structure-activity relationships will be established for each of the targeted LM. Finally, selected compounds will be scaled-up for in vivo animal model studies in Core D (Demonstration Core). Overall, this project will lead to the elucidation of the physiological and pathophysiological role of several topically active LM, particularly in host defense and inflammation. Therefore, this research may result in development of new molecules with novel anti-inflammatory properties with therapeutic potential in regulation of tissue-mediated injury, as in periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ONCOSTATIN M EXPRESSION AND ACTIVITY IN GINGIVAL CELLS Principal Investigator & Institution: Rose, Timothy M.; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2002 Summary: Periodontitis is a chronic infectious disease process which is highly prevalent in human populations. Although periodontitis is most common in adults, several forms of early onset periodontitis are seen in children and adolescents. An understanding of the basic biologic process leading to the formation of periodontal tissues during
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embryonic and childhood development, as well as their maintenance during adulthood is crucial doe the development of new approaches for the prevention, diagnosis and treatment of periodontitis. We have previously identified a pleiotropic cytokine called oncostatin M (OSM) (OSM) which is important in cell growth, regulation and differentiation during early development and maturation. We and others have shown that OSM acts as an anti- inflammatory molecule which has regenerative activities with regard to connective tissue and bone. We have recently demonstrated that OSM is expressed in gingival tissues in vivo and in vitro and that this expression is downregulated by bacterial components. Furthermore, we have evidence that the OSM specific receptor is abundantly expressed in several periodontal cell types. Although considerable work remains to establish the function of OSM in oral tissues, our data suggest that OSM may be important for the development and maintenance of the normal periodontium. Our studies suggest that the induction of OSM in or the addition of exogenous OSM to periodontal tissues could reverse the disease progression in periodontitis. We believe that the proposed research may provide a basis for therapeutic testing of OSM in vivo preclinical and clinical trials. In addition, this research will further our understanding of childhood susceptibility to oral diseases, with the potential for the development of new therapeutic interventions. In this application, we propose the following specific aims: 1) Determine the expression levels of OSM in serum, gingival crevicular fluids and gingival biopsies from children and adults with periodontal disease. 2) Assess the ability of periopathogenic bacteria and induced proinflammatory mediators to module the expression of OSM and the OSM receptor subunits in gingival epithelial cell cultures in vitro. 3) Determine the effects of OSM on gingival fibroblast and epithelial cells in vitro by analyzing the expression of genes for various cytokines, chemokines, tissue-specific genes, and proteinases and their inhibitors which are implicated in periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ORAL ACQUISITION OF HIV INFECTION Principal Investigator & Institution: Shafer, Kimberly P.; Assistant Adjunct Professor; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001; Project Start 15-APR-1999; Project End 31-MAR-2004 Summary: Although the number of case reports and epidemiologic evidence of orogenital transmission of HIV infection has increased in recent years, little is known about biological, behavioral or social risk factors that may be associated with this mode of transmission. We propose to identify risk factors for oral acquisition of HIV infection using a case-control study design. By using a uniform method of identifying recent seroconverters (dual or "detuned" enzyme immunoassay) who report only receptive oral sex as a mode of transmission, a uniform oral and periodontal exam, sexually transmitted disease screening, and standardized questionnaires, to measure biological, behavioral and sociodemographic data, we will study a question of great concern to communities at risk of HIV infection. The Specific Aims of this proposal are: 1. To assess whether host oral environment including signs and symptoms of periodontal disease (e.g. gingival bleeding or loss of attachment), and/or oral health practices are associated with increased odds of oral acquisition of HIV infection. 2. To assess which specific orogenital sexual practices and oral exposure to ejaculatory fluids (such as swallowing or not swallowing semen) are associated with increased or decreased odds of oral acquisition of HIV. 3. To assess whether comorbid conditions documented within the seroconversion period (e.g. sexually transmitted disease such as gonorrhea, chlamydia
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and other viral infections such as HSV-1 or 2) are associated with increased or decreased odds of oral acquisition of HIV. 4. To assess whether non-injecting substance use which may modify the oral or naso-pharyngeal mucosa and/or sexual behavior is associated with increased or decreased odds of oral acquisition of HIV. The case-control design cannot estimate infectivity or the rate of oral HIV infection, but is the only feasible way to study factors which may influence the risk of oral infection. Identification of the cofactors for orogenital HIV acquisition will provide us with the kind of data that can be used by AIDS prevention programs and by members of AIDS risk groups themselves so that the risk for HIV transmission can be lowered even further. For this reason, this study addresses a crucial public health goal, one that is long overdue for careful epidemiological study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ORAL ANTIMICROBIAL PEPTIDES IN HEALTH AND DISEASE Principal Investigator & Institution: Dale-Crunk, Beverly A.; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2004 Summary: Children have excellent defenses against oral infections. They lose deciduous teeth and erupt permanent teeth without infections and rarely get periodontal disease even in the presence of plaque. This project will investigate the role without infections and rarely get periodontal disease even in the presence of plaque. This project will investigate the role of beta- defensins, a newly recognized family of small, cationic peptides with anti- microbial activity, in oral health and disease susceptibility. Oral epithelia are constantly exposed to microbial challenges that lead to bacterially induced gingivitis, periodontal diseases and other infections. Recent findings show that mucosal epithelial cells, including gingival epithelial are the source of beta-defensins. These peptides are predicted to function as a first line of host defense against microbial pathogens and are now recognized as part of the innate or non-adaptive hot defense system. Two beta-defensin peptides, hBD-1 and hBD-2, are expressed and differentially regulated in gingival epithelial cells. This proposal is based on the hypotheses that (1) beta- defensin peptides produced by oral epithelial cells play an important role in determining the outcome of the host pathogen interaction at the oral mucosal barrier, (2) these peptides may be important in the normal protective function of the oral mucosa during development, and (3) variation in individual expression of these peptides may be a contributing factor to susceptibility to specific oral disorders in children and adults. These peptides have future potential for prevention and treatment of oral microbial disorders, including periodontal disease, caries, recurrent candidal infections, and oral mucositis. The goals of this study encompass basic investigations and applied studies. We seek to understand the regulation of beta-defensin mRNA expression emphasizing epithelial differentiation and cell signaling pathways for expression upon stimulation by examples of commensal and pathogenic organisms, and by a two-component biofilm; to explore the relationship of beta-defensin expression and that of inflammatory cytokines; to determine beta-defensin expression in non- invasively collected oral samples from children, and to explore variation in defensin expression as a function of age and to test the hypothesis that defensin expression has correlated with oral health status in test populations in collaboration with other Comprehensive Center investigators. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ORAL CELLULAR IMMUNE FUNCTION-IMMUNOCOMPROMISED PATIENTS Principal Investigator & Institution: Meiller, Timothy F.; Professor; Oral Diagnosis; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2007 Summary: (provided by applicant): Revised Application: The candidate for this K24 midcareer investigator award In patient-oriented research is Dr. Timothy F. Meiller, Professor of Oral Medicine and Diagnostic Sciences and Professor of Oncology at the Greenebaum Cancer Center at the University of Maryland, Baltimore. Dr. Meiller has fully approved funding of his projects through 2004, with additional pending grants through 2007. Dr. Meiller holds a DDS degree and a PhD in Virology/Immunology. He is Board Eligible in Oral Pathology and is a Diplomate of the American Board of Oral Medicine. He has been a full-time faculty member at the University of Maryland since 1977 arid earned his PhD from the Graduate School at the University in 1992. The K24 will allow Dr. Meiller dedicated clinical research time to: * work with mentored faculty/students in the direct patient assessment of oral disease * work with the mentees, standardizing the collection of data using oral indices * assessing the clinical significance of the findings after the hypothesis has been tested Mentoring of other faculty, dental students, graduate students, and post-doctoral students at the University has been a major component of Dr. Meiller's career. The availability of clinical cohorts of adult and pediatric patients, such as those with HIV associated oral diseases and those undergoing myelosuppressive chemotherapy for cancer, has allowed Dr. Meiller to establish a desirable clinical environment for mentoring. Plans for recruitment, selection, education, mentoring and assessment of outcomes related to faculty interested in clinical research are described. Specifically: * where Dr. Meiller will find the highly qualified potential mentees * what they will do as they work with Dr. Meiller to be socialized into the world of research * what will Dr. Mauler do to help them make the transition into academia or research; and * how will outcomes related to recognition/success be monitored, assessed and tracked after gaining independence The Research Plan outlined in the application describes clinical patient oriented investigations into oral complications, as studied in patients with chemotherapy induced or HIV disease induced immunosuppression. Mentoring opportunities are cited for the project components related to chemotherapy associated oral fungal infections and effects of immunosuppression on periodontal disease. The K24 award will guarantee Dr. Meiller the time for an intense period of clinical patient-oriented research activity and expanded opportunities for mentoring junior faculty. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ORAL CONDITIONS AND PREGNANCY--NEONATAL OUTCOMES Principal Investigator & Institution: Auten, Richard L.; Duke University Durham, Nc 27706 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2002 Summary: This supplemental application extends the evaluation of oral inflammation and infection, effects on pregnancy to the potential impact on premature newborns and the leading complications of prematurity, lung and brain damage. The general hypothesis is that subclinical infection, possibly originating in periodontal disease, affects the inflammatory and immune responses in women, placing them at higher risk for preterm labor and delivery. Pro-inflammatory cytokines, associated with periodontal disease and intrauterine infection, have been implicated in the initiation of
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preterm labor. Our proposed studies will assess how these maternal processes affect the inflammatory cascade in the premature low birth eight infant and the risk for inflammatory complication of prematurity. Prenatal infection and inflammation are associated with brain injury in premature newborns, in particular intraventricular hemorrhage and periventricular leukomalacia. Inflammatory cytokines are found in the tracheal secretions of premature newborns who later develop bronchopulmonary dysplasia. Necrotizing enterocolitis is another serious life-threatening complication of prematurity associated with elevations in pro-inflammatory cytokines. Genetic polymorphisms encoding IL-1beta and TNFalpha are associated with increased cytokine expression and may predispose to an exaggerated inflammatory response. We will measure pro-inflammatory cytokines in pregnant women and compare them to those in their premature newborns. Cytokines will be correlated with the inflammatory complications of prematurity: bronchopulmonary dysplasia, intraventricular hemorrhage/periventricular leukomalacia, and necrotizing enterocolitis, using logistic regression analysis. Polymorphisms will be identified and correlated with these inflammatory complications with the abundance of cytokine protein and mRNA in tracheal aspirates cells and in blood. We will test whether a panel of mediators identified at risk with high sensitivity and specificity. Our long-term aim is to develop markers that identify newborns at highest risk and provide the basis for future therapy to prevent these complications of prematurity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ORAL INFECTIONS, CAROTID ATHEROSCLEROSIS AND STROKE Principal Investigator & Institution: Desvarieux, Moise; Assistant Epidemiology; Columbia University Health Sciences New York, Ny 10032
Professor;
Timing: Fiscal Year 2001; Project Start 15-JUN-2000; Project End 31-MAY-2005 Summary: The overall aim of the proposal is to conduct a prospective cohort study to determine and quantify the independent contribution of periodontal infections to the risk of atherosclerosis and vascular disease in a tri-ethnic population. Seizing the opportunity of the initiation of a larger cohort of stroke incidence in a community of Northern Manhattan where Blacks, Whites and Hispanics live together, and utilize the same health care facilities, we have assembled a multidisciplinary team of investigators in the fields of dentistry, medicine, and public health. 1,050 patients will be randomly selected from the community for the first 18 months of the study and followed over a period of 3 years. At baseline, they will undergo a comprehensive periodontal examination assessing clinical, radiologic, microbiologic (species specific DNA probes), immunologic (species-specific antibodies to periodontal pathogens) and inflammatory (GCF cytokine levels and systematic C-reactive protein and fibrinogen levels) parameters in addition to their extensive investigation for vascular risk factors (lipid profile, homocysteine, glucose, EKG, echocardiography.). At baseline and at 3-year follow up, they will also undergo a high resolution B-mode Doppler ultrasound to measure carotid atherosclerosis. All subjects will be re-interviewed every year. Those who report a change in their clinical status suggestive of an outcome event in the period before the 3rd year assessment will be brought in for evaluation. The concurrent measures of local markers of infection and inflammation together with systemic markers of infection and inflammation should help determine which of the infection or the inflammation component of periodontal disease better explains the purported association with atherosclerosis and stroke. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: P GINGIVALIS HSP90 RECOGNITION IN PERIODONTAL DISEASE Principal Investigator & Institution: Sweier, Domenica G.; Biologic & Materials Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2004 Summary: This proposal is submitted as part of the application for a Research Career Award for Domenica G. Sweier, D.D.S. A Research Career Award will enable the applicant to complete her graduate dentist scientist training in the Oral Health Sciences Ph.D. Program at the University of Michigan School of Dentistry. The objective of this proposal is to investigate the role of the P. gingivalis Hsp90 homologue in the pathogenesis of the microorganism in periodontal disease. Heat shock proteins have been found to be important in many soft tissue infections and have been referred to as virulence factors in some models. For example, the overexpression of Saccharomyces cerevisiae Hsp90 enhances the virulence of this organism in mice (Hodgetts et al., 1996). In humans, anti-Hsp90 seroconversion is associated with a higher survival rate in systemic candidiasis. Moreover, in candidiasis, antibodies to a specific conserved epitope were shown to confer protection (Matthews et al., 1995). Heat shock proteins have also been implicated in adherence mechanisms. A 66kDa Hsp of Salmonella typhimurium is believed to be responsible for binding to the intestinal mucosa and is considered a virulence factor in this microorganism (Ensgraber and Loos, 1992). Elevated levels of serum antibodies to purified human Hsp90 in healthy adults were associated with periodontal health (manuscript in preparation). Healthy individuals had higher anti-Hsp90 serum antibodies than those individuals diagnosed with periodontal disease. Additionally, the P. gingivalis Hsp90 homologue has been found to cross-react with anti-human Hsp90 stress protein antibodies. We feel that further studies on the role of the Hsp90 homologue of P. gingivalis in host-bacteria interactions in periodontal disease will result in the development of new diagnostic and therapeutic modalities. The studies proposed in this application will address the following global hypothesis: Specific epitopes of the Porphyromonas gingivalis Hsp90 homologue are putative virulence determinants that may be blocked by antibodies in sera of healthy subjects. In order to begin to address this hypothesis, we proposed to: (1) clone and characterize the P. gingivalis hsp90 gene homologue, (2) express the P. gingivalis hsp90 gene homologue and harvest the protein, and (3) map the immunodominant epitopes recognized in health and disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: P GINGIVALIS INTERACTIONS W GINGIVAL EPITHELIAL CELLS Principal Investigator & Institution: Lamont, Richard J.; Professor; Oral Biology; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-APR-1995; Project End 31-MAR-2004 Summary: Periodontal diseases are one of the most common bacterial infections in developed countries. Although the identities of the bacteria responsible for the disease and the mechanisms of pathogenicity are understood to some degree, further insights into the molecular and cellular interactions between the pathogenic bacteria and the host are required before the disease can he brought under control. In this study, the interactions between Porphyromonas gingivalis, a periodontal pathogen, and gingival epithelial cells will be investigated. It has been established that P. gingivalis can invade primary cultures of gingival epithelial cells. The ultrastructural and biochemical requirements of P. gingivalis and of gingival epithelial cells that are necessary for
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invasion will be determined. A variety of inhibitors of epithelial cell functions, such as microfilament and microtubule formation, protein synthesis and energy metabolism, will be examined for their ability to inhibit the invasion process. Similarly, inhibitors of bacterial cell functions such as macromolecule synthesis and energy metabolism will be tested for their effects on invasion. Thus, the nature of the invasion process will be elucidated. The molecules of P. gingivalis that mediate adherence and induction of the invasion process will also be investigated. Surface molecules of P. gingivalis will be purified and examined for binding to epithelial cells. The genes for interactive molecules will be identified by cloning and transposon mutagenesis experiments. Finally, the physiology of the signal transduction, in particular calcium ion fluxes, that occurs in the epithelial cells subsequent to the initial interaction with P. gingivalis will be investigated. The information provided by these studies will enhance our understanding of how pathogenic bacteria and host cells interact during the disease process, thus facilitating the development of novel methods to control the disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: P.GINGIVALIS AND ORAL KERATINOCYTE-ECM INTERACTIONS Principal Investigator & Institution: Quaranta, Vito; Professor; Cancer Biology; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-MAY-2005 Summary: The goal of this application is testing the novel hypothesis that the periodontal pathogen Porphyromonas gingivalis (P.g.) interferes with the interactions between oral keratinocytes (OK) and extracellular matrix (ECM), and may cause loss of epithelial integrity. P.g. is a well-known oral pathogen with several distinct virulence factors, which may contribute to P.g. pathogenicity. We intend to focus on those factors that directly or indirectly affect OK/ECM interactions. Our preliminary data show that P.g. alters OK cell morphology, adhesion, migration and survival, and induces proteolysis of OK proteins. Our project is articulated into3 Aims, with the purpose of investigating the molecular mechanisms, both cellular and bacterial, which may underlie these P.g. effects on ECM related functions in OK. In Aim 1, we will analyze the specificity of P.g. interference towards ECM macromolecules that are characteristically found either in normal (e.g. laminin-5 and collagen) or in chronically diseased (e.g. fibronectin and vitronectin) periodontal tissue. To this end, adhesion, migration and survival assays on specific ECMs will be performed with continuous OK cell lines in the presence of P.g. Furthermore, we will compare cellular effects of P.g. with those possibly induced by other oral bacteria, both pathogenic and not. In Aim 2, we will determine whether P.g. alters ECM related functions in OK by interfering with integrin expression and activation state, cytoskeletal organization, and/or modification of integrin-proximal and distal transduction pathways, focusing on the effect of P.g. gingipains. In Aim 3, we will test specific P.g. and other bacterial factors such as proteinases and fimbriae for their possible effects on OK/ECM interactions, by comparing P.g. wild-type versus well-defined virulence mutant strains, using as a guide data from Aim 1 and 2. Results from these approaches will hopefully provide new and exciting molecular clues as to the mechanisms whereby P.g. may initiate and sustain periodontal disease. Such clues may be useful for devising new modalities of treatment and prevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PERIODONTAL GLYCOSYLATION
DISEASE:ROLE
OF
ABERRANT
IG
Principal Investigator & Institution: Mestecky, Jiri F.; Professor; Microbiology; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): Periodontal disease (PD) shares many common features with other human chronic inflammatory disease, such as rheumatoid arthritis, including production of autoantibodies, infiltration of lesions with plasma cells producing mainly IgG, and aberrant glycosylation of IgG-linked glycans. Particularly striking is the deficiency of galactose (Gal) in N-linked glycan side-chains on IgG molecules. Glycans have a profound effect on the biological activities of immunoglobulins (Ig). Deficiency of Gal residues renders such molecules pathogenic due to the fact that terminal N-acetylglucosamine residues, normally covered by Gal, became exposed and are recognized by the ubiquitous mannose-binding lectin resulting in the activation of complement with all the inflammatory consequences resulting in tissue damage. Based on considerable literature reports and our preliminary data, we propose to test the hypothesis that Ig-producing cells found in abundance in mononuclear cell infiltrates in PD secrete Ig molecules with aberrant glycosylation pattern of their glycan moieties. This in turn alters the biological properties of such Ig molecules with respect to their ability to activate complement and to interact with Fc receptors expressed on phagocytic cells resident in the inflamed lesions. Reduced glycosylation of Ig is likely to be due to the effect of cytokines locally produced by several cell types found in inflammatory lesions. Therefore, we propose the following Specific Aims: 1) Characterize the pattern of glycosylation aberrancies of Ig molecules in PD patients by reactivity with lectins highly specific for component monosaccharides and by direct carbohydrate analyses. 2) Determine the origin of aberrantly glycosylated Ig molecules by comparing glycosylation patterns of Ig in serum and lesions to determine whether Ig molecules with altered glycosylation are produced locally in the inflammatory lesions. 3) Determine if the aberrantly glycosylated Igs are specific for antigens of selected bacteria associated with PD. 4) Study mechanisms possibly involved in synthesis of Gal-deficient Ig in PD patients and the biological activities of Ig molecules with altered glycans. Results of these studies will generate information concerning previously unexplored inflammatory pathways that participate in the development of PD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF OSTEOCLASTIC BONE RESORPTION Principal Investigator & Institution: Baron, Roland E.; Orthopedics and Rehabilitation; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2001; Project Start 01-AUG-1977; Project End 31-DEC-2002 Summary: The research described in this application is aimed at understanding of the molecular mechanisms by which bone resorption is regulated. Bone resorption is performed by the osteoclast and acidification of the extracellular bone resorbing compartment constitutes one of the major physiological constraint on the osteoclast. Agents that regulate the differentiation and/or function of the osteoclast affect, albeit not exclusively, the ion transporters and attachment molecules involved in the acidification process. Investigation f the mechanisms by which peptide and steroid hormones affect these processes will therefore help refine our understanding of their regulation. Furthermore, to try to elucidate the mechanisms in which the non-receptor
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tyrosine kinase c-src is involved and so critically needed for normal osteoclast function may open new avenues for therapeutic intervention. The overall aim of this proposal is to further characterize the specific isoforms of the ion transporters involved in osteoclast-mediated acidification and the mechanisms by which their expression and/or function in bone resorption are regulated. This will include examples of the three main regulatory pathways, i.e., steroid hormones, peptide hormones and the tyrosine kinase signal transduction pathway. This proposal will address the following specific aims: (1) Further analyze the mechanisms by which the peptide hormone calcitonin regulates the processes of acidification by kidney cells and osteoclasts and compare them to the action of PTHrP 107-111 and RGD-containing peptides; (2) Further elucidate the mechanisms by which c-src regulates the function of the osteoclast and, possibly, some of the processes involved in acidification. (3) Further analyze the role of the steroid hormones 1,25- dihydroxyvitamin D3 and estrogens in the regulation of the expression of the various genes required for acidification by the osteoclast; This research program is particularly relevant to health related issues since a detailed analysis of the molecular mechanisms of bone resorption and its regulation can provide more specific and, thereby, more efficient, means to regulate these processes in vivo, whether to therapeutically activate osteoclasts in diseases involving a reduced rate of bone resorption (osteopetrosis, growth deficiencies for instance) or to inactivate osteoclasts in diseases involving an increased bone resorption (osteoporosis, osteoarthritis, periodontal disease, Paget's disease, etc.). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SEVERE PERIODONTITIS AS A RHEOLOGIC MODIFIER Principal Investigator & Institution: Engebretson, Steven P.; Division of Periodontics; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 01-FEB-2000; Project End 31-JAN-2004 Summary: Cytokines play a key role in the host response to microbial infection. These mediators are induced following contact with Gram (-) bacteria, and have a wide range of effects including influencing hemostatic factors, which are risk indicators for thrombotic events. Experimental evidence has conclusively established that a low-dose endotoxin bolus in healthy human volunteers alters rheologic parameters via a cytokine cascade resulting in a transient procoagulant state. Further, recent case-control studies have shown severe periodontal disease to be a strong independent risk factor for myocardial infarct and stroke. While causation has not been established, the initiating step is likely the transient bacteremia that result when the highly vascular, chronically inflamed periodontium is mechanically irritated by chewing, toothbrushing, and dental procedures. We hypothesize that chronic Gram(-) infection of the periodontium represents a potential source of circulating endotoxin which may adversely effect the coagulation system via a transient bacteremia-induced cytokine cascade, resulting in a net procoagulant state. The goal of this study is to explore the association of severe periodontitis and hemostatic variables. We suggest that patients with severe chronic adult periodontitis are at risk for altered rheologic and hemostatic variables as has been shown in experimental endotoxemia studies. Specifically, we will monitor the sera of 20 adults with severe periodontitis during common dental manipulations and periodontal treatment to determine the temporal appearance of endotoxin, inflammatory cytokines, and coagulation products, and to test whether conservative therapy can reduce serum levels of acute phase proteins. This study will help to define the pathophysiology of the thrombotic disorder-periodontitis relationship, and identify future thrombotic disorder prevention strategies. This study will be the first to experimentally demonstrate whether
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periodontal disease is a systemic modifier of clinically relevant hemostatic variables, and is designed to establish a molecular mechanism to explain this relationship. A positive finding in this regard should have broad ramifications for both dentistry and medicine. Dr. Engebretson will receive training in research methodology and molecular biology in order to explore the mechanisms of periodontal medicine through the conduct of human clinical studies as a career goal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SIALYL LEWIS X IN RISK ASSESSMENT FOR PERIODONTAL DISEASE Principal Investigator & Institution: Fisher, Susan J.; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2002 Summary: One of the most interesting and biologically important functions of salivary glycoproteins is their ability to serve as bacterial receptors. Although microbial adhesion and/or clearance from the oral cavity is the result of a complex interplay of many factors, interactions between bacterial proteins (e.g., adhesin, lectins) and the carbohydrate portions of the salivary molecules are often an important component of the process. Structural work from the Fisher laboratory that was completed over the last decade resulted in the unexpected finding that individual salivary glycoproteins carry unique oligosaccharide structures. In addition, we demonstrated that these glycoprotein-specific carbohydrate sequences can direct either bacterial or neutrophil adherence to the molecules they modify. Together, these results suggest that the manner in which salivary proteins are glycosylated could be an important factor in determining oral health. Very recently we showed that saliva samples from 5 of our 67 saliva donors lack the epitope that promotes leukocyte adherence, sialyl Lex (sLex), but still express oligosaccharides that act as bacterial receptors. Mice and humans who lack the glycosyltransferase that encodes sLex have greatly impaired immune function. In this context, we propose that individuals with saliva that lacks the epitope have an increased risk of developing oral infections. As a first step toward testing this hypothesis, we will determine whether the sLex-phenotype is associated with the development of periodontitis and/or smooth surface caries. If this hypothesis proves correct, than our laboratory findings could lead to a test for predicting oral health, analogous to using IL1 genotype as an indicator of susceptibility to severe periodontitis in adults. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SOCIAL INEQUALITIES IN PERIODONTAL DISEASES Principal Investigator & Institution: Borrell, Luisa N.; Epidemiology; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-MAY-2007 Summary: (provided by applicant): While some improvements in the health of the United States population have occurred over time, the persistence of disparities between groups, namely racial/ethnic or socioeconomic groups, indicates that such improvement has been uneven. Indeed, this improvement differential has actually contributed toward widening the disparities gap. Furthermore, although the long-standing focus of health comparisons in the US has been race/ethnicity, differences between the "haves" and the "have-nots" have been documented for years and remained pervasive. One such disparity is oral health, and more specifically periodontal disease disparities, which have been reported from national and local surveys for years. Previous studies show
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differences in periodontal health by race/ethnicity and personal socioeconomic indicators such as income and education. However, race/ethnicity, SES, and traditional risk factors do not fully explain the observed disparities in periodontal health. These findings suggest that the determinants of disparities in periodontal diseases may extend beyond individual characteristics. Therefore, to reduce the gap among groups, multilevel and interdisciplinary research approaches addressing more distant or upstream factors will need to be undertaken in studying periodontal health disparities (i.e., the place where people live and interact could influence and shape their health profiles and behaviors patterns). This career transition award will provide me with a unique opportunity to obtain new and innovative ways for studying not only the social determinants of periodontal diseases and other dental conditions but also health in general. Three areas of training are proposed: Oral Epidemiology, Advanced Epidemiological Methods and Statistical Analysis and Social Epidemiology. My training in these areas will be overseen by five mentors: Brian A. Burr, BDS, MPH, PhD; Rueben C. Warren DDS, DrPH, Ana V. Diez-Roux, MD, PhD; Bruce Link, PhD and Harold W. Neighbors, PhD. My goal is to become an independent investigator that tackles research questions using a social determinant of health approach including individuals as well as their immediate environment. The proposed research will extend our understanding on the determinants of periodontal diseases by: 1) assessing the contribution of both individual and neighborhood-level social factors; 2) examining the contribution of individual risk factors to racial/ethnic and socioeconomic differences in periodontal diseases; 3) investigating interactions across individual and neighborhood-level social factors; and 4) exploring periodontal health disparity trends over time. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STUDIES ACTINOMYCETEMCOMITANS
OF
THE
FLP
OPERON
IN
A.
Principal Investigator & Institution: Haase, Elaine M.; Oral Biology; State University of New York at Buffalo Suite 211 Ub Commons Amherst, Ny 14228 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2003 Summary: (provided by applicant) Actinobacillus actinomycetemcomitans (Aa) is a gram-negative bacterium whose primary habitat in humans is the subgingival sulcus. The association between Aa and aggressive periodontitis in adolescents (e.g. localized juvenile penodontitis, LJP) provides the most compelling evidence for bacterial specificity in periodontitis. Fresh isolates with a "rough," adherent colony phenotype spontaneously and irreversibly switch to a non-adherent, smooth colony phenotype when grown in broth. Recent preliminary studies in rats found only the rough phenotype cells capable of colonizing the oral cavity. The rough phenotype is primarily associated with numerous bundle-forming fimbriae on the cell surface. These fimbriae are encoded by a fimbrial operon (the flp operon) that has recently been identified in Aa. Transposon analysis has demonstrated that this operon is important in fimbrial expression. It likely influences phase variation, biofilm formation, and possibly leukotoxin association with the bacterial cell. Although the Flp fimbrillin subunit encoded by the first gene of this operon shares homology with type V-like fimbrillin, it is unique in several respects, especially its small size (6.5 kb). The focus of our study on regulation will be the 5' end of the operon, the flp to tadA sequence, based on previous complementation studies in transposon mutants. One of the SPECIFIC AIMS of this proposal is 1.) to determine the molecular basis of fimbrial phase variation through the study of transcription, translation, and cell localization of Flp fimbrillin subunit. By comparing the DNA sequence, transcription, and cell localization of the flp subunit in
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rough and spontaneous isogenic smooth variants, we will identify at what molecular level fimbrial expression is interrupted in the smooth variant, and identify potential cis regulatory sequences. Our preliminary transcriptional analysis of these genes suggests there may be more than one polycistronic message and more than one promoter within the operon. Our goal is 2.) to perform functional analysis of potential promoter regions and to determine the transcriptional organization of the flp operon through the study of selected deletion mutants. The experiments proposed in this application, when successfully completed, will provide the essential preliminary results for subsequent experiments to define the basis of fimbrial regulation in Aa. The information gained by these studies will ultimately aid in the development of novel strategies for preventing colonization of Aa and subsequent periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STUDY PLANS OF COMMUNICATION AND ORAL HEALTH DISPARITIES Principal Investigator & Institution: Koerber, Anne; Pediatric Dentistry; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-AUG-2004 Summary: (provided by applicant): This is a proposal for a planning grant to develop research approaches to discover whether dentist-patient communication leads to disparities in the prevalence of caries and periodontal disease in African American and Hispanic patients, and to identify testable methods to improve communication to avoid or alleviate those disparities. The specific aims are: Aim One: To create a research team and form an Advisory Board for the development of research plans, and to obtain training for the team. Aim Two: To look for methods of studying the effect of dental team communication on caries and periodontal disease of Hispanic and African American dental school patients. Aim Three: To determine what methods promote compliance and good communication between practitioners and Hispanic and African American patients, to identify training methods for the dental team, and to develop evaluation protocols to test the methods that can be used to apply for pilot funding or R01 funding, as appropriate. If dental teams are more likely to alienate or fail to make an effective working relationship with African American or Hispanic patients than with White patients, then they are less likely to obtain important information from that patient, they are less likely to have a positive influence on the patient's dental attendance or home care behavior, and they are less likely to convince the patient of the appropriate treatment plan. This is especially true if the treatment plan consists of regimens that require specific patient behaviors, such as plaque control programs. The methods to be used are 1) literature searches to identify variables and methods, 2) interviews and focus groups with patients, dental students, dental hygiene students, faculty and dental school staff to uncover potential difficulties and assure that important areas are identified, 3) an advisory board to review and advise about potential difficulties with the measures and methods, identify areas that should be explored, and to review the value of proposed research plans, 4) consultation and training with experts in measuring communication and in teaching cultural competence, and 5) statistical advice on measurement and analyses. A two year plan is proposed with the expectation of producing several research proposals aimed at both measuring the effect of doctorpatient communication on disparities and evaluating training methods to help dental providers communicate better with minorities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: T CELL RESPONSE TO A PERIODONTAL PATHOGEN Principal Investigator & Institution: Kraig, Ellen B.; Associate Professor; Cellular & Structural Biology; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2001; Project Start 15-FEB-1999; Project End 31-JAN-2003 Summary: We have focused on the periodontal pathogen, Actinobacillus actinomycetemcomitans (Aa). Individuals infected with this bacterium generate a specific humoral immune responses; some of the antigens recognized by serum antibodies have already been identified. On the other hand, the T cell epitopes on Aa have not yet been defined. Towards this end, we have undertaken an innovative, T cell hybridoma-based approach in order to dissect the T cell responses to Aa. In preliminary mice were orally inoculated with live bacteria and a panel of T cell hybridomas was generated. To our surprise, approximately 50% of the T cells reactive with Aa were specific for leukotoxin, a virulence factor produced by this oral pathogen. In order to characterize the immune response to Aa further, we now propose to: Aim 1. Clone genes that encode other T cell epitopes by direct screening of an Aa genomic library. The identities of the Aa proteins recognized by the T cell hybridomas will be determined and recombinant peptides generated for use in Aims 2 and 3. Aim 2: Characterize the nature of the immune response in vivo to individual Aa antigens. Mice will be: a) immunized with purified recombinant peptides, b) immunized with bacteria, or c) orally inoculated with viable Aa. Immune activation to individual T cell epitopes will then be assessed by studies of antibody production, T cell activation and cytokine production (Th1 versus Th2), and protection in a murine inflammation model. Aim 3. Determine whether the predominant T cell antigens in mice are similarly stimulatory in Aa-infected patients. Specifically, peripheral blood lymphocytes from EOP patients will be cultured in vitro with individual recombinant Aa peptides and T cell stimulation assessed by cytokine production and by spectrotyping. These aims will: i) provide the first evidence regarding T cell antigenic epitopes on this pathogen and ii) assess the relationship between T cell epitopes that are immunodominant in mice and those seen in humans. The long term goal is to develop and validate a model for evaluating host-parasite interactions, vaccine potency, and immune protection for periodontal diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE ROLE OF P38 MAP KINASE IN IL-6 GENE REGULATION Principal Investigator & Institution: Kirkwood, Keith L.; Periodontics and Endodontics; State University of New York at Buffalo Suite 211 Ub Commons Amherst, Ny 14228 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2004 Summary: (provided by applicant): Chronic production of cytokines mediates inflammatory diseases. Proinflammatory cytokine production in periodontal disease, as well as other chronic inflammatory bone diseases, results in a net bone loss that ultimately negatively affects host function. A complex cytokine network controlled by many cell types, dictates cellular response in bone resorption. Proinflammatory cytokines, such as interleukin (IL)-6, regulate bone resorption through interaction with downstream cytokines. Intracellular signaling pathways regulate IL-6 through a variety of potential mechanisms. This current proposal will focus on the role of p38 mitogen activated kinase (MAP) and how this kinase regulates IL-6 mRNA in osteoblasts, p38 has been shown to play a significant role in regulation of mRNA stability of several inflammatory mediators including IL-6, IL-8, and COX-2. Post-transcriptional control of mRNA stability has been implicated as a potential role of p38 MAP kinase. The
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molecular mechanisms that underlie p38 regulation are poorly understood, but increasing evident from other studies suggests that cis elements of the 3' untranslated region (UTR) may play a major role. Preliminary data obtained for this proposal indicates that a specific p38 MAP kinase inhibitor, SB203580, can inhibit IL-l-induced expression of IL-6 in a dose dependent manner. The mechanism has been shown to depend upon de novo protein synthesis and occurs at the post-transcriptional level where IL-6 mRNA stability in dramatic decreased in the presence of SB203580. Thus, this proposal will focus establishing the role of p38 MAP kinase in controlling IL-6 regulation. The proposed studies may be important because they could lead towards the development of novel pharmacological agents that regulate IL-6 expression at the posttranscriptional level. The specific aims of the proposal are the following: 1) To establish that p38 MAP kinase is a key regulator of IL-l-induced IL-6 production in osteoblastic cells through construction of dominate negative mutants of p38 MAP kinase and correlating p38 MAP kinase activity with IL-6 mRNA expression and stability, and 2) To determine the cis elements of IL-6 3' untranslated region (UTR) that mediate p38 MAP kinase-induced IL-6 mRNA stability. These studies will provide insight into how specific sequence elements of IL-6 are modulated by p38 MAP kinase and control mRNA decay rates. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSCRIPTION DIFFERENTIATION
FACTORS
CONTROL
OSTEOCLAST
Principal Investigator & Institution: Li, Yi-Ping; Forsyth Institute Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-FEB-1999; Project End 31-JAN-2003 Summary: Osteoclasts are multinucleated giant cells specialized for the removal of both the inorganic and organic phases of bone. Despite some recent insights from the effects of the targeted deletion of the c-fos, PU.1 and NF-kappaB transcription factor genes, the mechanisms by which transcription factors control the process of OC differentiation remain unclear. This has prompted us to develop a new method for generating osteoclastogenic cell lines (MOCP-5), isolated novel OC-specific cDNAs (i.e. cathepsin K) and their mouse genomic clones. Cathepsin K, which was recently cloned by the P.I. employing differential cDNA screening, and which plays a central role in normal bone remodeling as well as in pathological processes, is largely if not exclusively limited in its expression to OC and is a useful model protein for studies of osteoclast differentiation. The hypothesis of the proposed studies is that the determination of OC differentiation involves OC-specific transcription factors (OCTFs i.e. lineage-specific factors) which bind cis-regulatory elements of OC-specific genes, and function together with ubiquitous transcription factors (i.e. c-fos, PU.1 and NF-KB), to activate OC- specific genes expression, and hence control OC differentiation. Therefore, the cathepsin K gene critical cis-regulatory element-binding proteins (CCREBPs) should be OCTFs. In Aim 1, the mouse cathepsin K gene critical cis-regulatory elements (CCRE) will be mapped by mutagenesis of the cathepsin K promoter in vitro (MOCP-5 cells) and in vivo (transgenic mice). In Aim 2, The CCRE-binding protein(s) (CCREBP) will be characterized by mobility shift analyses and DNase I footprinting. CCREs homologs and function will be sought in other OC-expressed genes. In Aim 3, the cDNA encoding the CCREBP(s) will be isolated by Southwestern screening, or alternatively, by expression cloning or protein purification. The temporal and spatial expression of CCREBPs will be discerned by northern blot and in situ hybridization. Functional analysis of CCREBPs as putative OCTFs for regulation of OCs differentiation will be determined by co-transfection, forced expression and antisense blockade (Aim 4). The work proposed in this
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application should not only expand our basic understanding of the molecular mechanisms of OC differentiation, but will also aid our ability to develop therapeutic means of intervention in diseases involving increased bone resorption such as osteoporosis, periodontal disease, and arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: WHOLE GENOME SHOTGUN SEQUENCING OF STREPTOCOCCUS MITIS Principal Investigator & Institution: Tettelin, Herves' S.; Associate Investigator; Institute for Genomic Research Rockville, Md 20850 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-MAR-2003 Summary: (Adapted from the Investigator?s Abstract): The goal is to determine the complete genome sequence of the type strain of Streptococcus mitis, the predominant pioneer colonizer of tooth surfaces, and thus an initiator of dental plaque formation relevant to caries and periodontal disease. These pioneer streptococci facilitate or inhibit the establishment of late colonizers and oral pathogens. The predominance of IgA1 protease producing S. mitis variants in the pharynx is associated with allergic disease. S. mitis is a causative agent of endocarditits. It is an emerging source of septicemia in cancer patients, and the first vancomycin-resistant S. mitis isolate was reported in one such case. Phylogenetically, S. mitis and the overt pathogen S. pneumoniae, the causative agent of otitis, pneumoniae, septicemia and meningitis, are nearest neighbors. There is clear demonstration that the S. mitis type strain constitutes a reservoir of genetic determinants that contribute to penicillin resistance in pathogenic S. pneumoniae. The fear is that resistance to vancomycin will be transferred in a similar manner. The approach is a whole genome random sequencing strategy used successfully at TIGR to sequence twelve prokaryotic genomes. The yearlong project will consists of four phases: 1) Construction of small, medium and large insert size genomic libraries from S. mitis type strain, NCTC 12261. 2) Sequencing both ends of a sufficient number of small insert clones to provide 8-fold sequence coverage of the genome. Medium and large insert clones will be sequenced to 6-fold and 10-fold clone coverage, respectively. This will provide a sequence scaffold that will aid in verifying genome architecture. Further, 10-fold clone coverage from the large (50 kb) insert library will ensure a predicted sequence hit every 5,000 bp of the 2.2 Mb S. mitis genome. 3) Assembling the genome sequence from the collection of sequence reads, and closing remaining gaps. 4) Annotation of the genome sequence to identify all open reading frames, assignment of gene names and functional roles based on database similarity searches. Accomplishing this goal will provide a unique opportunity to compare the repertoire of genes in the commensal S. mitis to that of other streptococci, such as the highly virulent, type-4 S. pneumoniae strain, nearing completion at TIGR, allowing the identification of virulence-associated genes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National
3
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
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Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “periodontal disease” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for periodontal disease in the PubMed Central database: •
Activation of the interleukin-1beta precursor by Treponema denticola: a potential role in chronic inflammatory periodontal diseases. by Beausejour A, Deslauriers N, Grenier D.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175452
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Antiphosphorylcholine Antibody Levels Are Elevated in Humans with Periodontal Diseases. by Schenkein HA, Gunsolley JC, Best AM, Harrison MT, Hahn CL, Wu J, Tew JG.; 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96813
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CD26 immuno-expression and periodontal disease progression. by Manna PM, Costa JE, Gomez RS.; 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113778
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Incidence of Prevotella intermedia and Prevotella nigrescens Carriage among Family Members with Subclinical Periodontal Disease. by Fukui K, Kato N, Kato H, Watanabe K, Tatematsu N.; 1999 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=85513
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Molecular Epidemiology of Oral Treponemes Associated with Periodontal Disease. by Moter A, Hoenig C, Choi BK, Riep B, Gobel UB.; 1998 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=104836
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Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment. by Loesche WJ, Grossman NS.; 2001 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=89001
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Salivary Histatin 5 Is an Inhibitor of Both Host and Bacterial Enzymes Implicated in Periodontal Disease. by Gusman H, Travis J, Helmerhorst EJ, Potempa J, Troxler RF, Oppenheim FG.; 2001 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98034
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Systemic Inflammation in Cardiovascular and Periodontal Disease: Comparative Study. by Glurich I, Grossi S, Albini B, Ho A, Shah R, Zeid M, Baumann H, Genco RJ, De Nardin E.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=119918
4 With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with periodontal disease, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “periodontal disease” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for periodontal disease (hyperlinks lead to article summaries): •
A century of progress in understanding periodontal disease. Author(s): Williams RC. Source: Compend Contin Educ Dent. 2002 May; 23(5 Suppl): 3-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12789962&dopt=Abstract
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A longitudinal study of interleukin-1 gene polymorphisms and periodontal disease in a general adult population. Author(s): Cullinan MP, Westerman B, Hamlet SM, Palmer JE, Faddy MJ, Lang NP, Seymour GJ. Source: Journal of Clinical Periodontology. 2001 December; 28(12): 1137-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11737511&dopt=Abstract
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A new guide to nonsurgical management of periodontal disease. Author(s): Gottehrer NR, Shirdan TA. Source: Dent Today. 2002 September; 21(9): 54-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271843&dopt=Abstract
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A profile of the patient with periodontal disease? Author(s): Rees TD. Source: Periodontology 2000. 2003; 32: 9-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756029&dopt=Abstract
6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A retrospective investigation of advanced periodontal disease as a risk factor for septicemia in hematopoietic stem cell and bone marrow transplant recipients. Author(s): Akintoye SO, Brennan MT, Graber CJ, McKinney BE, Rams TE, Barrett AJ, Atkinson JC. Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2002 November; 94(5): 581-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12424452&dopt=Abstract
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Acquired immune suppression and other risk factors/indicators for periodontal disease progression. Author(s): Stanford TW, Rees TD. Source: Periodontology 2000. 2003; 32: 118-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756038&dopt=Abstract
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Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in human periodontal disease: occurrence and treatment. Author(s): Slots J, Ting M. Source: Periodontology 2000. 1999 June; 20: 82-121. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10522224&dopt=Abstract
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Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in periodontal disease: introduction. Author(s): Slots J. Source: Periodontology 2000. 1999 June; 20: 7-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10522220&dopt=Abstract
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Acupuncture: a unique effort to treat periodontal disease. Author(s): Schoor RS, Sussman HI, Kazandjian GK. Source: The Journal of the American Dental Association. 2001 December; 132(12): 1705-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11780990&dopt=Abstract
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Amplified crevicular leukocyte activity in aggressive periodontal disease. Author(s): Buchmann R, Hasilik A, Van Dyke TE, Lange DE. Source: Journal of Dental Research. 2002 October; 81(10): 716-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12351672&dopt=Abstract
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An update on HIV and periodontal disease. Author(s): Ryder MI. Source: J Periodontol. 2002 September; 73(9): 1071-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12296594&dopt=Abstract
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Antigen-presenting cells in human periodontal disease tissues. Author(s): Gemmell E, Carter CL, Hart DN, Drysdale KE, Seymour GJ. Source: Oral Microbiology and Immunology. 2002 December; 17(6): 388-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485331&dopt=Abstract
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Antiproliferative effect of topic hyaluronic acid gel. Study in gingival biopsies of patients with periodontal disease. Author(s): Mesa FL, Aneiros J, Cabrera A, Bravo M, Caballero T, Revelles F, del Moral RG, O'Valle F. Source: Histology and Histopathology. 2002; 17(3): 747-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12168783&dopt=Abstract
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Are cytokines linked to collagen breakdown during periodontal disease progression? Author(s): Ejeil AL, Gaultier F, Igondjo-Tchen S, Senni K, Pellat B, Godeau G, Gogly B. Source: J Periodontol. 2003 February; 74(2): 196-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666708&dopt=Abstract
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Assessing periodontal disease risk: a comparison of clinicians' assessment versus a computerized tool. Author(s): Persson GR, Mancl LA, Martin J, Page RC. Source: The Journal of the American Dental Association. 2003 May; 134(5): 575-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12785492&dopt=Abstract
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Association between bone loss in periodontal disease and polymorphism of Nacetyltransferase (NAT2). Author(s): Kocher T, Sawaf H, Fanghanel J, Timm R, Meisel P. Source: Journal of Clinical Periodontology. 2002 January; 29(1): 21-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11846845&dopt=Abstract
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Association between interleukin-1 genotype and periodontal disease in a diabetic population. Author(s): Guzman S, Karima M, Wang HY, Van Dyke TE. Source: J Periodontol. 2003 August; 74(8): 1183-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514232&dopt=Abstract
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Association between nanobacteria and periodontal disease. Author(s): Ciftcioglu N, McKay DS, Kajander EO. Source: Circulation. 2003 August 26; 108(8): E58-9; Author Reply E58-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939248&dopt=Abstract
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Association between periodontal disease and left ventricle mass in essential hypertension. Author(s): Angeli F, Verdecchia P, Pellegrino C, Pellegrino RG, Pellegrino G, Prosciutti L, Giannoni C, Cianetti S, Bentivoglio M. Source: Hypertension. 2003 March; 41(3): 488-92. Epub 2003 February 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623948&dopt=Abstract
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Associations of medical status and physical fitness with periodontal disease. Author(s): Wakai K, Kawamura T, Umemura O, Hara Y, Machida J, Anno T, Ichihara Y, Mizuno Y, Tamakoshi A, Lin Y, Nakayama T, Ohno Y. Source: Journal of Clinical Periodontology. 1999 October; 26(10): 664-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10522778&dopt=Abstract
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Bacterial mediators in periodontal disease. Author(s): Loesche WJ. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1993 June; 16 Suppl 4: S203-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8324120&dopt=Abstract
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Bacterial penetration into the gingival tissue in periodontal disease. Author(s): Saglie R, Elbaz JJ. Source: J West Soc Periodontol Periodontal Abstr. 1983; 31(3): 85-93. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6227754&dopt=Abstract
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Bacteriocin production by Actinobacillus actinomycetemcomitans isolated from the oral cavity of humans with periodontal disease, periodontally healthy subjects and marmosets. Author(s): Lucia LF, Farias FF, Eustaquio CJ, Auxiliadora M, Carvalho R, Alviano CS, Farias LM. Source: Research in Microbiology. 2002 January-February; 153(1): 45-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11881898&dopt=Abstract
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Bacteriocin production by Fusobacterium isolates recovered from the oral cavity of human subjects with and without periodontal disease and of marmosets. Author(s): Oliveira AA, Farias LM, Nicoli JR, Costa JE, Carvalho MA. Source: Research in Microbiology. 1998 September; 149(8): 585-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9795996&dopt=Abstract
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Bacteriological diagnosis of periodontal disease. Author(s): Okuda K. Source: Bull Tokyo Dent Coll. 1994 August; 35(3): 107-19. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8620588&dopt=Abstract
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Bacteriology of periodontal disease. Author(s): Russell RR. Source: Curr Opin Dent. 1992 September; 2: 66-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1392003&dopt=Abstract
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Bacteroides forsythus prtH genotype in periodontitis patients: occurrence and association with periodontal disease. Author(s): Tan KS, Song KP, Ong G. Source: Journal of Periodontal Research. 2001 December; 36(6): 398-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11762876&dopt=Abstract
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Biased T cell receptor V gene usage in tissues with periodontal disease. Author(s): Nakajima T, Yamazaki K, Hara K. Source: Journal of Periodontal Research. 1996 January; 31(1): 2-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8636872&dopt=Abstract
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Biologically active factors in the treatment of periodontal disease. Author(s): Terranova VP. Source: Curr Opin Periodontol. 1993; : 129-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8401835&dopt=Abstract
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Black-pigmented Bacteroides species, Capnocytophaga species, and Actinobacillus actinomycetemcomitans in human periodontal disease: virulence factors in colonization, survival, and tissue destruction. Author(s): Slots J, Genco RJ. Source: Journal of Dental Research. 1984 March; 63(3): 412-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6583243&dopt=Abstract
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Black-pigmenting gram-negative bacteria in periodontal disease. I. Topographic distribution in the human dentition. Author(s): Mombelli A, McNabb H, Lang NP. Source: Journal of Periodontal Research. 1991 July; 26(4): 301-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1831497&dopt=Abstract
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Black-pigmenting gram-negative bacteria in periodontal disease. II. Screening strategies for detection of P. gingivalis. Author(s): Mombelli A, McNabb H, Lang NP. Source: Journal of Periodontal Research. 1991 July; 26(4): 308-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1831498&dopt=Abstract
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Bleeding on probing. A predictor for the progression of periodontal disease? Author(s): Lang NP, Joss A, Orsanic T, Gusberti FA, Siegrist BE. Source: Journal of Clinical Periodontology. 1986 July; 13(6): 590-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3489010&dopt=Abstract
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Blocking periodontal disease progression by inhibiting tissue-destructive enzymes: a potential therapeutic role for tetracyclines and their chemically-modified analogs. Author(s): Rifkin BR, Vernillo AT, Golub LM. Source: J Periodontol. 1993 August; 64(8 Suppl): 819-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8410621&dopt=Abstract
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Blocking periodontal disease progression with anti-inflammatory agents. Author(s): Howell TH. Source: J Periodontol. 1993 August; 64(8 Suppl): 828-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8410622&dopt=Abstract
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Bug hunt may turn up keys to periodontal disease. Author(s): Jones DG. Source: J Calif Dent Assoc. 2000 March; 28(3): 171-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11326531&dopt=Abstract
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Burkitt-like lymphoma presenting as a periodontal disease in AIDS patients: a report of two cases. Author(s): Nittayananta W, Apinawatavorngul S, Chungpanich S, Pongpanich S, Kietthubthew S. Source: Oral Diseases. 1998 December; 4(4): 281-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10200708&dopt=Abstract
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Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease. Author(s): Kido J, Nakamura T, Kido R, Ohishi K, Yamauchi N, Kataoka M, Nagata T. Source: Journal of Clinical Periodontology. 1999 October; 26(10): 653-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10522776&dopt=Abstract
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Cell-surface proteoglycan expression by lymphocytes from peripheral blood and gingiva in health and periodontal disease. Author(s): Manakil JF, Sugerman PB, Li H, Seymour GJ, Bartold PM. Source: Journal of Dental Research. 2001 August; 80(8): 1704-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11669479&dopt=Abstract
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Change of antibiotic susceptibility following periodontal therapy. A pilot study in aggressive periodontal disease. Author(s): Buchmann R, Muller RF, Van Dyke TE, Lange DE. Source: Journal of Clinical Periodontology. 2003 March; 30(3): 222-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631180&dopt=Abstract
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Chemokines in human periodontal disease tissues. Author(s): Gemmell E, Carter CL, Seymour GJ. Source: Clinical and Experimental Immunology. 2001 July; 125(1): 134-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11472436&dopt=Abstract
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Clinical and microbiological studies of periodontal disease in Sjogren syndrome patients. Author(s): Kuru B, McCullough MJ, Yilmaz S, Porter SR. Source: Journal of Clinical Periodontology. 2002 February; 29(2): 92-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11908470&dopt=Abstract
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Clinical outcome observed in subjects with recurrent periodontal disease following local treatment with 25% metronidazole gel. Author(s): Jansson H, Bratthall G, Soderholm G. Source: J Periodontol. 2003 March; 74(3): 372-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710758&dopt=Abstract
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Clinical usefulness of microbiological diagnostic tools in the management of periodontal disease. Author(s): Suchett-Kaye G, Morrier JJ, Barsotti O. Source: Research in Microbiology. 2001 September; 152(7): 631-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11605983&dopt=Abstract
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Clinical, pathological and immunological aspects of periodontal disease. Author(s): Kinane DF, Lappin DF. Source: Acta Odontologica Scandinavica. 2001 June; 59(3): 154-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501884&dopt=Abstract
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Comparison of body composition and periodontal disease using nutritional assessment techniques: Third National Health and Nutrition Examination Survey (NHANES III). Author(s): Wood N, Johnson RB, Streckfus CF. Source: Journal of Clinical Periodontology. 2003 April; 30(4): 321-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694430&dopt=Abstract
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Comparison of periodontal disease status of adults in two untreated indigenous populations of Guatemala, Central America. Author(s): Dowsett SA, Eckert GJ, Kowolik MJ. Source: Journal of Clinical Periodontology. 2002 August; 29(8): 784-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390578&dopt=Abstract
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Comprehensive treatment concept in a young adult patient with severe periodontal disease: a case report. Author(s): Hofer D, Hammerle CH, Lang NP. Source: Quintessence Int. 2002 September; 33(8): 567-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12238687&dopt=Abstract
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Coping with stress: its influence on periodontal disease. Author(s): Wimmer G, Janda M, Wieselmann-Penkner K, Jakse N, Polansky R, Pertl C. Source: J Periodontol. 2002 November; 73(11): 1343-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12479640&dopt=Abstract
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Coronary artery disease and periodontal disease: is there a link? Author(s): Abou-Raya S, Naeem A, Abou-El KH, El BS. Source: Angiology. 2002 March-April; 53(2): 141-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952103&dopt=Abstract
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Costimulatory molecules in human periodontal disease tissues. Author(s): Gemmell E, McHugh GB, Grieco DA, Seymour GJ. Source: Journal of Periodontal Research. 2001 April; 36(2): 92-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11327084&dopt=Abstract
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Current concepts and future trends for periodontal disease and periodontal therapy, Part 1: Etiology, risk factors, natural history, and systemic implications. Author(s): Lamster IB. Source: Dent Today. 2001 January; 20(1): 50-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524887&dopt=Abstract
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Current concepts and future trends for periodontal disease and periodontal therapy, Part 2: Classification, diagnosis, and nonsurgical and surgical therapy. Author(s): Lamster IB. Source: Dent Today. 2001 March; 20(3): 86-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524874&dopt=Abstract
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Current evidence regarding periodontal disease as a risk factor in preterm birth. Author(s): Jeffcoat MK, Geurs NC, Reddy MS, Goldenberg RL, Hauth JC. Source: Ann Periodontol. 2001 December; 6(1): 183-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887462&dopt=Abstract
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Current research in diagnostic methods for assessing periodontal disease. Author(s): Anil S, Baiju FM. Source: Indian J Dent Res. 1998 October-December; 9(4): 120-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10530198&dopt=Abstract
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Cytokines in periodontal disease: where to from here? Author(s): Seymour GJ, Gemmell E. Source: Acta Odontologica Scandinavica. 2001 June; 59(3): 167-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501886&dopt=Abstract
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Cytolethal distending toxin of Actinobacillus actinomycetemcomitans. Occurrence and association with periodontal disease. Author(s): Tan KS, Song KP, Ong G. Source: Journal of Periodontal Research. 2002 August; 37(4): 268-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200970&dopt=Abstract
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Defensin-induced adaptive immunity in mice and its potential in preventing periodontal disease. Author(s): Brogden KA, Heidari M, Sacco RE, Palmquist D, Guthmiller JM, Johnson GK, Jia HP, Tack BF, McCray PB. Source: Oral Microbiology and Immunology. 2003 April; 18(2): 95-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654098&dopt=Abstract
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Dental bacterial plaques. Nature and role in periodontal disease. Author(s): Christersson LA, Zambon JJ, Genco RJ. Source: Journal of Clinical Periodontology. 1991 July; 18(6): 441-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1890226&dopt=Abstract
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Dental caries and periodontal disease (prevention and control methods). Author(s): Juan SP. Source: J Philipp Dent Assoc. 1999 June-August; 51(1): 29-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10808358&dopt=Abstract
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Dental caries and periodontal disease in Down's syndrome patients. Author(s): Chan AR. Source: Univ Tor Dent J. 1994; 7(1): 18-21. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9584771&dopt=Abstract
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Design, characterisation and preliminary clinical evaluation of a novel mucoadhesive topical formulation containing tetracycline for the treatment of periodontal disease. Author(s): Jones DS, Woolfson AD, Brown AF, Coulter WA, McClelland C, Irwin CR. Source: Journal of Controlled Release : Official Journal of the Controlled Release Society. 2000 July 3; 67(2-3): 357-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10825567&dopt=Abstract
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Destructive membranous periodontal disease (Ligneous periodontitis). Author(s): Gunhan O, Gunhan M, Berker E, Gurgan CA, Yildirim H. Source: J Periodontol. 1999 August; 70(8): 919-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10476902&dopt=Abstract
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Destructive periodontal disease in adults 30 years of age and older in the United States, 1988-1994. Author(s): Albandar JM, Brunelle JA, Kingman A. Source: J Periodontol. 1999 January; 70(1): 13-29. Erratum In: J Periodontol 1999 March; 70(3): 351. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10052767&dopt=Abstract
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Diabetes and periodontal disease. Author(s): Roeder LB, Dennison DK. Source: J Gt Houst Dent Soc. 1998 September; 70(2): 13-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9796525&dopt=Abstract
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Diabetes and periodontal disease: two sides of a coin. Author(s): Mealey BL. Source: Compend Contin Educ Dent. 2000 November; 21(11): 943-6, 948, 950, Passim; Quiz 956. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11968145&dopt=Abstract
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Diabetes as a modifier of periodontal disease expression. Author(s): Yalda B, Offenbacher S, Collins JG. Source: Periodontology 2000. 1994 October; 6: 37-49. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9673169&dopt=Abstract
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Diagnosis and progression of periodontal disease: current status of bleeding as a diagnostic indicator. Author(s): Polson AM. Source: Dtsch Zahnarztl Z. 1987 May; 42(5): 414-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3503735&dopt=Abstract
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Diagnosis of periodontal disease using rapid identification of “activity-related” gramnegative species. Author(s): Tanner AC, Dzink JL, Socransky SS, Des Roches CL. Source: Journal of Periodontal Research. 1987 May; 22(3): 207-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2955099&dopt=Abstract
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Diagnostic tests for periodontal disease activity. Author(s): Smith AJ. Source: Dent Update. 1995 May; 22(4): 140-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9601215&dopt=Abstract
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Diagnostic tests for periodontal disease. Author(s): Geurs NC, Wang IC. Source: J Indiana Dent Assoc. 1999 Spring; 78(1): 30-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10740491&dopt=Abstract
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Dietary vitamin C and the risk for periodontal disease. Author(s): Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ. Source: J Periodontol. 2000 August; 71(8): 1215-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10972636&dopt=Abstract
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Differences in periodontal disease-associated microorganisms of subgingival plaque in prepubertal, pubertal and postpubertal children. Author(s): Wojcicki CJ, Harper DS, Robinson PJ. Source: J Periodontol. 1987 April; 58(4): 219-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3473218&dopt=Abstract
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Differential expression of costimulatory molecules in chronic inflammatory periodontal disease tissue. Author(s): Orima K, Yamazaki K, Aoyagi T, Hara K. Source: Clinical and Experimental Immunology. 1999 January; 115(1): 153-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9933436&dopt=Abstract
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Dinucleotide repeat polymorphism in the interleukin-10 gene promoter (IL-10.G) and genetic susceptibility to early-onset periodontal disease. Author(s): Hennig BJ, Parkhill JM, Chapple IL, Heasman PA, Taylor JJ. Source: Genes and Immunity. 2000 August; 1(6): 402-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11196688&dopt=Abstract
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Distribution of periodontal disease in a Swedish adult population 1973, 1983 and 1993. Author(s): Hugoson A, Norderyd O, Slotte C, Thorstensson H. Source: Journal of Clinical Periodontology. 1998 July; 25(7): 542-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9696253&dopt=Abstract
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Dynamics of systemic antibody responses in periodontal disease. Author(s): Ebersole JL, Frey DE, Taubman MA, Haffajee AD, Socransky SS. Source: Journal of Periodontal Research. 1987 May; 22(3): 184-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2955094&dopt=Abstract
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Effect of estrogen supplementation on periodontal disease. Author(s): Grossi SG. Source: Compend Contin Educ Dent Suppl. 1998; (22): S30-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12089759&dopt=Abstract
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Effect of gallium arsenide diode laser on human periodontal disease: a microbiological and clinical study. Author(s): Yilmaz S, Kuru B, Kuru L, Noyan U, Argun D, Kadir T. Source: Lasers in Surgery and Medicine. 2002; 30(1): 60-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11857606&dopt=Abstract
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Effect of initial treatment of chronic inflammatory periodontal disease on the frequency of peripheral blood T-lymphocytes specific to periodontopathic bacteria. Author(s): Mahanonda R, Seymour GJ, Powell LW, Good MF, Halliday JW. Source: Oral Microbiology and Immunology. 1991 August; 6(4): 221-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1667435&dopt=Abstract
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Effect of vitamin E gel, placebo gel and chlorhexidine on periodontal disease. Author(s): Cohen RE, Ciancio SG, Mather ML, Curro FA. Source: Clin Prev Dent. 1991 September-October; 13(5): 20-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1809525&dopt=Abstract
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Effects of smoking on the prevalence and severity of periodontal disease. Author(s): Tanur E. Source: Tex Dent J. 2001 October; 118(10): 922-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11764623&dopt=Abstract
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Effects of specific nutrients on periodontal disease onset, progression and treatment. Author(s): Neiva RF, Steigenga J, Al-Shammari KF, Wang HL. Source: Journal of Clinical Periodontology. 2003 July; 30(7): 579-89. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834494&dopt=Abstract
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Ehlers-Danlos syndrome with severe early-onset periodontal disease (EDS-VIII) is a distinct, heterogeneous disorder with one predisposition gene at chromosome 12p13. Author(s): Rahman N, Dunstan M, Teare MD, Hanks S, Douglas J, Coleman K, Bottomly WE, Campbell ME, Berglund B, Nordenskjold M, Forssell B, Burrows N, Lunt P, Young I, Williams N, Bignell GR, Futreal PA, Pope FM. Source: American Journal of Human Genetics. 2003 July; 73(1): 198-204. Epub 2003 May 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776252&dopt=Abstract
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Elevated levels of collagen cross-link residues in gingival tissues and crevicular fluid of teeth with periodontal disease. Author(s): Jepsen S, Springer IN, Buschmann A, Hedderich J, Acil Y. Source: European Journal of Oral Sciences. 2003 June; 111(3): 198-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786949&dopt=Abstract
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Enamel pearls and cervical enamel projections on 2 maxillary molars with localized periodontal disease: case report and histologic study. Author(s): Risnes S, Segura JJ, Casado A, Jimenez-Rubio A. Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2000 April; 89(4): 493-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10760733&dopt=Abstract
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Environmental tobacco smoke and periodontal disease in the United States. Author(s): Arbes SJ Jr, Agustsdottir H, Slade GD. Source: American Journal of Public Health. 2001 February; 91(2): 253-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11211634&dopt=Abstract
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Epidemiologic associations between periodontal disease and chronic obstructive pulmonary disease. Author(s): Garcia RI, Nunn ME, Vokonas PS. Source: Ann Periodontol. 2001 December; 6(1): 71-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887473&dopt=Abstract
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Epidemiology of periodontal disease among older adults: a review. Author(s): Locker D, Slade GD, Murray H. Source: Periodontology 2000. 1998 February; 16: 16-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10337302&dopt=Abstract
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Epidemiology of periodontal disease in children and adolescents. Author(s): Jenkins WM, Papapanou PN. Source: Periodontology 2000. 2001; 26: 16-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11452904&dopt=Abstract
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Epidemiology of periodontal disease: a review and clinical perspectives. Author(s): Irfan UM, Dawson DV, Bissada NF. Source: J Int Acad Periodontol. 2001 January; 3(1): 14-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666973&dopt=Abstract
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Epidemiology of periodontal disease: a review. Author(s): Dummett CO. Source: Military Medicine. 1983 July; 148(7): 606-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6413896&dopt=Abstract
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Estimation of interleukin-1beta levels in the gingival crevicular fluid in health and in inflammatory periodontal disease. Author(s): Faizuddin M, Bharathi SH, Rohini NV. Source: Journal of Periodontal Research. 2003 April; 38(2): 111-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12608903&dopt=Abstract
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Evidence for an association between periodontal disease and cardiovascular disease. Author(s): Taylor BA, Tofler GH. Source: Ann R Australas Coll Dent Surg. 2002 October; 16: 82-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507144&dopt=Abstract
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Explanatory models for clinical and subjective indicators of periodontal disease in an adult population. Author(s): Unell L, Soderfeldt B, Halling A, Birkhed D. Source: Journal of Clinical Periodontology. 2000 January; 27(1): 22-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10674958&dopt=Abstract
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Exploring interrelationships between diabetes and periodontal disease in African Americans. Author(s): Taylor GW. Source: Compend Contin Educ Dent. 2001 July; 22(3 Spec No): 42-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11913252&dopt=Abstract
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Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction. Author(s): Liu D, Xu JK, Figliomeni L, Huang L, Pavlos NJ, Rogers M, Tan A, Price P, Zheng MH. Source: International Journal of Molecular Medicine. 2003 January; 11(1): 17-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12469211&dopt=Abstract
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Factors affecting IL-1-mediated collagen metabolism by fibroblasts and the pathogenesis of periodontal disease: a review of the literature. Author(s): Havemose-Poulsen A, Holmstrup P. Source: Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists. 1997; 8(2): 217-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9167094&dopt=Abstract
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Factors associated with active and inactive root caries in patients with periodontal disease. Author(s): Ravald N, Birkhed D. Source: Caries Research. 1991; 25(5): 377-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1747889&dopt=Abstract
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Factors in virulence expression and their role in periodontal disease pathogenesis. Author(s): Holt SC, Bramanti TE. Source: Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists. 1991; 2(2): 177-281. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1912148&dopt=Abstract
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Factors influencing the diagnosis and management of periodontal disease by general dental practitioners. Author(s): Chestnutt IG, Kinane DF. Source: British Dental Journal. 1997 November 8; 183(9): 319-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9401142&dopt=Abstract
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Failure of macrophage activation in destructive periodontal disease. Author(s): Chapple CC, Srivastava M, Hunter N. Source: The Journal of Pathology. 1998 November; 186(3): 281-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10211117&dopt=Abstract
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Familial transmission of periodontal pathogens as a risk factor for periodontal disease progression. Author(s): Zambon JJ. Source: Compendium. 1994 August; 15(8): 996, 998-1000. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7987900&dopt=Abstract
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Family ties may be a link to periodontal disease. Author(s): O'Hehir TE. Source: Rdh. 1994 July; 14(7): 19. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7997599&dopt=Abstract
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Features of severe periodontal disease in a teenager with Chediak-Higashi syndrome. Author(s): Delcourt-Debruyne EM, Boutigny HR, Hildebrand HF. Source: J Periodontol. 2000 May; 71(5): 816-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10872965&dopt=Abstract
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Fetal cartilage graft in periodontal disease. Author(s): Han JQ, Liang RX. Source: Chinese Medical Journal. 1987 May; 100(5): 429-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3115717&dopt=Abstract
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Fibronectin levels of unstimulated saliva from naval recruits with and without chronic inflammatory periodontal disease. Author(s): Lamberts BL, Pederson ED, Bial JJ, Tombasco PK. Source: Journal of Clinical Periodontology. 1989 July; 16(6): 342-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2668347&dopt=Abstract
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Flow cytometric approach to human polymorphonuclear leukocyte activation induced by gingival crevicular fluid in periodontal disease. Author(s): Biselli R, Ferlini C, Di Murro C, Paolantonio M, Fattorossi A. Source: Inflammation. 1995 August; 19(4): 479-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7558252&dopt=Abstract
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Fluoridation effects on periodontal disease among adults. Author(s): Grembowski D, Fiset L, Spadafora A, Milgrom P. Source: Journal of Periodontal Research. 1993 May; 28(3): 166-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8496780&dopt=Abstract
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Focus on primary care: periodontal disease: implications for women's health. Author(s): Zeeman GG, Veth EO, Dennison DK. Source: Obstetrical & Gynecological Survey. 2001 January; 56(1): 43-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11140863&dopt=Abstract
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For the dental patient. Preventing periodontal disease. Author(s): American Dental Association. Source: The Journal of the American Dental Association. 2001 September; 132(9): 1339. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11665361&dopt=Abstract
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Formulation of a drug delivery system based on a mixture of monoglycerides and triglycerides for use in the treatment of periodontal disease. Author(s): Norling T, Lading P, Engstrom S, Larsson K, Krog N, Nissen SS. Source: Journal of Clinical Periodontology. 1992 October; 19(9 Pt 2): 687-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1447387&dopt=Abstract
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Free amino acid levels in oral fluids of normal subjects and patients with periodontal disease. Author(s): Syrjanen SM, Alakuijala L, Alakuijala P, Markkanen SO, Markkanen H. Source: Archives of Oral Biology. 1990; 35(3): 189-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2190545&dopt=Abstract
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Free amino-acid content of wax-stimulated human whole saliva as related to periodontal disease. Author(s): Syrjanen S, Piironen P, Markkanen H. Source: Archives of Oral Biology. 1987; 32(9): 607-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3481959&dopt=Abstract
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Frequency distribution of individuals aged 20-70 years according to severity of periodontal disease experience in 1973 and 1983. Author(s): Hugoson A, Laurell L, Lundgren D. Source: Journal of Clinical Periodontology. 1992 April; 19(4): 227-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1569222&dopt=Abstract
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From plaque formation to periodontal disease, is there a role for nitric oxide? Author(s): Rausch-Fan X, Matejka M. Source: European Journal of Clinical Investigation. 2001 October; 31(10): 833-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11737219&dopt=Abstract
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Fructosamine as a possible monitoring parameter in non-insulin dependent diabetes mellitus patients with periodontal disease. Author(s): Unal T, Firatli E, Sivas A, Meric H, Oz H. Source: J Periodontol. 1993 March; 64(3): 191-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8463941&dopt=Abstract
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Gamma delta T lymphocytes in human periodontal disease tissue. Author(s): Gemmell E, Seymour GJ. Source: J Periodontol. 1995 September; 66(9): 780-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7500244&dopt=Abstract
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GCF IL-1beta profiles in periodontal disease. Author(s): Engebretson SP, Grbic JT, Singer R, Lamster IB. Source: Journal of Clinical Periodontology. 2002 January; 29(1): 48-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11846849&dopt=Abstract
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Gender and smoking-related risk reduction of periodontal disease with variant myeloperoxidase alleles. Author(s): Meisel P, Krause T, Cascorbi I, Schroeder W, Herrmann F, John U, Kocher T. Source: Genes and Immunity. 2002 April; 3(2): 102-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11960308&dopt=Abstract
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General considerations in the treatment of periodontal disease: infection control, medications, and wound healing. Author(s): Cattabriga M, Di Murro C, Paolantonio M. Source: Curr Opin Dent. 1991 February; 1(1): 66-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1912635&dopt=Abstract
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Generalized cervical root resorption associated with periodontal disease. Author(s): Beertsen W, Piscaer M, Van Winkelhoff AJ, Everts V. Source: Journal of Clinical Periodontology. 2001 November; 28(11): 1067-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11686829&dopt=Abstract
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Genetic and heritable risk factors in periodontal disease. Author(s): Michalowicz BS. Source: J Periodontol. 1994 May; 65(5 Suppl): 479-88. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8046564&dopt=Abstract
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Genetic and inheritance considerations in periodontal disease. Author(s): Michalowicz BS. Source: Curr Opin Periodontol. 1993; : 11-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8401833&dopt=Abstract
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Genetic considerations of risk in human periodontal disease. Author(s): Hart TC. Source: Curr Opin Periodontol. 1994; : 3-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8032464&dopt=Abstract
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Genetic risk for severe periodontal disease. Author(s): Newman MG. Source: Compend Contin Educ Dent. 1997 September; 18(9): 881-4, 886, 888 Passim; Quiz 894. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9533366&dopt=Abstract
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Genetic susceptibility to periodontal disease. Author(s): Nevins M, Nevins ML. Source: Dent Today. 1998 February; 17(2): 94-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9560673&dopt=Abstract
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Gingival crevicular fluid antibody to Actinobacillus actinomycetemcomitans in periodontal disease. Author(s): Ebersole JL, Cappelli D. Source: Oral Microbiology and Immunology. 1994 December; 9(6): 335-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7870468&dopt=Abstract
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Gingival crevicular fluid gelatinase and its relationship to periodontal disease in human subjects. Author(s): Teng YT, Sodek J, McCulloch CA. Source: Journal of Periodontal Research. 1992 September; 27(5): 544-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1403585&dopt=Abstract
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Gingival crevicular fluid of patients with gingivitis or periodontal disease: evaluation of elastase-alpha 1 proteinase inhibitor complex. Author(s): Huynh C, Roch-Arveiller M, Meyer J, Giroud JP. Source: Journal of Clinical Periodontology. 1992 March; 19(3): 187-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1556247&dopt=Abstract
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Gingival recession in smokers and non-smokers with minimal periodontal disease. Author(s): Muller HP, Stadermann S, Heinecke A. Source: Journal of Clinical Periodontology. 2002 February; 29(2): 129-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11895540&dopt=Abstract
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Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population. Author(s): Tsai C, Hayes C, Taylor GW. Source: Community Dentistry and Oral Epidemiology. 2002 June; 30(3): 182-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12000341&dopt=Abstract
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Glycosaminoglycans and periodontal disease: analysis of GCF by safranin O. Author(s): Giannobile WV, Riviere GR, Gorski JP, Tira DE, Cobb CM. Source: J Periodontol. 1993 March; 64(3): 186-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8463940&dopt=Abstract
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Guided tissue regeneration in the treatment of human periodontal disease. Author(s): Vallone D, Dyer B, Caffesse PG. Source: J Gt Houst Dent Soc. 1990 May; 61(10): 6-10. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2375847&dopt=Abstract
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Guided tissue regeneration procedure applied to the treatment of endodonticperiodontal disease: analysis of a case. Author(s): Zorzano LA, Sanchez AL, Chacartegi JE, Llamosas RM, Cundin EE, Zuazua JS. Source: Quintessence Int. 1997 February; 28(2): 87-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10332360&dopt=Abstract
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Health promotion and behavioral approaches in the prevention of periodontal disease in children and adolescents. Author(s): Kallio PJ. Source: Periodontology 2000. 2001; 26: 135-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11452902&dopt=Abstract
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Heat shock proteins in the human periodontal disease process. Author(s): Ando T, Kato T, Ishihara K, Ogiuchi H, Okuda K. Source: Microbiology and Immunology. 1995; 39(5): 321-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7565172&dopt=Abstract
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Hepatocyte growth factor (HGF) in periodontal disease: detection of HGF in gingival crevicular fluid. Author(s): Ohshima M, Sakai A, Ito K, Otsuka K. Source: Journal of Periodontal Research. 2002 February; 37(1): 8-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11842942&dopt=Abstract
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Hepatocyte growth factor in saliva: a possible marker for periodontal disease status. Author(s): Ohshima M, Fujikawa K, Akutagawa H, Kato T, Ito K, Otsuka K. Source: J Oral Sci. 2002 March; 44(1): 35-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12058868&dopt=Abstract
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Herpesviruses in human periodontal disease. Author(s): Contreras A, Slots J. Source: Journal of Periodontal Research. 2000 February; 35(1): 3-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10791704&dopt=Abstract
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Higher risk of preterm birth and low birth weight in women with periodontal disease. Author(s): Lopez NJ, Smith PC, Gutierrez J. Source: Journal of Dental Research. 2002 January; 81(1): 58-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11820369&dopt=Abstract
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High-tech periodontics: new weaponry for scaling back periodontal disease. Author(s): Farr C. Source: Dent Today. 1996 October; 15(10): 66, 70-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9567843&dopt=Abstract
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HIV disease as a risk factor for periodontal disease. Author(s): Murray PA. Source: Compendium. 1994 August; 15(8): 1052, 1054-63; Quiz 1064. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7987897&dopt=Abstract
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HIV infection and periodontal disease. Author(s): Yeung SC. Source: Ann R Australas Coll Dent Surg. 2000 October; 15: 331-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11709967&dopt=Abstract
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HIV-associated periodontal disease. Author(s): Cobb CM. Source: Northwest Dent. 1993 September-October; 72(5): 25-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8041599&dopt=Abstract
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HIV-associated periodontal disease: new oral spirochete found. Author(s): Rosenstein DI, Riviere GR, Elott KS. Source: The Journal of the American Dental Association. 1993 July; 124(7): 76-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8335802&dopt=Abstract
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Hormonal factors in periodontal disease. Author(s): Soory M. Source: Dent Update. 2000 October; 27(8): 380-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11218530&dopt=Abstract
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Host mechanisms in the pathogenesis of periodontal disease. Author(s): Landi L, Amar S, Polins AS, Van Dyke TE. Source: Curr Opin Periodontol. 1997; 4: 3-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9655015&dopt=Abstract
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Host modulation as a therapeutic strategy in the treatment of periodontal disease. Author(s): Kornman KS. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1999 March; 28(3): 520-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10194070&dopt=Abstract
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How do data from deepest pocket per quadrant relate to full-mouth scores? Progression of untreated periodontal disease in young Indonesians. Author(s): Timmerman MF, Van der Weijden GA, Hart AA, Abbas F, Winkel EG, Van der Velden U. Source: Journal of Clinical Periodontology. 2002 March; 29(3): 219-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11940141&dopt=Abstract
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How periodontal disease may contribute to cardiovascular disease. Author(s): Kinane DF, Lowe GD. Source: Periodontology 2000. 2000 June; 23: 121-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11276758&dopt=Abstract
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Humoral immune response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in periodontal disease. Author(s): Kinane DF, Mooney J, Ebersole JL. Source: Periodontology 2000. 1999 June; 20: 289-340. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10522229&dopt=Abstract
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Humoral immune response to an antigen from Porphyromonas gingivalis 381 in periodontal disease. Author(s): Kurihara H, Nishimura F, Nakamura T, Nakagawa M, Tanimoto I, Nomura Y, Kokeguchi S, Kato K, Murayama Y. Source: Infection and Immunity. 1991 August; 59(8): 2758-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1855992&dopt=Abstract
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Humoral immune responses in periodontal disease may have mucosal and systemic immune features. Author(s): Kinane DF, Lappin DF, Koulouri O, Buckley A. Source: Clinical and Experimental Immunology. 1999 March; 115(3): 534-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10193430&dopt=Abstract
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Humoral immunity to stress proteins and periodontal disease. Author(s): Lopatin DE, Shelburne CE, Van Poperin N, Kowalski CJ, Bagramian RA. Source: J Periodontol. 1999 October; 70(10): 1185-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10534073&dopt=Abstract
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Identification of lysine decarboxylase as a mammalian cell growth inhibitor in Eikenella corrodens: possible role in periodontal disease. Author(s): Levine M, Progulske-Fox A, Denslow ND, Farmerie WG, Smith DM, Swearingen WT, Miller FC, Liang Z, Roe BA, Pan HQ. Source: Microbial Pathogenesis. 2001 April; 30(4): 179-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11312612&dopt=Abstract
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Identification of periodontal disease-associated bacteria in the “plaque-free zone”. Author(s): Noiri Y, Ebisu S. Source: J Periodontol. 2000 August; 71(8): 1319-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10972648&dopt=Abstract
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Immunodominant antigens in periodontal disease: a real or illusive concept? Author(s): Podmore M, Ebersole JL, Kinane DF. Source: Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists. 2001; 12(2): 179-85. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11345527&dopt=Abstract
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Importance of periodontal disease in the kidney patient. Author(s): Craig RG, Spittle MA, Levin NW. Source: Blood Purification. 2002; 20(1): 113-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11803168&dopt=Abstract
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Incidence of Prevotella intermedia and Prevotella nigrescens carriage among family members with subclinical periodontal disease. Author(s): Fukui K, Kato N, Kato H, Watanabe K, Tatematsu N. Source: Journal of Clinical Microbiology. 1999 October; 37(10): 3141-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10488167&dopt=Abstract
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Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses? Author(s): Brandtzaeg P. Source: Acta Odontologica Scandinavica. 2001 August; 59(4): 235-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11570527&dopt=Abstract
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Influence of periodontal disease on Th1/Th2-type cytokines in saliva of HIV-positive individuals. Author(s): Vastardis S, Leigh JE, Wozniak K, Yukna R, Fidel PL Jr. Source: Oral Microbiology and Immunology. 2003 April; 18(2): 88-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654096&dopt=Abstract
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Initial outcome and long-term effect of surgical and non-surgical treatment of advanced periodontal disease. Author(s): Serino G, Rosling B, Ramberg P, Socransky SS, Lindhe J. Source: Journal of Clinical Periodontology. 2001 October; 28(10): 910-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11686808&dopt=Abstract
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Insulin resistance and periodontal disease: an epidemiologic overview of research needs and future directions. Author(s): Donahue RP, Wu T. Source: Ann Periodontol. 2001 December; 6(1): 119-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887454&dopt=Abstract
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Insulin resistance linked to periodontal disease. Author(s): McBride DL. Source: Journal of Dental Hygiene : Jdh / American Dental Hygienists' Association. 2000 Summer; 74(3): 172. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11314635&dopt=Abstract
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Interdisciplinary treatment plannning for patients with advanced periodontal disease. Author(s): Evans RI, Dawson AS, Hyde MT. Source: Ann R Australas Coll Dent Surg. 2002 October; 16: 95-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507147&dopt=Abstract
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Interleukin 1 beta, interleukin 6, beta 2-microglobulin, and transforming growth factor-alpha in gingival crevicular fluid from human periodontal disease. Author(s): Mogi M, Otogoto J, Ota N, Inagaki H, Minami M, Kojima K. Source: Archives of Oral Biology. 1999 June; 44(6): 535-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10401533&dopt=Abstract
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Interleukin-1 haplotype and periodontal disease progression following therapy. Author(s): Ehmke B, Kress W, Karch H, Grimm T, Klaiber B, Flemmig TF. Source: Journal of Clinical Periodontology. 1999 December; 26(12): 810-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10599909&dopt=Abstract
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Intraoral distribution of Actinobacillus actinomycetemcomitans in young adults with minimal periodontal disease. Author(s): Muller HP, Heinecke A, Fuhrmann A, Eger T, Zoller L. Source: Journal of Periodontal Research. 2001 April; 36(2): 114-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11327078&dopt=Abstract
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Investigation of the association between angiographically defined coronary artery disease and periodontal disease. Author(s): Malthaner SC, Moore S, Mills M, Saad R, Sabatini R, Takacs V, McMahan AC, Oates TW Jr. Source: J Periodontol. 2002 October; 73(10): 1169-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416775&dopt=Abstract
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Involvement of T-lymphocytes in periodontal disease and in direct and indirect induction of bone resorption. Author(s): Taubman MA, Kawai T. Source: Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists. 2001; 12(2): 125-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11345523&dopt=Abstract
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Is estrogen deficiency a risk factor for periodontal disease? Author(s): Genco RJ, Grossi SG. Source: Compend Contin Educ Dent Suppl. 1998; (22): S23-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12089758&dopt=Abstract
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Is periodontal disease a risk factor for coronary artery disease (CAD)? Author(s): Lavelle C. Source: Journal (Canadian Dental Association). 2002 March; 68(3): 176-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11911814&dopt=Abstract
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Is there a relationship between rheumatoid arthritis and periodontal disease? Author(s): Mercado F, Marshall RI, Klestov AC, Bartold PM. Source: Journal of Clinical Periodontology. 2000 April; 27(4): 267-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10783841&dopt=Abstract
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Isotypic antibody response to plaque anaerobes in periodontal disease. Author(s): Plombas M, Gobert B, De March AK, Sarda MN, Sixou M, Bene MC, Miller N, Faure GC. Source: J Periodontol. 2002 December; 73(12): 1507-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546101&dopt=Abstract
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Knowledge, attitude and practice of dental caries and periodontal disease prevention among primary school teachers in Udupi municipality. Author(s): Goel P, Shetty V. Source: J Indian Soc Pedod Prev Dent. 1997 December; 15(4): 124-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10635125&dopt=Abstract
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Lack of effect of oral hygiene training on periodontal disease progression over 3 years in adolescents. Author(s): Albandar JM, Buischi YA, Oliveira LB, Axelsson P. Source: J Periodontol. 1995 April; 66(4): 255-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7782978&dopt=Abstract
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Legal aspects of orthodontic practice: risk management concepts. Periodontal disease in orthodontic practice. Author(s): Machen DE. Source: American Journal of Orthodontics and Dentofacial Orthopedics : Official Publication of the American Association of Orthodontists, Its Constituent Societies, and the American Board of Orthodontics. 1989 May; 95(5): 445-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2718975&dopt=Abstract
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Less than 20% of the US population has periodontal disease. Author(s): Hillam DG. Source: Journal of Clinical Periodontology. 1999 April; 26(4): 264-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10223400&dopt=Abstract
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Leukotoxic activity in Actinobacillus (Haemophilus) actinomycetemcomitans isolated from periodontal disease patients. Author(s): Ohta H, Kokeguchi S, Fukui K, Kato K. Source: Microbiology and Immunology. 1987; 31(4): 313-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3613993&dopt=Abstract
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Levels of interleukin 1 beta in tissue from sites of active periodontal disease. Author(s): Stashenko P, Fujiyoshi P, Obernesser MS, Prostak L, Haffajee AD, Socransky SS. Source: Journal of Clinical Periodontology. 1991 August; 18(7): 548-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1894750&dopt=Abstract
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Lipoxin A(4) analogues inhibit leukocyte recruitment to Porphyromonas gingivalis: a role for cyclooxygenase-2 and lipoxins in periodontal disease. Author(s): Pouliot M, Clish CB, Petasis NA, Van Dyke TE, Serhan CN. Source: Biochemistry. 2000 April 25; 39(16): 4761-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10769133&dopt=Abstract
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Local and systemic chemotherapy in the management of periodontal disease: an opinion and review of the concept. Author(s): Addy M, Renton-Harper P. Source: Journal of Oral Rehabilitation. 1996 April; 23(4): 219-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8730268&dopt=Abstract
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Local and systemic production of immunoglobulins to periodontopathogens in periodontal disease. Author(s): Suzuki JB, Martin SA, Vincent JW, Falkler WA Jr. Source: Journal of Periodontal Research. 1984 November; 19(6): 599-603. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6241235&dopt=Abstract
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Local and systemic TCR V gene expression in advanced periodontal disease. Author(s): Berglundh T, Liljenberg B, Tarkowski A, Lindhe J. Source: Journal of Clinical Periodontology. 1998 February; 25(2): 125-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9495611&dopt=Abstract
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Local antimicrobial therapies in periodontal disease. Author(s): Kinane DF. Source: Ann R Australas Coll Dent Surg. 2000 October; 15: 57-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11709978&dopt=Abstract
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Local production of IgA- and IgM-rheumatoid factors in adult periodontal disease. Author(s): Hirsch HZ, Tarkowski A, Koopman WJ, Mestecky J. Source: Journal of Clinical Immunology. 1989 July; 9(4): 273-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2671009&dopt=Abstract
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Longitudinal changes in periodontal disease in untreated subjects. Author(s): Lindhe J, Okamoto H, Yoneyama T, Haffajee A, Socransky SS. Source: Journal of Clinical Periodontology. 1989 November; 16(10): 662-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2613935&dopt=Abstract
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Longitudinal comparison of the periodontal status of patients with moderate to severe periodontal disease receiving no treatment, non-surgical treatment, and surgical treatment utilizing individual sites for analysis. Author(s): Harrel SK, Nunn ME. Source: J Periodontol. 2001 November; 72(11): 1509-19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11759862&dopt=Abstract
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Longitudinal periodontal tissue alterations during supportive therapy. Findings from subjects with normal and high susceptibility to periodontal disease. Author(s): Rosling B, Serino G, Hellstrom MK, Socransky SS, Lindhe J. Source: Journal of Clinical Periodontology. 2001 March; 28(3): 241-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11284537&dopt=Abstract
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Longitudinal study of predictive factors for periodontal disease and tooth loss. Author(s): Machtei EE, Hausmann E, Dunford R, Grossi S, Ho A, Davis G, Chandler J, Zambon J, Genco RJ. Source: Journal of Clinical Periodontology. 1999 June; 26(6): 374-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10382577&dopt=Abstract
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Long-term effect of surgical/non-surgical treatment of periodontal disease. Author(s): Lindhe J, Westfelt E, Nyman S, Socransky SS, Haffajee AD. Source: Journal of Clinical Periodontology. 1984 August; 11(7): 448-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6378986&dopt=Abstract
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Long-term maintenance of patients treated for advanced periodontal disease. Author(s): Lindhe J, Nyman S. Source: Journal of Clinical Periodontology. 1984 September; 11(8): 504-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6384275&dopt=Abstract
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Loss-of-function mutations in the cathepsin C gene result in periodontal disease and palmoplantar keratosis. Author(s): Toomes C, James J, Wood AJ, Wu CL, McCormick D, Lench N, Hewitt C, Moynihan L, Roberts E, Woods CG, Markham A, Wong M, Widmer R, Ghaffar KA, Pemberton M, Hussein IR, Temtamy SA, Davies R, Read AP, Sloan P, Dixon MJ, Thakker NS. Source: Nature Genetics. 1999 December; 23(4): 421-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10581027&dopt=Abstract
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Low levels of destructive periodontal disease in a rural population in west Bengal, India. Author(s): Maity AK, Banerjee K, Pal TK. Source: Community Dentistry and Oral Epidemiology. 1994 February; 22(1): 60-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8143446&dopt=Abstract
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Low metacarpal bone density, tooth loss, and periodontal disease in Japanese women. Author(s): Inagaki K, Kurosu Y, Kamiya T, Kondo F, Yoshinari N, Noguchi T, Krall EA, Garcia RI. Source: Journal of Dental Research. 2001 September; 80(9): 1818-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11926240&dopt=Abstract
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Malocclusion as an etiologic factor in periodontal disease: a retrospective essay. Author(s): Geiger AM. Source: American Journal of Orthodontics and Dentofacial Orthopedics : Official Publication of the American Association of Orthodontists, Its Constituent Societies, and the American Board of Orthodontics. 2001 August; 120(2): 112-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11500651&dopt=Abstract
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Management of molar teeth with periodontal disease. Author(s): Dowell P, McLaughlin WS. Source: Dent Update. 2000 January-February; 27(1): 25, 28-32, 34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11218264&dopt=Abstract
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Managing risk factors in successful nonsurgical treatment of periodontal disease. Author(s): Gottehrer NR. Source: Dent Today. 2003 January; 22(1): 64-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12616891&dopt=Abstract
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Maternal periodontal disease and preterm low birthweight: case-control study. Author(s): Davenport ES, Williams CE, Sterne JA, Murad S, Sivapathasundram V, Curtis MA. Source: Journal of Dental Research. 2002 May; 81(5): 313-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12097443&dopt=Abstract
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Maternal periodontal disease is associated with an increased risk for preeclampsia. Author(s): Boggess KA, Lieff S, Murtha AP, Moss K, Beck J, Offenbacher S. Source: Obstetrics and Gynecology. 2003 February; 101(2): 227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576243&dopt=Abstract
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Matrix molecules and growth factors as indicators of periodontal disease activity. Author(s): Giannobile WV, Al-Shammari KF, Sarment DP. Source: Periodontology 2000. 2003; 31: 125-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656999&dopt=Abstract
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Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Author(s): Janket SJ, Baird AE, Chuang SK, Jones JA. Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2003 May; 95(5): 559-69. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738947&dopt=Abstract
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Metastatic breast carcinoma mimicking periodontal disease on radiographs. Author(s): Ogutcen-Toller M, Metin M, Yildiz L. Source: Journal of Clinical Periodontology. 2002 March; 29(3): 269-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11940148&dopt=Abstract
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Microbiology of destructive periodontal disease in adolescent patients with congenital neutropenia. A report of 3 cases. Author(s): van Winkelhoff AJ, Schouten-van Meeteren AY, Baart JA, VandenbrouckeGrauls CM. Source: Journal of Clinical Periodontology. 2000 November; 27(11): 793-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11073320&dopt=Abstract
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Microbiology of periodontal disease in children and young adults. Author(s): Darby I, Curtis M. Source: Periodontology 2000. 2001; 26: 33-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11452905&dopt=Abstract
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Microorganisms as risk indicators for periodontal disease. Author(s): Ezzo PJ, Cutler CW. Source: Periodontology 2000. 2003; 32: 24-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756031&dopt=Abstract
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Mineral status of skeleton and advanced periodontal disease. Author(s): Klemetti E, Collin HL, Forss H, Markkanen H, Lassila V. Source: Journal of Clinical Periodontology. 1994 March; 21(3): 184-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8157771&dopt=Abstract
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Molecular interaction of Porphyromonas gingivalis with host cells: implication for the microbial pathogenesis of periodontal disease. Author(s): Amano A. Source: J Periodontol. 2003 January; 74(1): 90-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12593602&dopt=Abstract
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Monitoring untreated periodontal disease. Author(s): Harley A, Floyd P, Watts T. Source: Journal of Clinical Periodontology. 1987 April; 14(4): 221-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3473089&dopt=Abstract
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Monocyte-derived RANTES is intrinsically elevated in periodontal disease while MCP-1 levels are related to inflammation and are inversely correlated with IL-12 levels. Author(s): Fokkema SJ, Loos BG, van der Velden U. Source: Clinical and Experimental Immunology. 2003 March; 131(3): 477-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605701&dopt=Abstract
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Mouthrinses and periodontal disease. Author(s): FDI Commission. Source: Int Dent J. 2002 October; 52(5): 346-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12418603&dopt=Abstract
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Multiple dental extractions using general anesthesia for a patient with Down and Eisenmenger syndromes and periodontal disease. Author(s): Bozich JG, Albert TW. Source: Spec Care Dentist. 1990 March-April; 10(2): 51-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11100206&dopt=Abstract
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My love affair with periodontal disease. Author(s): Glasscoe D. Source: Rdh. 1999 October; 19(10): 70-2, 74, 76 Passim. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10921370&dopt=Abstract
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Negative effects of chronic inflammatory periodontal disease on diabetes mellitus. Author(s): Nishimura F, Kono T, Fujimoto C, Iwamoto Y, Murayama Y. Source: J Int Acad Periodontol. 2000 April; 2(2): 49-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666961&dopt=Abstract
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Neutrophil-mediated tissue injury in periodontal disease pathogenesis: findings from localized aggressive periodontitis. Author(s): Kantarci A, Oyaizu K, Van Dyke TE. Source: J Periodontol. 2003 January; 74(1): 66-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12593599&dopt=Abstract
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New antimicrobial delivery systems join the fight against periodontal disease. Interview by Phillip Bonner. Author(s): Drisko CH. Source: Dent Today. 1999 October; 18(10): 96, 98. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10803147&dopt=Abstract
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New concepts regarding the pathogenesis of periodontal disease in HIV infection. Author(s): Lamster IB, Grbic JT, Mitchell-Lewis DA, Begg MD, Mitchell A. Source: Ann Periodontol. 1998 July; 3(1): 62-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9722691&dopt=Abstract
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Nicotine effects on polymorphonuclear cell apoptosis and lipopolysaccharideinduced monocyte functions. A possible role in periodontal disease? Author(s): Mariggio MA, Guida L, Laforgia A, Santacroce R, Curci E, Montemurro P, Fumarulo R. Source: Journal of Periodontal Research. 2001 February; 36(1): 32-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11246702&dopt=Abstract
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Nitric oxide synthesis and severity of human periodontal disease. Author(s): Batista AC, Silva TA, Chun JH, Lara VS. Source: Oral Diseases. 2002 September; 8(5): 254-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12363110&dopt=Abstract
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Nitric oxide synthesis is increased in periodontal disease. Author(s): Matejka M, Partyka L, Ulm C, Solar P, Sinzinger H. Source: Journal of Periodontal Research. 1998 November; 33(8): 517-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9879526&dopt=Abstract
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Noninflammatory destructive periodontal disease (NDPD). Author(s): Page RC, Sturdivant EC. Source: Periodontology 2000. 2002; 30: 24-39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12236893&dopt=Abstract
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Nutrition, infection, and periodontal disease. Author(s): Boyd LD, Madden TE. Source: Dent Clin North Am. 2003 April; 47(2): 337-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699235&dopt=Abstract
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Nutrition, inflammation, and periodontal disease. Author(s): Ritchie CS, Kinane DF. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2003 May; 19(5): 475-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714106&dopt=Abstract
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Obesity and periodontal disease in young, middle-aged, and older adults. Author(s): Al-Zahrani MS, Bissada NF, Borawskit EA. Source: J Periodontol. 2003 May; 74(5): 610-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816292&dopt=Abstract
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Occlusal forces as a risk factor for periodontal disease. Author(s): Harrel SK. Source: Periodontology 2000. 2003; 32: 111-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756037&dopt=Abstract
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On the association between hypercholesterolemia, cardiovascular disease and severe periodontal disease. Author(s): Katz J, Chaushu G, Sharabi Y. Source: Journal of Clinical Periodontology. 2001 September; 28(9): 865-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11493357&dopt=Abstract
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Oral hygiene in the prevention of caries and periodontal disease. Author(s): Loe H. Source: Int Dent J. 2000 June; 50(3): 129-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10967765&dopt=Abstract
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Oral scurvy and periodontal disease. Author(s): Touyz LZ. Source: Journal (Canadian Dental Association). 1997 December; 63(11): 837-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9433025&dopt=Abstract
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Oro-antral fistula: an unusual complication of HIV-associated periodontal disease. Author(s): Felix DH, Wray D, Smith GL, Jones GA. Source: British Dental Journal. 1991 July 20; 171(2): 61-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1873097&dopt=Abstract
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Orthodontic movement into infrabony defects in patients with advanced periodontal disease: a clinical and radiological study. Author(s): Corrente G, Abundo R, Re S, Cardaropoli D, Cardaropoli G. Source: J Periodontol. 2003 August; 74(8): 1104-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514223&dopt=Abstract
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Osteoporosis and periodontal disease progression. Author(s): Geurs NC, Lewis CE, Jeffcoat MK. Source: Periodontology 2000. 2003; 32: 105-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756036&dopt=Abstract
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Osteoporosis and periodontal disease: is there a relationship? Author(s): Krejci CB. Source: J West Soc Periodontol Periodontal Abstr. 1996; 44(2): 37-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9477863&dopt=Abstract
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Oxygen sufficiency in the gingiva of smokers and non-smokers with periodontal disease. Author(s): Hanioka T, Tanaka M, Ojima M, Takaya K, Matsumori Y, Shizukuishi S. Source: J Periodontol. 2000 December; 71(12): 1846-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156041&dopt=Abstract
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Partial-mouth assessment of periodontal disease in an adult population of the United States. Author(s): Owens JD, Dowsett SA, Eckert GJ, Zero DT, Kowolik MJ. Source: J Periodontol. 2003 August; 74(8): 1206-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514235&dopt=Abstract
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Periodontal disease among the middle-aged Vietnamese population. Author(s): Do LG, Spencer JA, Roberts-Thomson K, Ha DH, Tran TV, Trinh HD. Source: J Int Acad Periodontol. 2003 July; 5(3): 77-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12887146&dopt=Abstract
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Periodontal disease and diabetes mellitus. Bidirectional relationship. Author(s): Mealey BL, Rethman MP. Source: Dent Today. 2003 April; 22(4): 107-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733412&dopt=Abstract
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Periodontal disease and preterm birth: results of a pilot intervention study. Author(s): Jeffcoat MK, Hauth JC, Geurs NC, Reddy MS, Cliver SP, Hodgkins PM, Goldenberg RL. Source: J Periodontol. 2003 August; 74(8): 1214-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514236&dopt=Abstract
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Periodontal disease and preterm low birth weight deliveries. Author(s): Zachariasen RD, Dennison DK. Source: J Gt Houst Dent Soc. 1998 November; 70(4): 16-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10530117&dopt=Abstract
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Periodontal disease as a risk factor for cardiovascular disease and myocardial infarction. Author(s): Stein H. Source: Ont Dent. 1999 January-February; 76(1): 16-20. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10518886&dopt=Abstract
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Periodontal disease incidence, progression and rate of tooth loss in a general dental practice: the results of a 12-year retrospective analysis of patient's clinical records. Author(s): Nicholls C. Source: British Dental Journal. 2003 May 10; 194(9): 485-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835778&dopt=Abstract
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Periodontal disease: a look at historical, current, and future approaches to therapy. Author(s): Suzuki JB. Source: J Indiana Dent Assoc. 2003 Spring; 82(1): 16-21. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12815935&dopt=Abstract
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Prevalence assessment of periodontal disease in 3-5 year old children through PSR-population study. Author(s): Andrade IT, Rapp GE. Source: J Int Acad Periodontol. 2002 October; 4(4): 126-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12670092&dopt=Abstract
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Prevalence assessment of periodontal disease in 3-6 year old children through PSR--a pilot study. Author(s): Rapp GE, Garcia RV, Motta AC, Andrade IT, Biao MA, Carvalho PB. Source: J Int Acad Periodontol. 2001 July; 3(3): 75-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666945&dopt=Abstract
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Qualitative and quantitative studies of Gc (vitamin D-binding protein) in normal subjects and patients with periodontal disease. Author(s): Krayer JW, Emerson DL, Goldschmidt-Clermont PJ, Nel AE, Werner PA, Galbraith RM. Source: Journal of Periodontal Research. 1987 July; 22(4): 259-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2957481&dopt=Abstract
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Quantitative relationship of Treponema denticola to severity of periodontal disease. Author(s): Simonson LG, Goodman CH, Bial JJ, Morton HE. Source: Infection and Immunity. 1988 April; 56(4): 726-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3346072&dopt=Abstract
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Relationship between periodontal disease and C-reactive protein among adults in the Atherosclerosis Risk in Communities study. Author(s): Slade GD, Ghezzi EM, Heiss G, Beck JD, Riche E, Offenbacher S. Source: Archives of Internal Medicine. 2003 May 26; 163(10): 1172-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767953&dopt=Abstract
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Relationship between periodontal disease in pregnant women and the nutritional condition of their newborns. Author(s): Romero BC, Chiquito CS, Elejalde LE, Bernardoni CB. Source: J Periodontol. 2002 October; 73(10): 1177-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416776&dopt=Abstract
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Relationship between periodontal disease, tooth loss, and carotid artery plaque: the Oral Infections and Vascular Disease Epidemiology Study (INVEST). Author(s): Desvarieux M, Demmer RT, Rundek T, Boden-Albala B, Jacobs DR Jr, Papapanou PN, Sacco RL; Oral Infections and Vascular Disease Epidemiology Study (INVEST). Source: Stroke; a Journal of Cerebral Circulation. 2003 September; 34(9): 2120-5. Epub 2003 July 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12893951&dopt=Abstract
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Relationship between stress factors and periodontal disease. Author(s): Pistorius A, Krahwinkel T, Willershausen B, Boekstegen C. Source: European Journal of Medical Research. 2002 September 30; 7(9): 393-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435617&dopt=Abstract
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Relationship of destructive periodontal disease to the acute-phase response. Author(s): Craig RG, Yip JK, So MK, Boylan RJ, Socransky SS, Haffajee AD. Source: J Periodontol. 2003 July; 74(7): 1007-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12931763&dopt=Abstract
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Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities (ARIC) study. Author(s): Beck JD, Elter JR, Heiss G, Couper D, Mauriello SM, Offenbacher S. Source: Arteriosclerosis, Thrombosis, and Vascular Biology. 2001 November; 21(11): 1816-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11701471&dopt=Abstract
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Replantation of avulsed central incisor with advanced periodontal disease: a case report. Author(s): Casterline AC. Source: Endodontics & Dental Traumatology. 1999 June; 15(3): 135-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10530158&dopt=Abstract
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Resolution of crevicular fluid leukocyte activity in patients treated for aggressive periodontal disease. Author(s): Buchmann R, Hasilik A, Van Dyke TE, Lange DE. Source: J Periodontol. 2002 September; 73(9): 995-1002. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12296600&dopt=Abstract
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Risk factors for periodontal disease progression among elderly people. Author(s): Ogawa H, Yoshihara A, Hirotomi T, Ando Y, Miyazaki H. Source: Journal of Clinical Periodontology. 2002 July; 29(7): 592-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12354083&dopt=Abstract
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Risk of severe periodontal disease in a Swedish adult population. A longitudinal study. Author(s): Norderyd O, Hugoson A, Grusovin G. Source: Journal of Clinical Periodontology. 1999 September; 26(9): 608-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10487312&dopt=Abstract
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Salt and periodontal disease. Author(s): Khoury NS. Source: British Dental Journal. 2003 May 10; 194(9): 467. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835762&dopt=Abstract
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Serum markers of periodontal disease status and inflammation in hemodialysis patients. Author(s): Rahmati MA, Craig RG, Homel P, Kaysen GA, Levin NW. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2002 November; 40(5): 983-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12407643&dopt=Abstract
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Serum modulation of neutrophil response to Porphyromonas gingivalis LPS in periodontal disease. Author(s): Soolari AS, Champagne C, Punzi JS, Amar S, Van Dyke TE. Source: J Int Acad Periodontol. 1999 October; 1(4): 101-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666954&dopt=Abstract
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Simultaneous measurement of the viability, aggregation, and live and dead adherence of Streptococcus crista, Streptococcus mutans and Actinobacillus actinomycetemcomitans in human saliva in relation to indices of caries, dental plaque and periodontal disease. Author(s): Rudney JD, Staikov RK. Source: Archives of Oral Biology. 2002 May; 47(5): 347-59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12015215&dopt=Abstract
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Single-nucleotide polymorphism in the CD14 promoter and periodontal disease expression in a Japanese population. Author(s): Yamazaki K, Ueki-Maruyama K, Oda T, Tabeta K, Shimada Y, Tai H, Nakajima T, Yoshie H, Herawati D, Seymour GJ. Source: Journal of Dental Research. 2003 August; 82(8): 612-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885845&dopt=Abstract
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Smoking and periodontal disease. Author(s): Rivera-Hidalgo F. Source: Periodontology 2000. 2003; 32: 50-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756033&dopt=Abstract
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Some risk factors for the progression of periodontal disease. Author(s): Skaleric U, Kovac-Kavcic M. Source: J Int Acad Periodontol. 2000 January; 2(1): 19-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666982&dopt=Abstract
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Specific fibronectin fragments as markers of periodontal disease status. Author(s): Huynh QN, Wang S, Tafolla E, Gansky SA, Kapila S, Armitage GC, Kapila YL. Source: J Periodontol. 2002 October; 73(10): 1101-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416766&dopt=Abstract
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Systemic antibiotics in the treatment of periodontal disease. Author(s): Slots J, Ting M. Source: Periodontology 2000. 2002; 28: 106-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12013339&dopt=Abstract
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Systemic disorders in patients with periodontal disease. Author(s): Lagervall M, Jansson L, Bergstrom J. Source: Journal of Clinical Periodontology. 2003 April; 30(4): 293-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694426&dopt=Abstract
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The distribution of periodontal disease and loss of attachment in jaw sextants in different age groups--cross-sectional study. Author(s): Spalj S, Plancak D. Source: Coll Antropol. 2003; 27 Suppl 1: 183-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12955908&dopt=Abstract
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The effect of a triclosan-containing dentifrice on the progression of periodontal disease in an adult population. Author(s): Cullinan MP, Westerman B, Hamlet SM, Palmer JE, Faddy MJ, Seymour GJ. Source: Journal of Clinical Periodontology. 2003 May; 30(5): 414-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716333&dopt=Abstract
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The genetic relationship to periodontal disease. Author(s): Nares S. Source: Periodontology 2000. 2003; 32: 36-49. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756032&dopt=Abstract
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The owner-animal-environment triad in the treatment of canine periodontal disease. Author(s): Hale FA. Source: J Vet Dent. 2003 June; 20(2): 118-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14528858&dopt=Abstract
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The prevention of dental caries and periodontal disease from the cradle to the grave: what is the best available evidence? Author(s): Davies RM. Source: Dent Update. 2003 May; 30(4): 170-6, 178-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830693&dopt=Abstract
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The relationship between coronary artery disease and periodontal disease. Author(s): Johnson-Leong C, Patel G, Messieha Z. Source: Dent Today. 2003 February; 22(2): 100-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680268&dopt=Abstract
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The relationship of palato-gingival grooves and cervical enamel projections to localized periodontal disease. A review of the literature. Author(s): Jackson P. Source: Ont Dent. 1999 January-February; 76(1): 21-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10518887&dopt=Abstract
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The role of acquired immunity and periodontal disease progression. Author(s): Teng YT. Source: Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists. 2003; 14(4): 237-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907693&dopt=Abstract
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The role of herpesviruses in periodontal disease. Author(s): Simonian K. Source: J West Soc Periodontol Periodontal Abstr. 2003; 51(1): 5-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830822&dopt=Abstract
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Topical antimicrobials: new horizons for management of periodontal disease in general practice? Author(s): Urquhart E, Addy M. Source: Dent Update. 1995 April; 22(3): 104-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10495702&dopt=Abstract
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Unification of the “burst” and “linear” theories of periodontal disease progression: a multilevel manifestation of the same phenomenon. Author(s): Gilthorpe MS, Zamzuri AT, Griffiths GS, Maddick IH, Eaton KA, Johnson NW. Source: Journal of Dental Research. 2003 March; 82(3): 200-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598549&dopt=Abstract
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Untreated periodontal disease in Indonesian adolescents. Clinical and microbiological baseline data. Author(s): Timmerman MF, Van der Weijden GA, Armand S, Abbas F, Winkel EG, Van Winkelhoff AJ, Van der Velden U. Source: Journal of Clinical Periodontology. 1998 March; 25(3): 215-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9543192&dopt=Abstract
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Untreated periodontal disease in Indonesian adolescents. Longitudinal clinical data and prospective clinical and microbiological risk assessment. Author(s): Timmerman MF, Van der Weijden GA, Abbas F, Arief EM, Armand S, Winkel EG, Van Winkelhoff AJ, Van der Velden U. Source: Journal of Clinical Periodontology. 2000 December; 27(12): 932-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11140561&dopt=Abstract
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Untreated periodontal disease in Indonesian adolescents. Subgingival microbiota in relation to experienced progression of periodontitis. Author(s): Timmerman MF, Van der Weijden GA, Arief EM, Armand S, Abbas F, Winkel EG, Van Winkelhoff AJ, Van der Velden U. Source: Journal of Clinical Periodontology. 2001 July; 28(7): 617-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422582&dopt=Abstract
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Untreated periodontal disease: a follow-up on 30 cases. Author(s): Harris RJ. Source: J Periodontol. 2003 May; 74(5): 672-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816300&dopt=Abstract
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Update on Actinobacillus Actinomycetemcomitans and Porphyromonas gingivalis in human periodontal disease. Author(s): Slots J. Source: J Int Acad Periodontol. 1999 October; 1(4): 121-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666957&dopt=Abstract
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Update on general health risk of periodontal disease. Author(s): Slots J. Source: Int Dent J. 2003; 53 Suppl 3: 200-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875309&dopt=Abstract
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Upregulation of co-stimulatory molecule expression and dendritic cell marker (CD83) on B cells in periodontal disease. Author(s): Mahanonda R, Sa-Ard-Iam N, Yongvanitchit K, Wisetchang M, Ishikawa I, Nagasawa T, Walsh DS, Pichyangkul S. Source: Journal of Periodontal Research. 2002 June; 37(3): 177-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12113551&dopt=Abstract
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Use of aspartate aminotransferase in diagnosing periodontal disease: a comparative study of clinical and microbiological parameters. Author(s): Barbosa e Silva E, Salvador SL, Fogo JC, Marcantonio RA. Source: J Oral Sci. 2003 March; 45(1): 33-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816362&dopt=Abstract
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Using host response modifiers in the treatment of periodontal disease. Author(s): Novak MJ, Donley TG. Source: Pract Proced Aesthet Dent. 2002 November-December; 14(9): Suppl 3-10; Quiz 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12685424&dopt=Abstract
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Validation of smoking status in clinical research into inflammatory periodontal disease. Author(s): Scott DA, Palmer RM, Stapleton JA. Source: Journal of Clinical Periodontology. 2001 August; 28(8): 715-22. Review. English, French, German. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11442730&dopt=Abstract
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Validity and accuracy of a risk calculator in predicting periodontal disease. Author(s): Page RC, Krall EA, Martin J, Mancl L, Garcia RI. Source: The Journal of the American Dental Association. 2002 May; 133(5): 569-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12036161&dopt=Abstract
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Validity of a self-reported periodontal disease measure. Author(s): Joshipura KJ, Douglass CW, Garcia RI, Valachovic R, Willett WC. Source: J Public Health Dent. 1996 Summer; 56(4): 205-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8906704&dopt=Abstract
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Variational expression of functionally different macrophage markers (27E10, 25F9, RM3/1) in normal gingiva and inflammatory periodontal disease. Author(s): Schlegel Gomez R, Langer P, Pelka M, von den Driesch P, Johannessen AC, Simon M Jr. Source: Journal of Clinical Periodontology. 1995 May; 22(5): 341-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7541406&dopt=Abstract
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Vascular endothelial growth factor in human periodontal disease. Author(s): Booth V, Young S, Cruchley A, Taichman NS, Paleolog E. Source: Journal of Periodontal Research. 1998 November; 33(8): 491-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9879523&dopt=Abstract
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Vascular remodelling in chronic inflammatory periodontal disease. Author(s): Chapple CC, Kumar RK, Hunter N. Source: Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology. 2000 November; 29(10): 500-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11048966&dopt=Abstract
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Videodensitometrical study of the alveolar bone crest in periodontal disease. Author(s): Landini G. Source: J Periodontol. 1991 August; 62(8): 528-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1920021&dopt=Abstract
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Vitamin D receptor alleles, periodontal disease progression, and tooth loss in the VA dental longitudinal study. Author(s): Inagaki K, Krall EA, Fleet JC, Garcia RI. Source: J Periodontol. 2003 February; 74(2): 161-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666703&dopt=Abstract
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VLA-4/VCAM-1 pathway in human periodontal disease. Author(s): Tsurumachi T, Nishi K, Hayashi M, Saito T, Saito I, Moro I. Source: Advances in Experimental Medicine and Biology. 1995; 371B: 1131-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7502768&dopt=Abstract
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Volatile sulfur compounds in mouth air from clinically healthy subjects and patients with periodontal disease. Author(s): Yaegaki K, Sanada K. Source: Journal of Periodontal Research. 1992 July; 27(4 Pt 1): 233-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1640345&dopt=Abstract
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Wake up to periodontal disease. Author(s): Derdivanis JP. Source: Cda J. 1983 October; 11(10): 60. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6586302&dopt=Abstract
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Will implants survive well in patients with a history of inflammatory periodontal disease? Author(s): Nevins M. Source: J Periodontol. 2001 January; 72(1): 113-7. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11210068&dopt=Abstract
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CHAPTER 2. NUTRITION AND PERIODONTAL DISEASE Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and periodontal disease.
Finding Nutrition Studies on Periodontal Disease The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “periodontal disease” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following information is typical of that found when using the “Full IBIDS Database” to search for “periodontal disease” (or a synonym): •
Antineutrophil cytoplasmic antibodies: a missing link in the pathogenesis of periodontal disease? Author(s): Universidad del Zulia, Facultad de Odontolgia, Hospital Central, Maracaibo, Venezuela. Source: Novo, E Viera, N J-Periodontal-Res. 1996 July; 31(5): 365-8 0022-3484
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Ascorbic acid and periodontal disease. Source: Alvares, O. Vitamin C in health and disease /. New York : M. Dekker, 1997. page 505-516. ISBN: 0824793137 (hardcover : alk paper)
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Characteristics and responses of EBV immortalized B cells from periodontal disease patients. Author(s): Department of Periodontics, University of Texas Health Science Center at San Antonio 78284, USA. Source: Celenligil, H Ebersole, J L Oral-Dis. 1997 December; 3(4): 262-71 1354-523X
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Correlation of diet, other chewing activities and periodontal disease in North American client-owned dogs. Author(s): Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104-6010, USA. Source: Harvey, C E Shofer, F S Laster, L J-Vet-Dent. 1996 September; 13(3): 101-5 08987564
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Cytokines and prostaglandins in immune homeostasis and tissue destruction in periodontal disease. Author(s): Department of Oral Biology, School of Dentistry, University of Queensland, Australia. Source: Gemmell, E Marshall, R I Seymour, G J Periodontol-2000. 1997 June; 14112-43 0906-6713
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Design, characterisation and preliminary clinical evaluation of a novel mucoadhesive topical formulation containing tetracycline for the treatment of periodontal disease. Author(s): School of Pharmacy, The Queen's University of Belfast, Medical Biology Centre, 97, Lisburn Road, BT9 7BL, Northern Ireland, Belfast, UK.
[email protected] Source: Jones, D S Woolfson, A D Brown, A F Coulter, W A McClelland, C Irwin, C R JControl-Release. 2000 July 3; 67(2-3): 357-68 0168-3659
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Diet and periodontal disease in dogs and cats. Author(s): Department of Veterinary Clinical Sciences, University of Sydney, New South Wales. Source: Watson, A D Aust-Vet-J. 1994 October; 71(10): 313-8 0005-0423
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Epidemiology of periodontal disease in poodles. Author(s): Department of Periodontology, Dental School of Technical University of Dresden, Germany. Source: Hoffmann, T Gaengler, P J-Small-Anim-Pract. 1996 July; 37(7): 309-16 0022-4510
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Generalized cervical root resorption associated with periodontal disease. Author(s): Departments of Periodontology. Source: Beertsen, W Piscaer, M Van Winkelhoff, A J Everts, V J-Clin-Periodontol. 2001 November; 28(11): 1067-73 0303-6979
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Histological features of chronic periodontal disease in rats maintained on a soft diet. Source: Heely, J D Dobeck, J M Ellis, C H Int-J-Periodontics-Restorative-Dent. 1987; 7(6): 58-72 0198-7569
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Local antimicrobial therapies in periodontal disease. Author(s): University of Glasgow Dental School, 378 Sauchiehall Street, Glasgow G2 3JZ, Scotland, UK. Source: Kinane, D F Ann-R-Australas-Coll-Dent-Surg. 2000 October; 15: 57-60 0158-1570
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Oral malodor and its relevance to periodontal disease in the dog. Author(s): Waltham Centre For Pet Nutrition, Leicestershire, England. Source: Culham, N Rawlings, J M J-Vet-Dent. 1998 December; 15(4): 165-8 0898-7564
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Osteoclast activation in inflammatory periodontal diseases. Author(s): Department of Physiology, Faculty of Dentistry, University of Western Ontario, London, Canada. Source: Wiebe, S H Hafezi, M Sandhu, H S Sims, S M Dixon, S J Oral-Dis. 1996 June; 2(2): 167-80 1354-523X
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Osteoporosis and periodontal disease: is there a relationship? Author(s): Department of Periodontics, School of Dentistry, Case Western Reserve University, Cleveland, Ohio, USA. Source: Krejci, C B J-West-Soc-Periodontol-Periodontal-Abstr. 1996; 44(2): 37-42 01484893
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Oxidative injury and inflammatory periodontal diseases: the challenge of antioxidants to free radicals and reactive oxygen species. Author(s): Institute of Biochemistry, Faculty of Medicine, University of Ancona, Italy. Source: Battino, M Bullon, P Wilson, M Newman, H Crit-Rev-Oral-Biol-Med. 1999; 10(4): 458-76 1045-4411
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Periodontal disease and leucopenia. Author(s): Riverstone Veterinary Hospital, Australia. Source: Lonsdale, T J-Small-Anim-Pract. 1995 December; 36(12): 542-6 0022-4510
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Practical periodontics. Awareness of periodontal disease--the patient. Source: Croxson, L J Int-Dent-J. 1998 June; 48(3 Suppl 1): 256-60 0020-6539
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Qualitative and quantitative studies of Gc (vitamin D-binding protein) in normal subjects and patients with periodontal disease. Source: Krayer, J W Emerson, D L Goldschmidt Clermont, P J Nel, A E Werner, P A Galbraith, R M J-Periodontal-Res. 1987 July; 22(4): 259-63 0022-3484
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Radiographic bone loss correlations and technetium-99m-MDP bone uptake in ligature-induced periodontal disease in the beagle. Author(s): College of Veterinary Medicine, Mississippi State University, Mississippi State 39762-9825, USA. Source: Holland, M Boring, J G Boyle, C R Pickrum, H M Jeffcoat, M K Vet-RadiolUltrasound. 1998 Jul-August; 39(4): 366-74 1058-8183
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Receptor for advanced glycation end products, inflammation, and accelerated periodontal disease in diabetes: mechanisms and insights into therapeutic modalities. Author(s): School of Dental & Oral Surgery, Columbia University, New York, New York, USA. Source: Lalla, E Lamster, I B Stern, D M Schmidt, A M Ann-Periodontol. 2001 December; 6(1): 113-8
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Relationship between diet, dental calculus and periodontal disease in domestic and feral cats in Australia. Source: Clarke, D E Cameron, A Aust-Vet-J. 1998 October; 76(10): 690-3 0005-0423
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Relationship of sulphated glycosaminoglycans in human gingival crevicular fluid with active periodontal disease. Author(s): Department of Basic Dental Science, Dental School, Wales, Cardiff, UK. Source: Waddington, R J Langley, M S Guida, L Iuorio, G Labella, R Embery, G Caruso, F J-Periodontal-Res. 1996 April; 31(3): 168-70 0022-3484
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Reliability of a self-reported health questionnaire in a periodontal disease study. Author(s): State University of New York at Buffalo, School of Dental Medicine, Department of Oral Biology, NY 14214-3092, USA. Source: Ho, A W Grossi, S G Dunford, R G Genco, R J J-Periodontal-Res. 1997 November; 32(8): 646-50 0022-3484
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Resolution of inflammation: a new paradigm for the pathogenesis of periodontal diseases. Author(s): Department of Periodontology and Oral Biology, Boston University, Goldman School of Dental Medicine, 100 East Newton Street, Boston, MA 02118, USA.
[email protected] Source: Van Dyke, T E Serhan, C N J-Dent-Res. 2003 February; 82(2): 82-90 0022-0345
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Salivary antioxidants and periodontal disease status. Author(s): Centre for Healthcare Education, University College Northampton, UK.
[email protected] Source: Sculley, D V Langley Evans, S C Proc-Nutr-Soc. 2002 February; 61(1): 137-43 0029-6651
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Self-heat shock protein 60 induces tumour necrosis factor-alpha in monocyte-derived macrophage: possible role in chronic inflammatory periodontal disease. Author(s): Division of Periodontology, Department of Oral Biological Sciences, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. Source: Ueki, K Tabeta, K Yoshie, H Yamazaki, K Clin-Exp-Immunol. 2002 January; 127(1): 72-7 0009-9104
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Smoking and periodontal disease. Author(s): Periodontology and Oral Immunology, University of Glasgow Dental Hospital and School, Scotland, UK. Source: Kinane, D F Chestnutt, I G Crit-Rev-Oral-Biol-Med. 2000; 11(3): 356-65 1045-4411
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The association of two recombinant proteinases of a feline strain of Porphyromonas gingivalis with periodontal disease in cats. Source: Norris, J.M. Love, D.N. Vet-microbiol. Amsterdam, The Netherlands : Elsevier Science B.V. January 2000. volume 71 (1/2) page 69-80. 0378-1135
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The effect of ketoprofen creams on periodontal disease in rhesus monkeys. Author(s): Block Drug Company, Inc., Jersey City, NJ, USA. Source: Li, K L Vogel, R Jeffcoat, M K Alfano, M C Smith, M A Collins, J G Offenbacher, S J-Periodontal-Res. 1996 November; 31(8): 525-32 0022-3484
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The natural history of periodontal disease in man. Risk factors for progression of attachment loss in individuals receiving no oral health care. Author(s): University of Detroit-Mercy, School of Dentistry, Department of Periodontology and Dental Hygiene, MI 48219-0900, USA.
[email protected] Source: Neely, A L Holford, T R Loe, H Anerud, A Boysen, H J-Periodontol. 2001 August; 72(8): 1006-15 0022-3492
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The periodontal-systemic connection: implications for treatment of patients with osteoporosis and periodontal disease. Author(s): Department of Health Policy and Health Services Research, Boston University Goldman School of Dental Medicine, Boston, Massachusetts, USA. Source: Krall, E A Ann-Periodontol. 2001 December; 6(1): 209-13
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The prevention of periodontal disease. Source: Manson, J D Eley, B M Dent-Update. 1989 June; 16(5): 189-95 0305-5000
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The role of non-steroidal anti-inflammatory drugs in the management of periodontal disease. Source: Heasman, P A J-Dent. 1988 December; 16(6): 247-57 0300-5712
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Zinc in etiology of periodontal disease. Author(s): Stomatological Clinic, Medical Faculty, Charles University, Pilsen, Czechoslovakia. Source: Polenik, P Med-Hypotheses. 1993 March; 40(3): 182-5 0306-9877
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to periodontal disease; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Folic Acid Source: Healthnotes, Inc.; www.healthnotes.com Folic Acid Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,887,00.html Vitamin B12 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin C Source: Healthnotes, Inc.; www.healthnotes.com Vitamin C Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin C Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,904,00.html Vitamin C and Flavonoids Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,935,00.html Vitamin E Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,906,00.html
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Minerals Calcium Source: Healthnotes, Inc.; www.healthnotes.com Calcium Source: Integrative Medicine Communications; www.drkoop.com Calcium Source: Prima Communications, Inc.www.personalhealthzone.com Calcium Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,884,00.html Folate Source: Prima Communications, Inc.www.personalhealthzone.com Hmg-coa Reductase Inhibitors (statins) Source: Integrative Medicine Communications; www.drkoop.com Magnesium Source: Prima Communications, Inc.www.personalhealthzone.com Selenium Source: Healthnotes, Inc.; www.healthnotes.com Zinc Source: Prima Communications, Inc.www.personalhealthzone.com
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Food and Diet Cinnamon Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,271,00.html
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CHAPTER 3. ALTERNATIVE MEDICINE AND PERIODONTAL DISEASE Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to periodontal disease. At the conclusion of this chapter, we will provide additional sources.
The Combined Health Information Database The Combined Health Information Database (CHID) is a bibliographic database produced by health-related agencies of the U.S. federal government (mostly from the National Institutes of Health) that can offer concise information for a targeted search. The CHID database is updated four times a year at the end of January, April, July, and October. Check the titles, summaries, and availability of CAM-related information by using the “Simple Search” option at the following Web site: http://chid.nih.gov/simple/simple.html. In the drop box at the top, select “Complementary and Alternative Medicine.” Then type “periodontal disease” (or synonyms) in the second search box. We recommend that you select 100 “documents per page” and to check the “whole records” options. The following was extracted using this technique: •
NIH Funds Multi-Site, Collaborative ACM Studies in Portland, Oregon Source: Alternative and Complementary Therapies. 6(1): 32-37. February 2000. Summary: This journal article describes the collaborative alternative and complementary medicine (ACM) studies under way in Portland, Oregon. The studies were made possible by grants from the National Institutes of Health to the Oregon Health Sciences University (OHSU) and the Kaiser Permanente Center for Health Research (CHR). The money will fund collaboration among these two institutions and four of Portland's ACM colleges: the National College of Naturopathic Medicine, the Oregon College of Oriental Medicine, the Western States Chiropractic College, and the Oregon School of Massage. OHSU researchers will investigate the effects of ginkgo in neurologic disease and age-related cognitive disorders, the effects of antioxidants in multiple sclerosis (MS), and the effects of yoga in older people with MS. CHR studies
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will examine the effects of nutritional and herbal supplements on periodontal disease; the effects of acupuncture, chiropractic, and massage therapy on temporomandibular joint disorder (TMD); and the effects of traditional Chinese medicine (TCM) and naturopathic medicine in the treatment of women with TMD and multiple health problems. The article includes brief descriptions of the collaborating institutions, the TCM protocol for TMD, and 2 references.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to periodontal disease and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “periodontal disease” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to periodontal disease: •
Acupuncture: a unique effort to treat periodontal disease. Author(s): Schoor RS, Sussman HI, Kazandjian GK. Source: The Journal of the American Dental Association. 2001 December; 132(12): 1705-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11780990&dopt=Abstract
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Assessment of a novel screening test for neutrophil collagenase activity in the diagnosis of periodontal diseases. Author(s): Mancini S, Romanelli R, Laschinger CA, Overall CM, Sodek J, McCulloch CA. Source: J Periodontol. 1999 November; 70(11): 1292-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10588492&dopt=Abstract
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Effect of LongoVital treatment on development of periodontal disease in rats. Author(s): Klausen B, Apostolopoulos A, Stoltze K, Norgaard F. Source: Scand J Dent Res. 1993 February; 101(1): 33-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8382835&dopt=Abstract
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Effects of specific nutrients on periodontal disease onset, progression and treatment. Author(s): Neiva RF, Steigenga J, Al-Shammari KF, Wang HL. Source: Journal of Clinical Periodontology. 2003 July; 30(7): 579-89. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834494&dopt=Abstract
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Functional role of interleukin 1 in periodontal disease: induction of interleukin 1 production by Bacteroides gingivalis lipopolysaccharide in peritoneal macrophages from C3H/HeN and C3H/HeJ mice. Author(s): Hanazawa S, Nakada K, Ohmori Y, Miyoshi T, Amano S, Kitano S.
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Source: Infection and Immunity. 1985 October; 50(1): 262-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3876285&dopt=Abstract •
Herbal medicine for periodontal diseases. Author(s): Cao CF, Sun XP. Source: Int Dent J. 1998 June; 48(3 Suppl 1): 316-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9779114&dopt=Abstract
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Isoquinoline alkaloids in local periodontal disease therapy (preliminary notice). Author(s): Cerna H, Fiala B, Lenfeld J, Marsalek E, Preininger V, Simanek V. Source: Acta Univ Palacki Olomuc Fac Med. 1984; 107: 159-62. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6242637&dopt=Abstract
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Non-proteolytic activation of latent human neutrophil collagenase and its role in matrix destruction in periodontal diseases. Author(s): Sorsa T, Saari H, Konttinen YT, Suomalainen K, Lindy S, Uitto VJ. Source: Int J Tissue React. 1989; 11(4): 153-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2561361&dopt=Abstract
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Occurrence of doxycycline resistant bacteria in the oral cavity after local administration of doxycycline in patients with periodontal disease. Author(s): Larsen T. Source: Scandinavian Journal of Infectious Diseases. 1991; 23(1): 89-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2028232&dopt=Abstract
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Periodontal disease and diet in domestic pets. Author(s): Gorrel C. Source: The Journal of Nutrition. 1998 December; 128(12 Suppl): 2712S-2714S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9868248&dopt=Abstract
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Periodontal disease and tooth loss. Author(s): Ong G. Source: Int Dent J. 1998 June; 48(3 Suppl 1): 233-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9779103&dopt=Abstract
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Periodontal disease in the prehistoric Ipiutak and Tigara skeletal remains from Point Hope, Alaska. Author(s): Costa RL Jr. Source: American Journal of Physical Anthropology. 1982 September; 59(1): 97-110. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6753601&dopt=Abstract
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Periodontal disease. Etiology and pathogenesis. Author(s): Colmery B 3rd, Frost P. Source: The Veterinary Clinics of North America. Small Animal Practice. 1986 September; 16(5): 817-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3490036&dopt=Abstract
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Periodontal disease. Therapy and prevention. Author(s): Hawkins BJ. Source: The Veterinary Clinics of North America. Small Animal Practice. 1986 September; 16(5): 835-49. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3532504&dopt=Abstract
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Potential adjunctive applications of hypnosis in the management of periodontal diseases. Author(s): Wood GJ, Zadeh HH. Source: Am J Clin Hypn. 1999 January; 41(3): 212-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10554383&dopt=Abstract
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Prevention and control of periodontal diseases in developing and industrialized nations. Author(s): Axelsson P, Albandar JM, Rams TE. Source: Periodontology 2000. 2002; 29: 235-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12102711&dopt=Abstract
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Prevention of periodontal disease. Author(s): DuPont GA. Source: The Veterinary Clinics of North America. Small Animal Practice. 1998 September; 28(5): 1129-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9779544&dopt=Abstract
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Psychosocial factors in inflammatory periodontal diseases. A review. Author(s): da Silva AM, Newman HN, Oakley DA. Source: Journal of Clinical Periodontology. 1995 July; 22(7): 516-26. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7560234&dopt=Abstract
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Reliability of a self-reported health questionnaire in a periodontal disease study. Author(s): Ho AW, Grossi SG, Dunford RG, Genco RJ. Source: Journal of Periodontal Research. 1997 November; 32(8): 646-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9409459&dopt=Abstract
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Serum fatty acid imbalance in bone loss: example with periodontal disease. Author(s): Requirand P, Gibert P, Tramini P, Cristol JP, Descomps B.
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Source: Clinical Nutrition (Edinburgh, Lothian). 2000 August; 19(4): 271-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10952799&dopt=Abstract •
The natural history of periodontal disease in man. Risk factors for progression of attachment loss in individuals receiving no oral health care. Author(s): Neely AL, Holford TR, Loe H, Anerud A, Boysen H. Source: J Periodontol. 2001 August; 72(8): 1006-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11525431&dopt=Abstract
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The owner-animal-environment triad in the treatment of canine periodontal disease. Author(s): Hale FA. Source: J Vet Dent. 2003 June; 20(2): 118-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14528858&dopt=Abstract
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The periodontal-systemic connection: implications for treatment of patients with osteoporosis and periodontal disease. Author(s): Krall EA. Source: Ann Periodontol. 2001 December; 6(1): 209-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887467&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
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The following is a specific Web list relating to periodontal disease; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Gingivitis Source: Healthnotes, Inc.; www.healthnotes.com Gum Disease Source: Integrative Medicine Communications; www.drkoop.com Periodontal Disease Alternative names: Gum Disease Source: Prima Communications, Inc.www.personalhealthzone.com Sickle Cell Anemia Source: Healthnotes, Inc.; www.healthnotes.com
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Alternative Therapy Hypnotherapy Source: Integrative Medicine Communications; www.drkoop.com
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Chinese Medicine Bushen Guchi Wan Alternative names: Bushen Guchi Pills Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Bushen%20Guchi%20Wan&m h=10&sb=---&view_records=View+Records
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Herbs and Supplements Alpha2-adrenergic Agonists Source: Integrative Medicine Communications; www.drkoop.com Beta-blockers Source: Integrative Medicine Communications; www.drkoop.com Bloodroot Alternative names: Sanguinaria canadensis Source: Healthnotes, Inc.; www.healthnotes.com Bloodroot Source: Prima Communications, Inc.www.personalhealthzone.com
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Caraway Alternative names: Carum carvi Source: Healthnotes, Inc.; www.healthnotes.com Centella Alternative names: Gotu Kola; Centella asiatica (Linn.) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Chamomile Alternative names: Matricaria recutita Source: Healthnotes, Inc.; www.healthnotes.com Chamomile Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,766,00.html Coenzyme Q Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,768,00.html Coenzyme Q10 Source: Healthnotes, Inc.; www.healthnotes.com Coenzyme Q10 Source: Integrative Medicine Communications; www.drkoop.com Coenzyme Q10 (coq10) Source: Prima Communications, Inc.www.personalhealthzone.com Coq10 Source: Integrative Medicine Communications; www.drkoop.com Cranberry Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10019,00.html Echinacea Alternative names: Echinacea purpurea, Echinacea angustifolia, Echinacea pallida Source: Healthnotes, Inc.; www.healthnotes.com Eucalyptus Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,778,00.html Eugenia Clove Alternative names: Cloves; Eugenia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Fibric Acid Derivatives Source: Integrative Medicine Communications; www.drkoop.com Flavonoids Source: Healthnotes, Inc.; www.healthnotes.com German Chamomile Alternative names: Matricaria recutita Source: Integrative Medicine Communications; www.drkoop.com Glycyrrhiza1 Alternative names: Licorice; Glycyrrhiza glabra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Goldenrod Alternative names: Solidago virgaurea Source: Integrative Medicine Communications; www.drkoop.com Gotu Kola Source: Prima Communications, Inc.www.personalhealthzone.com Matricaria Recutita Source: Integrative Medicine Communications; www.drkoop.com Melaleuca Alternative names: Tea Tree Oil; Melaleuca alternifolia Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Myrrh Alternative names: Commiphora molmol Source: Healthnotes, Inc.; www.healthnotes.com Peppermint Alternative names: Mentha piperita Source: Healthnotes, Inc.; www.healthnotes.com Phenothiazine Derivatives Source: Integrative Medicine Communications; www.drkoop.com Sage Alternative names: Salvia officinalis Source: Healthnotes, Inc.; www.healthnotes.com Solidago Virgaurea Source: Integrative Medicine Communications; www.drkoop.com Spirulina and Kelp Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10058,00.html
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Sulfonylureas Source: Integrative Medicine Communications; www.drkoop.com Tea Tree Source: Prima Communications, Inc.www.personalhealthzone.com Thiazide Diuretics Source: Integrative Medicine Communications; www.drkoop.com Thioxanthene Derivatives Source: Integrative Medicine Communications; www.drkoop.com Thuja Plicata Alternative names: Western Red Cedar Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Tricyclic Antidepressants (tcas) Source: Integrative Medicine Communications; www.drkoop.com Vasodilators Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON PERIODONTAL DISEASE Overview In this chapter, we will give you a bibliography on recent dissertations relating to periodontal disease. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “periodontal disease” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on periodontal disease, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Periodontal Disease ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to periodontal disease. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
In Vitro Studies of Collagen Catabolism in Progressive Periodontal Disease in Beagle Dogs by Gates, Donald James; Phd from University of Alberta (canada), 1982 http://wwwlib.umi.com/dissertations/fullcit/NK60302
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Methods for Studying Geochemical - Dental-disease Interrelationships, Including the Assessment of Periodontal Disease by Digital Imaging (missouri) by Hildebolt, Charles Floyd, Phd from Washington University, 1987, 301 pages http://wwwlib.umi.com/dissertations/fullcit/8722459
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Oral Contraceptive Use and Periodontal Diseases among United States Women: an Analysis of Nhanes Data by Taichman, Linda Susan; Phd from University of Michigan, 2002, 147 pages http://wwwlib.umi.com/dissertations/fullcit/3058058
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Stress-induced Porphyromonas Gingivalis Gene Expression in Periodontal Disease by Shelburne, Charles Edward; Phd from Queen's University of Belfast (united Kingdom), 2002 http://wwwlib.umi.com/dissertations/fullcit/f411729
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The Role of Mucopolysaccharidase-producing Anaerobic Oral Bacteria in the Pathogenesis of Inflammatory Periodontal Disease by Tam, You-cheuk; Phd from Mcgill University (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NL24043
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. DISEASE
CLINICAL TRIALS AND PERIODONTAL
Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning periodontal disease.
Recent Trials on Periodontal Disease The following is a list of recent trials dedicated to periodontal disease.8 Further information on a trial is available at the Web site indicated. •
Effect of 3 periodontal therapies in current and non-smokers Condition(s): Periodontitis; Periodontal Diseases Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Dental and Craniofacial Research (NIDCR) Purpose - Excerpt: The purpose of this study is to determine in current and non-smokers the clinical and microbiological effects of 3 therapies: scaling and root planing (SRP) alone; SRP in combination with the orally administered antibiotic metronidazole; and SRP with the orally administered antibiotics metronidazole and amoxicillin along with the locally delivered antibiotic doxycycline at periodontal pockets >= 4 mm. Phase(s): Phase II Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00066066
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Microbial associations in periodontal health and disease Condition(s): Periodontitis; Periodontal Diseases Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Dental and Craniofacial Research (NIDCR)
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These are listed at www.ClinicalTrials.gov.
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Purpose - Excerpt: The purpose of this study is to determine the clinical and microbiological effects of systemically administered metronidazole alone or in combination with professional plaque removal on periodontally diseased patients. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00066001 •
Norplant and Irregular Bleeding/Spotting Condition(s): Endometrial bleeding; Periodontal Disease Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: Irregular or prolonged menstrual bleeding and/or spotting are common side effects in patients using progestin-only hormonal contraception such as levonorgestrel implants (Norplant). Doxycyline, a drug approved by the Food and Drug Administration (FDA) to treat gum disease, may reduce the occurrence of uterine bleeding and spotting in women who use Norplant. This study will evaluate the effects of doxycycline on uterine bleeding/spotting in women using Norplant. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00064766
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Study of the Composition of Dental Plaque Condition(s): Dental Caries; Dental Plaque; Periodontal Disease Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Dental and Craniofacial Research (NIDCR) Purpose - Excerpt: This study will examine the composition of dental plaque-a naturally occurring substance that sticks to the teeth and can cause tooth decay and gum disease. A better understanding of how plaque builds up in the mouth may help in developing improved ways of controlling it. Healthy normal volunteers between the ages of 18 and 65 who work at the National Institutes of Health main campus in Bethesda, Maryland, may participate in this study. Candidates will be screened for eligibility with a medical and dental history. This study involves a maximum of five visits to the dental clinic. At the first visit, participants will have a dental examination, and a mold will be made of the mouth. To make the mold, a small plastic tray containing impression material will be placed in the volunteer's mouth and held in place for about 2 minutes to set. The tray will then be removed and a mold will be made from the impression. The mold will be used to make the mouthpiece used in study 1, described below, and the tooth fittings used in study 2, also described below. Volunteers will participate in one of these two studies. Study 1. Volunteers in study 1 will have their mouthpiece checked at the second visit, have a teeth cleaning, and have the mold put in place. The mouthpiece will be worn for up to 8 hours, during which time soft foods can be eaten. Mouthwash should not be used while the device is in place. At the volunteer's third (last) visit, the mouthpiece will be removed and the volunteer will spit into a tube to collect saliva for
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examination for bacteria. Study 2. Volunteers in study 2 will have their teeth cleaned at the second visit and the tooth fittings placed onto the back teeth with a dental adhesive. The fittings will be worn for up to 72 hours, during which time volunteers can eat a regular diet and brush their teeth. Mouthwash should not be used while the fittings are in place. At the third, fourth and fifth visits, some of the fittings will be removed and, if necessary, the tooth surface will be polished. The last of the fittings will be removed at the fifth visit and the volunteer will spit into a tube to collect saliva for examination for bacteria. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001726 •
Periodontal Therapy Outcomes Condition(s): Periodontal Disease Study Status: This study is not yet open for patient recruitment. Sponsor(s): National Institute of Dental and Craniofacial Research (NIDCR) Purpose - Excerpt: This trial compares proven surgical methods for treating periodontal infections with newer medical methods using antibiotics. The objective is to determine whether one method or the other provides a better outcome in terms of tooth stability (a clinician's perspective), and tooth function (a patient's perspective). In addition we will determine the relative costs of the two approaches so that one can determine which approach makes most sense financially. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00016809
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Treating Periodontal Infection Condition(s): Periodontal Disease; Diabetes Mellitus, Non-Insulin-Dependent Study Status: This study is not yet open for patient recruitment. Sponsor(s): National Institute of Dental and Craniofacial Research (NIDCR) Purpose - Excerpt: The purpose of this project is to obtain preliminary data about the effects of treating periodontal infection on blood glucose control in people with type 2 diabetes. This is a pilot study which will provide important information that will help in the design of a full scale clinical trial. 45 subjects with type 2 diabetes and periodontal disease will be treated and evaluated at 3-month intervals for 15 months to obtain information regarding the effects of the periodontal treatment procedures on changes in hemoglobin A1c (HbA1c). This project will also provide an opportunity to explore the effects of treating periodontal infection on levels of periodontitis- and glucose metabolism-related inflammatory mediators (TNFa,IL-1B,IL-6) and levels of serum cholesterol, triglyceride and lipids in patients with type 2 diabetes mellitus. The periodontal treatment that will be evaluated will include ultrasonic scaling, local antimicrobial treatment and oral systemic antibiotics. If results provide significant evidence that treating periodontal infection contributes to improved blood glucose control, then diagnosis and treatment of periodontal infection in patients with type 2 diabetes could be an important component in management of type 2 diabetes. Phase(s): Phase II
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00016835
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “periodontal disease” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON PERIODONTAL DISEASE Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “periodontal disease” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on periodontal disease, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Periodontal Disease By performing a patent search focusing on periodontal disease, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. 9Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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The following is an example of the type of information that you can expect to obtain from a patent search on periodontal disease: •
Anatomical interproximal dental stimulator Inventor(s): White; Dennis J. (51 Nostrand Rd., Plainsboro, NJ 08512) Assignee(s): none reported Patent Number: 6,283,751 Date filed: January 15, 1998 Abstract: A dental/gingival stimulating article is disclosed that provides interdental stimulation and plaque removal to the interproximal areas. This toothbrush like design holds bristle tips that terminate in a vee shaped design. The instrument is held in one hand and directed with appropriate direction and force to guide fiber ends into the spaces between the gum and teeth interproximally. Its vee shape will allow nonrestricted passage around the interdental papilla. The rotational direction used on the handle will dissipate to a massaging motion within the sulci. Therefore, the threat of interproximal caries is reduced and the occurrence of periodontal disease is minimized. Excerpt(s): This invention relates a dental article to stimulate gums and clean teeth in interproximal areas, which is both efficient and easy to use. Regarding dental hygiene, it has been found desirable to remove residual food particles and plaque harboring between the teeth and under the gums. In fact, irritation occurs when food and plaque are left to remain between the teeth. This leads to tooth decay and periodontitis. Moderate to severe periodontitis will cause recession of gums, mobility of teeth, and eventual tooth loss. Teeth must be brushed and adjacent soft tissue massaged in order to maintain oral health. Oral health is critical for certain individuals. Patients with heart defects are susceptible to further heart damage due to a bacteremia originating from inflamed gums. Orthopedic patients with total joint replacements are also candidates for similar infections due to unhealthy gums. An Advisory Statement of 1997 by the American Academy of Orthopaedic Surgeons strongly outlines the need for healthy oral tissues. Effective daily oral hygiene is important to all of us as well as in the above specificities. Web site: http://www.delphion.com/details?pn=US06283751__
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Anti-inflammatory composition comprising tetracycline Inventor(s): Gardner; Wallace J. (1791 Mass Ave., Cambridge, MA 02140) Assignee(s): none reported Patent Number: 6,610,274 Date filed: December 18, 2001 Abstract: Therapeutic composition having anti-infective activity. The therapeutic composition is a formulation comprising an antibiotic, preferably a tetracycline, most preferably doxycycline, which has not been chemically modified to eliminate antimicrobial efficacy. The antibiotic is preferably in a liquid vehicle, most preferably one that contains at least 20% alcohol by volume. The therapeutic composition is preferably in local delivery form and is self-administered orally or via the nasal cavity. Administration of the therapeutic composition of the present invention treats diseases that originate from the oral cavity or that do not originate in the oral cavity, but are
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affected by contaminants, such as viruses or bacteria, in the oral cavity entering the bloodstream including but not limited to periodontal disease, sinusitis, gingivitis, the common cold, sore throat, influenza, allergies (particularly to tree pollen), resistant pneumonia, diseases of the gastrointestinal tract, inflammatory diseases such as rheumatoid arthritis, cancer, ulcers, heart disease, etc. Excerpt(s): The accumulation bacteria in the oral cavity, such as on the teeth or tongue has been identified as a contributor or cause of various inflammatory conditions, including gingivitis, periodontitis and other gum diseases. Treatment of the oral cavity with antibiotics to reduce or eliminate the effects of bacteria is known. For example, broad spectrum antibiotics such as tetracyclines and metronidazole have been used in the treatment of periodontal disease to reduce oral cavity microflora. Typically such use has been systemic, which can result in various undesirable side effects, including the threat or danger or building allergies or immunity to the antibiotic, overgrowth of opportunistic yeast and fungi and intestinal disturbances. Many other common inflammatory diseases, such as sinusitis, diseases of the gastrointestinal tract (including those that manifest themselves in stomach and bowel problems), the common cold, influenza, allergies, halitosis, pneumonia, etc., also may be caused by viruses and/or bacteria. Often the source of the bacteria and viruses is the oral cavity, especially the ear, nose and throat passages, and the sinuses. Once the bacteria and/or viruses are resident in the oral cavities or sinuses (e.g., the maxillary, frontal and ethmoid), they can continually cause infection through circulation in the blood stream. Continual reduction or elimination of these bacteria and viruses would reduce chronic infection in the body. The problems of the prior art have been overcome by the present invention, which provides a therapeutic composition having anti-infective activity. In a preferred embodiment, the therapeutic composition is a formulation comprising an antibiotic, preferably a tetracycline, most preferably doxycycline, which has not been chemically modified to eliminate antimicrobial efficacy. The antibiotic is preferably in a liquid vehicle, most preferably one that contains at least 20% alcohol by volume. The therapeutic composition is preferably in local delivery form and is preferably selfadministered orally or via-the nasal cavity. The therapeutic composition most preferably is a self-delivered formulation in local delivery form that consists essentially of a tetracycline, most preferably doxycline, which has not been chemically modified to eliminate antimicrobial efficacy, and a liquid vehicle, more preferably one which contains at least 20% alcohol by volume, and most preferably one which consists essentially of sterile water or Listerine or the like, which tetracyline is preferably present in the formulation in the amount of between 50 to 100 mgs per ounce of liquid vehicle. Web site: http://www.delphion.com/details?pn=US06610274__ •
Benzene butyric acids and their derivatives as inhibitors of matrix metalloproteinases Inventor(s): Purchase, Jr.; Claude Forsey (Ann Arbor, MI), Roth; Bruce David (Plymouth, MI), White; Andrew David (Pinckney, MI) Assignee(s): Warner-Lambert Company (Morris Plains, NJ) Patent Number: 6,541,521 Date filed: July 12, 1999 Abstract: Benzene butyric acid compounds and derivatives are described as well as methods for the preparation and pharmaceutical compositions of same, which are useful as inhibitors of matrix metalloproteinases, particularly gelatinase A, collagenase-3, and stromelysin-1 and for the treatment of multiple sclerosis, atherosclerotic plaque rupture,
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aortic aneurysm, heart failure, left ventricular dilation, restenosis, periodontal disease, corneal ulceration, treatment of burns, decubital ulcers, wound healing, cancer, inflammation, pain, arthritis, osteoporosis, renal disease, or other autoimmune or inflammatory disorders dependent upon tissue invasion by leukocytes or other activated migrating cells, acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. Excerpt(s): The present invention relates to novel benzene butyric acid compounds and their derivatives useful as pharmaceutical agents, to methods for their production, to pharmaceutical compositions which include these compounds and a pharmaceutically acceptable carrier, and to pharmaceutical methods of treatment. The novel compounds of the present invention are inhibitors of matrix metalloproteinases, e.g., gelatinase A (MMP-2), collagenase-3 (MMP-13), and stromelysin-1 (MMP-3). More particularly, the novel compounds of the present invention are useful in the treatment of atherosclerotic plaque rupture, aortic aneurism, heart failure, left ventricular dilation, restenosis, periodontal disease, corneal ulceration, treatment of bums, decubital ulcers, wound repair, cancer, inflammation, pain, arthritis, osteoporosis, multiple sclerosis, renal disease, and other autoimmune or inflammatory disorders dependent on the tissue invasion of leukocytes or other activated migrating cells. Additionally, the compounds of the present invention are useful in the treatment of acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. Gelatinase A and stromelysin-1 are members of the matrix metalloproteinase (MMP) family (Woessner J. F., FASEB J., 1991;5:2145-2154). Other members include fibroblast collagenase, neutrophil collagenase, gelatinase B (92 kDa gelatinase), stromelysin-2, stromelysin-3, matrilysin, collagenase 3 (Freije J. M., Diez-Itza I., Balbin M., Sanchez L. M., Blasco R., Tolivia J., and Lopez-Otin C., J. Biol. Chem., 1994;269:16766-16773), and the newly discovered membrane-associated matrix metalloproteinases (Sato H., Takino T., Okada Y., Cao J., Shinagawa A., Yamamoto E., and Seiki M., Nature, 1994;370:61-65). The catalytic zinc in matrix metalloproteinases is a focal point for inhibitor design. The modification of substrates by introducing chelating groups has generated potent inhibitors such as peptide hydroxymates and thiolcontaining peptides. Peptide hydroxamates and the natural endogenous inhibitors of MMPs (TIMPs) have been used successfully to treat animal models of cancer and inflammation. Web site: http://www.delphion.com/details?pn=US06541521__ •
Dental floss dispenser and method Inventor(s): Francis; Shlomo (6604 N. Richmond St., Chicago, IL 60645) Assignee(s): none reported Patent Number: 6,488,036 Date filed: November 2, 1999 Abstract: A single support dental flosser with improved maneuverability; to provide the user with increased leverage and dexterity to easily and thoroughly clean food, debris, and dental plaque so as to prevent proximal caries and periodontal disease. The dental flosser includes a handle section, an intermediate section, and an upstanding dental
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floss support section. In an embodiment of the invention, the dental flosser includes a preset strand of floss attached to the upstanding dental floss support section. In an other embodiment, the dental flosser includes a main body portion having a cylindrical shape for ease of handling. A hollow interior containing a metered floss dispenser, and a floss support containing a through hole to supply floss. The metered floss dispenser has a simplified construction and is especially designed to fit into a cylindrically shaped handle. The floss support is slender to deem the device suitable for use by orthodontic patients where the maneuverability is especially crucial to allow thorough cleaning under orthodontic appliances. Excerpt(s): The present invention relates to easily maneuvered dental flossing devices and methods of flossing teeth using the same. More particularly it relates to single posted dental flossing devices with improved maneuverability including assemblies for metered floss dispention which are capable of being contained in such dental flossing devices and slender floss supports which allow the use of such dental flossing devices in orthodontic patients. Attempts to provide dental flossers that are suitable for orthodontic patients have generally produced dental flossers that include two floss supports and a I strand of floss suspended between them. This frees the user from the necessity of grasping the floss with his fingers, but has the decided disadvantage of restricting maneuverability within the clearance. All of the prior art had to be moved as one inflexible unit. The one post and a flexible floss design provide increased maneuverability and access within the clearance. (a) Since the prior art is maneuvered as one inflexible unit, it does not allow vertiginous maneuvering within the clearance. This limitation increases difficulty and decreases cleaning efficiency of flossing. Web site: http://www.delphion.com/details?pn=US06488036__ •
Enteric coated formulation of bishosphonic acid compounds and associated therapeutic methods Inventor(s): Chen; Feng-Jing (Salt Lake City, UT), Patel; Mahesh V. (Salt Lake City, UT) Assignee(s): Lipocine, Inc. (Salt Lake City, UT) Patent Number: 6,468,559 Date filed: April 28, 2000 Abstract: Oral dosage forms are provided for the administration of a bisphosphonic acid compound in the prevention and treatment of conditions involving calcium or phosphate metabolism, i.e., conditions associated with bone resorption such as osteoporosis, Paget's disease, periprosthetic bone loss, osteolysis, malignant hypercalcemia, metastatic bone disease, multiple myeloma, and periodontal disease. The dosage forms are either enterically coated capsules housing the drug in a liquid or semi-solid carrier, or enterically coated osmotically activated drug delivery devices. Excerpt(s): The present invention relates generally to drug delivery, and more specifically relates to novel enteric coated pharmaceutical dosage forms that for oral administration of bisphosphonic acid compounds. The invention additionally relates to methods for administering a bisphosphonic acid compound using the novel dosage forms. A number of bisphosphonic acids are known as pharmaceutical agents, particularly in the diagnosis and treatment of disorders and conditions related to bone resorption, calcium metabolism and phosphate metabolism. Such disorders and conditions include, for example, osteoporosis, Paget's disease, periprosthetic bone loss or osteolysis, metastatic bone disease, hypercalcemia of malignancy, multiple myeloma,
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periodontal disease, and tooth loss. The bisphosphonic acids, or "bisphosphonates," which are known to be useful in treating such disorders and conditions fall into three categories: a first generation of drugs, including etidronate, which have significant activity but do not reliably suppress bone resorption, and result in undesirable side effects (etidronate, for example, can give rise to osteomalacia, resulting in a decrease in bone mineralization; see Boyce et al. (1984) Lancet 1(8381):821-824, and Gibbs et al. (1986) Br. Med. J. 2:1227-1229); a second generation of drugs, e.g., pamidronate, which reliably suppress bone resorption when administered parenterally, but are not orally active; and a third generation of drugs typified by alendronate and risedronate, that exhibit both oral and parenteral efficacy. The known bisphosphonic acids include 1hydroxyethane-1,1-diphosphonic acid (etidronic acid, salts of which are referred to as "etidronate"), 1,1-dichloromethylene-1,1-bisphosphonic acid (clodronic acid, salts of which are is referred to as "clodronate"), 3-amino-1-hydroxypropylidene-1,1bisphosphonic acid (pamidronic acid, salts of which are referred to as "pamidronate"), 4amino-1-hydroxybutylidene-1,1-bisphosphonic acid (alendronic acid, salts of which are referred to as "alendronate), 6-amino-1-hydroxy-hexylidene-1,1-bisphosphonic acid (neridronic acid, salts of which are referred to as "neridronate"), (4-chlorophenyl)thiomethane-1,1-diphosphonic acid (tiludronic acid, salts of which are referred to as "tiludronate"), 2-(3-pyridinyl)-1-hydroxy-2-(3-pyridinyl)-ethylidene-1,1-bisphosphonic acid (risedronic acid, salts of which are referred to as "residronate"), cycloheptylaminomethylene-1,1-bisphosphonic acid (cimadronic acid, salts of which are referred to as "cimadronate"), 1-hydroxy-3-(N-methyl-N-pentylamino)-propylidene-1,1bisphosphonic acid (ibandronic acid, salts of which are referred to as "ibandronate"), 3(dimethylamino)-1-hydroxypropylidene-1,1-bisphosphonic acid (olpadronic acid, salts of which are referred to as "olpadronate"), [2-(2-pyridinyl)-ethylidene]-1,1bisphosphonic acid (piridronic acid, salts of which are referred to as "piridronate") and 1-hydroxy-2-(1H-imidazol-1-yl)ethylidene-1,1-bisphosphonic acid (zoledronic acid, salts of which are referred to as "zoledronate"). Although the bisphosphonic acids are therapeutically effective, oral administration of the drugs is problematic, primarily because of adverse gastrointestinal effects, particularly irritation of the esophagus. Pamidronate has been associated with esophageal ulcers, as has alendronate, although to a lesser extent. See, for example, Lufkin et al. (1994) Osteoporosis International 4:320322; De Groen et al. (1996), N. Eng. J. Med. 335(124):1016-1021; Castell et al. (1996) N. Eng. J. Med. 335(124):1058-1059; and Lieberman et al. (1996) N. Eng. J. Med. 3(124):10691070. Even with risedronate, which because of its potency can be administered at relatively low doses, complaints such as heartburn and esophageal burning are frequent. Web site: http://www.delphion.com/details?pn=US06468559__ •
Inhibitors of proteasomal activity and production for stimulating bone growth Inventor(s): Garrett; I. Ross (San Antonio, TX), Mundy; Gregory R. (San Antonio, TX), Rossini; G. (San Antonio, TX) Assignee(s): OsteoScreen, Inc. (San Antonio, TX) Patent Number: 6,462,019 Date filed: July 10, 1998 Abstract: Compounds that inhibit the activity of NF-.kappa.B or inhibit the activity of the proteasome or both promote bone formation and are thus useful in treating osteoporosis, bone fracture or deficiency, primary or secondary hyperparathyroidism,
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periodontal disease or defect, metastatic bone disease, osteolytic bone disease, postplastic surgery, post-prosthetic joint surgery, and post-dental implantation. Excerpt(s): The invention relates to compositions and methods for use in treating skeletal system disorders in a vertebrate at risk for bone loss, and in treating conditions that are characterized by the need for bone growth, in treating fractures, and in treating cartilage disorders. More specifically, the invention concerns the use of inhibitors of proteasomal activity and of NF-.kappa.B activity for this purpose. Bone is subject to constant breakdown and resynthesis in a complex process mediated by osteoblasts, which produce new bone, and osteoclasts, which destroy bone. The activities of these cells are regulated by a large number of cytokines and growth factors, many of which have now been identified and cloned. There is a plethora of conditions which are characterized by the need to enhance bone formation or to inhibit bone resorption. Perhaps the most obvious is the case of bone fractures, where it would be desirable to stimulate bone growth and to hasten and complete bone repair. Agents that enhance bone formation would also be useful in facial reconstruction procedures. Other bone deficit conditions include bone segmental defects, periodontal disease, metastatic bone disease, osteolytic bone disease and conditions where connective tissue repair would be beneficial, such as healing or regeneration of cartilage defects or injury. Also of great significance is the chronic condition of osteoporosis, including age-related osteoporosis and osteoporosis associated with post-menopausal hormone status. Other conditions characterized by the need for bone growth include primary and secondary hyperparathyroidism, disuse osteoporosis, diabetes-related osteoporosis, and glucocorticoid-related osteoporosis. Web site: http://www.delphion.com/details?pn=US06462019__ •
Method for predicting refractory periodontal disease Inventor(s): Levine; Martin (505 Kensington Rd., Norman, OK 73072) Assignee(s): none reported Patent Number: 6,576,435 Date filed: August 24, 2000 Abstract: A kit and method of predicting a refractory response in a subject diagnosed as having periodontal disease by measuring serum concentrations of actinomyces antibodies, streptococcal antibodies and lysine decarboxylase antibodies and using the measurement along with other subject information in a set of derived equations. Excerpt(s): Inflammatory adult periodontitis is a major cause of tooth loss in the middle aged and elderly. The gingival sulci of teeth become infected with a complex mixture of bacteria that impair tooth attachment. Mechanical debridement of the teeth-surfaces (scaling and root planing, SRP) is the current basis of prevention. Many patients preserve tooth attachment with regular SRP and home care, but some,.defined as refractory, continue to lose attachment, even after additional therapy, tetracycline and surgery, to supplement SRP efficacy [1,2]. The severity of prior attachment loss increases the likelihood that a patient will be refractory to therapy [3,4], as also does attachment loss in response to initial SRP [5]. The ability to identify refractory subjects at initial examination would provide several functions that are currently lacking in periodontics. It would indicate how patients should be divided to determine differences in host response or bacterial flora a priori, what patients would benefit most from new and experimental therapies and provide an objective criterion for periodontists to warn
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patients of failure before treatment is begun. Although patients develop antibody responses to various bacterial antigens, responses to specific bacteria have not been related to disease severity or progression except in a general way. The odds ratio of being refractory increased from 3-fold to 19-fold as the number of bacterial taxa with an antibody concentration >50.mu.g/ml increased from 3 to 17, out of a total of 85 bacterial taxa examined [6]. Measuring antibody levels to 85 taxa is difficult. A more specific response was the antibody to Hemophilus aphrophilus being >50.mu.g/ml, but the rationale for measuring antibodies to this organism is not clear and a second, more complex laboratory procedure, measuring bacterial DNA to Streptococcus constellatus, is also required [6]. The proposed procedure requires only antibody levels, and clinical measurements that all periodontists obtain prior to therapy. Recent findings suggest that, of 40 bacterial species detected in the sulci pre-therapy, 37% of the variance in attachment level change after initial SRP was predicted by only the amount of Actinomyces naeslundii serotype 2 and Treponema denticola [5]. A. naeslundii extrudes an ornithine-rich antigen that contains an epitope to which an IgG antibody is directed in human serum [7,8]. An antibody response to this Actinomyces antigen is increased in subjects with less plaque, gingivitis and caries [9]. The sulci of refractory patients contain increased numbers of constellatus/anginosus streptococci [2] that possess a streptococcal antigen (e.g., D-alanyl lipoteichoic acid (D-alanyl-LTA)), whereas mitis/oralis streptococci do not possess D-alanyl LTA and increase in healthy sulci [10,11]. Web site: http://www.delphion.com/details?pn=US06576435__ •
Method for treating periodontal disease Inventor(s): Kurtz; Seymour J. (211 E. Ontario St., Suite 1195, Chicago, IL 60611) Assignee(s): none reported Patent Number: 6,261,597 Date filed: December 3, 1999 Abstract: A method of improving the periodontal condition of a person is disclosed. A suspension of small, unilamellar vesicles composed primarily of phospholipids, similar in nature to those of egg phosphatidylcholine, is administered parenterally to a person suffering from periodontal disease. In the method, liposomes are infused over an extended period of time of at least several weeks, until a desired improvement in gum condition is achieved. Excerpt(s): The present invention relates to methods for improving the periodontal health of a subject by intravenous administration of a suspension of liposomes. The invention also relates to methods for improving hair regrowth of a subject by intravenous administration of a suspension of liposomes. Amselem, S., et al., LIPOSOME TECHNOLOGY (Gregoriadis, G., Ed.), pp. 501-524, CRC Press, Boca Raton, Fla. (1993). Barenholz, Y., et al., Biochemistry 16:2806 (1977). Web site: http://www.delphion.com/details?pn=US06261597__
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Method of testing for periodontal disease Inventor(s): Lamster; Ira B. (Wycoff, NJ) Assignee(s): The Trustees of Columbia University in the City of New York (New York, NY) Patent Number: 6,277,587 Date filed: May 14, 1999 Abstract: This invention provides a method of testing for periodontal disease in a subject which comprises detecting an elevated concentration of.beta.-glucuronidase in saliva from the subject relative to the concentration of.beta.-glucuronidase present in saliva from a healthy subject. The concentration of.beta.-glucuronidase in the subject's saliva is determined by adding to a sample of the saliva a substrate for.beta.glucuronidase and measuring the amount of a product produced by the action of.beta.glucuronidase in the substrate. Also, the concentration of.beta.-glucuronidase in the subject's saliva is determined by adding to a sample of saliva a labeled antibody specific for.beta.-glucuronidase and measuring the amount of labeled antibody which forms a complex with.beta.-glucuronidase present in the saliva. Excerpt(s): Throughout this application, various publications are referenced by author and date. Full citations for these publications may be found listed alphabetically at the end of the specification immediately before the claims. The disclosures of these publications in their entireties are hereby incorporated by reference into this application in order to more fully describe the state of the art as known to those skilled therein. Conventional diagnostic evaluation of periodontal disease has relied on measuring clinical parameters, such as probing depth, attachment level, and plaque accumulation, and on measuring the height of the alveolar bone using radiographs. One shortcoming of these conventional tests is that they only define the status of the periodontium at the time of examination. In the past 10 to 15 years, studies have shown that clinical parameters of periodontal disease are poor predictors of when and at which sites patients that would experience active disease (Haffajee, A. D., et al., 1993). In addition, measurement of alveolar bone loss using intraoral radiographs is of limited value because it provides only a historical record of past disease and cannot be used to determine when the loss of crestal bone occurred. Due to these limitations, researchers have investigated alternative methods for evaluating patients with periodontal disease (Lamster, I. B., et al., 1993). Web site: http://www.delphion.com/details?pn=US06277587__
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Methods and compositions for treating periodontal disease with an inhibitor of secretory phospholipase A2 Inventor(s): Draheim; Susan E. (6125 Burlington Ave., Indianapolis, IN 46220) Assignee(s): none reported Patent Number: 6,325,991 Date filed: August 24, 1999 Abstract: The present invention relates to methods of treating periodontal disease in a mammal. The methods include administering to an animal an s effective amount of an inhibitor of sPLA.sub.2. The inhibitors may be advantageously delivered as a composition that includes various carriers. In certain aspects of the invention, inhibitors
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used in the method include substituted indole or substituted pyrrole sPLA.sub.2 inhibitors. Also provided are compositions that include the sPLA.sub.2 carriers for oral delivery of the inhibitors. Excerpt(s): Periodontal disease is an oral inflammatory disease that begins when inflammation of gingival tissues (gingivitis) progresses to an inflammation of the periodontal attachment tissues. This inflammation may eventually lead to breakdown of the periodontal attachment, periodontal pocket formation and bone loss-periodontitis. The disease may progress to the extent of causing tooth loss due to destruction of the tooth supporting bone. A similar course of events can take place in the tissues surrounding dental implants (peri-implantitis), and can result in gradual loosening and eventual loss of the implant. The rate of progression of periodontal disease is extremely variable. It is believed to be modulated by a complex interaction between subgingival bacterial, the host defense system (including immune and inflammatory responses), and other local tissue factors. Methods of treatment, however, have traditionally focused on the bacterial component of the disease. The conventional approach to the treatment of periodontal disease involves initially removing subgingival bacterial plaque and calculus deposits with scaling and root planing procedures and following-up with improved oral hygiene procedures. If this treatment does not halt progression of the disease, surgical reduction of periodontal tissues is often performed, with the intention of decreasing the depth of the periodontal pocket, thus decreasing the area available for bacterial colonization and aiding mechanical removal of the microorganisms. Concurrent treatment with an antibacterial agent may also be used to further reduce bacterial numbers. Web site: http://www.delphion.com/details?pn=US06325991__ •
Oral hygiene powder composition and method Inventor(s): Anderson; Michael R. (1355 W. Palmetto Park Rd. #129, Boca Raton, FL 33486) Assignee(s): none reported Patent Number: 6,645,472 Date filed: September 13, 2002 Abstract: A anhydrous tooth and gum powdered dentifrice formulated of calcium or magnesium peroxide, sodium bicarbonate, methylsufonymethane, ascorbic acid, colostrum, and optionally menthol, flavoring agent, sweetening agent, sodium laurel sulfate and green tea extract that has a long shelf life but when activated by water or saliva, functions to effect a synergistic chemical and mechanical action to whiten, brighten, polish teeth and reduce bacteria so as to aid in the prevention and treatment of periodontal disease, dental caries and mouth odor. Excerpt(s): The invention relates to a storable, normally inactive, anhydrous oral dentifrice which promotes oral hygiene and which is activated by saliva and/or water, then applied onto the surface of teeth and adjacent gum tissues. The composition and method includes calcium or magnesium peroxide, sodium bicarbonate, ascorbic acid, methylsulfonymethane, and colostrum which are believed to function synergistically to cosmetically whiten, brighten, and bleach (to make whiter or lighter) teeth and therapeutically to cleanse the teeth and surrounding oral tissues and to kill the bacteria which contribute to the formation of dental plaque, caries, and mouth odor. Optionally green tea extract, sodium laurel sulfate, flavors, and sweeteners may be added. The
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desire of people to have white teeth has been present in our society for decades. This desire is heightened by the presence of stains on teeth caused from the food we eat, smoking tobacco, medications, and poor oral hygiene, just to name a few. Many materials, compositions and processes have been developed over the years in attempts to solve this problem. These approaches are not without drawbacks, the most common being product instability, cost, product harshness to teeth and gums, specially trained personnel being required for product application, necessity of wearing specially crafted dental appliances often referred to as "splints". Thus, it is clear that a need exists for a tooth whitener and cleanser that is stable until use, reasonably priced, safe, easy to use, requires no special apparatus or trained personnel to apply, is not harmful to teeth, gums, and other surrounding tissues, and combats tooth and gum diseases commonly caused by bacteria. To a large degree, dental caries and periodontal disease are connected closely to the formation of dental plaque. The literature has long reported that a majority of the world's population suffers from periodontal disease. According to the Merck Manual, 14th ed. 1982, P. 2104, the most common types of periodontal disease are gingivitis and periodontitis. Gingivitis (early stage gum disease) is an inflammation of the gums, characterized by swelling, redness, change in normal contours, and bleeding. If gingivitis is allowed to progress, periodontitis (late, stage gum disease), characterized by loss of tooth-supporting bone, will follow. The greatest single source of periodontal disease is poor hygiene, indicated by the appearance of bacterial and calcified plaque. Web site: http://www.delphion.com/details?pn=US06645472__ •
Periodontal disease preventive and ameliorative agent Inventor(s): Aoe; Seiichirou (Sayama, JP), Dousako; Shunichi (Urawa, JP), Serizawa; Atsusi (Kawagoe, JP), Suguri; Toshiaki (Tokyo, JP), Takada; Yukihiro (Kawagoe, JP) Assignee(s): Snow Brand Milk Products Co., Ltd. (Hokkai-do, JP) Patent Number: 6,544,498 Date filed: March 20, 2000 Abstract: A periodontal disease preventive and ameliorative agent with milk-derived basic protein as its effective ingredient, which protein is obtained by contacting a milk or milk-derived ingredient with cation-exchange resin, and then eluting a fraction adsorbed by the resin using an elution solution and which protein has an isoelectric point within a range of 7.5.about.11, and food/drink and a medicament such as toothpaste and gargling agents, which contain this periodontal disease preventive and ameliorative agent. Excerpt(s): The application claims the priority of PCT International Application No. PCT/JP99/02223, filed Apr. 27, 1999 and Japanese patent document No. 10-134243, filed Apr. 30, 1998, the disclosure of which is expressly incorporated by reference herein. This invention relates to a periodontal disease preventive and ameliorative agent with a milk-derived basic protein as an effective ingredient. This invention also relates to the utilization of the periodontal disease preventive and ameliorative agent with a milkderived basic protein as an effective ingredient for a food/drink and medicament. In recent years, periodontal disease has become an object of public concern. Unlike dental caries, periodontal disease is a disease wherein the foundation of the teeth becomes weak and the use of teeth other than a decayed tooth is eventually lost. In addition, it is said that there are a large number of people who show symptoms of periodontal disease. In this sense, periodontal disease is a more serious disease than dental caries.
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Web site: http://www.delphion.com/details?pn=US06544498__ •
Piperazine derivatives for treating bone deficit conditions Inventor(s): Piggott; James R. (Bothell, WA) Assignee(s): Zymogenetics, Inc. (Seattle, WA) Patent Number: 6,268,367 Date filed: February 23, 1998 Abstract: Piperazine derivatives useful in treating osteoporosis, bone fracture or deficiency, primary or secondary hyperparathyroidism, periodontal disease or defect, metastatic bone disorder, osteolytic bone disease, post-plastic surgery, post-prosthetic joint surgery and post-dental implantation. Excerpt(s): Bone is not a static tissue. It is subject to constant breakdown and resynthesis in a complex process mediated by osteoblasts, which produce new bone, and osteoclasts, which destroy bone. The activities of these cells are regulated by a large number of cytokines and growth factors, many of which have now been identified and cloned. Mundy has described the current knowledge related to these factors (Mundy, Clin. Orthop. 324:24-28, 1996; Mundy, J. Bone Miner. Res. 8:S505-10, 1993). Although there is a great deal of information available on the factors which influence the breakdown and resorption of bone, information on growth factors which stimulate the formation of new bone is more limited. Investigators have searched for sources of such activities, and have found that bone tissue itself is a storehouse for factors which have the capacity for stimulating bone cells. Thus, extracts of bovine bone tissue obtained from slaughterhouses contain not only structural proteins which are responsible for maintaining the structural integrity of bone, but also biologically active bone growth factors which can stimulate bone cells to proliferate. Among these latter factors are transforming growth factor.beta., the heparin-binding growth factors (acidic and basic fibroblast growth factor), the insulin-like growth factors (insulin-like growth factor I and insulin-like growth factor II), and a recently described family of proteins called bone morphogenetic proteins (BMPs). All of these growth factors have effects on other types of cells, as well as on bone cells. The BMPs are novel factors in the extended transforming growth factor.beta. superfamily. They were first identified by Wozney J. et al. Science 242:1528-34, 1980, using gene cloning techniques, following earlier descriptions characterizing the biological activity in extracts of demineralized bone (Urist, Science 150:893-99, 1965). Recombinant BMP2 and BMP4 can induce new bone formation when they are injected locally into the subcutaneous tissues of rats (Wozney, Molec. Reprod. Dev. 32:160-67, 1992). These factors are expressed by normal osteoblasts as they differentiate, and have been shown to stimulate osteoblast differentiation and bone nodule formation in vitro as well as bone formation in vivo (Harris et al., J. Bone. Miner. Res. 9:855-63, 1994). This latter property suggests potential usefulness as therapeutic agents in diseases which result in bone loss. Web site: http://www.delphion.com/details?pn=US06268367__
Patents 167
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Sulfonamide inhibitors of matrix metalloproteinases Inventor(s): Ortwine; Daniel F. (Saline, MI), Purchase, Jr.; Claude F. (Ann Arbor, MI), White; Andrew D. (Lakeland, MI) Assignee(s): Warner-Lambert Company (Morris Plains, NJ) Patent Number: 6,297,247 Date filed: June 22, 2000 Abstract: Sulfonamide compounds are described which are inhibitors of matrix metalloproteinases, particularly stromelysin-1 and gelatinase A (72 kD gelatinase). Also described are methods for the treatment of multiple sclerosis, atherosclerotic plaque rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, burns, decubital ulcers, chronic ulcers or wounds, cancer metastasis, tumor angiogenesis, arthritis, or other autoimmune or inflammatory disorders dependent upon tissue invasion by leukocytes using the compounds. Excerpt(s): The present invention relates to sulfonamide compounds that inhibit matrix metalloproteinases, pharmaceutical compositions that include these compounds, and pharmaceutical methods of treatment using these compounds. The novel compounds of the present invention are inhibitors of matrix metalloproteinases, e.g., stromelysin-1 and gelatinase A (72 kDa gelatinase). More particularly, the compounds of the present invention are useful in the treatment of atherosclerotic plaque rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, burns, decubital ulcers, chronic ulcers or wounds, cancer metastasis, tumor angiogenesis, arthritis, multiple sclerosis, and other autoimmune or inflammatory disorders dependent on the tissue invasion of leukocytes or other activated migrating cells. Stromelysin-1 and gelatinase A are members of the matrix metalloproteinase (MMP) family (Woessner J. F., FASEB J. 1991;5:2145-2154). Other members include fibroblast collagenase, neutrophil collagenase, gelatinase B (92 kDa gelatinase), stromelysin-2, stromelysin-3, matrilysin, collagenase 3 (Freije J. M., Diez-Itza I., Balbin M., Sanchez L. M., Blasco R., Tolivia J., and Lopez-Otin C., J. Biol. Chem., 1994; 269:16766-16773), and the newly discovered membrane-associated matrix metalloproteinases (Sato H., Takino T., Okada Y., Cao J., Shinagawa A., Yamamoto E., and Seiki M., Nature, 1994;370:61-65). Web site: http://www.delphion.com/details?pn=US06297247__
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Suppression, by 5-lipoxygenase inhibitors, of bone resorption Inventor(s): Bonewald; Lynda F. (San Antonio, TX), Gallwitz; Wolf E. (San Antonio, TX), Mundy; G. R. (San Antonio, TX) Assignee(s): Board of Regents, The University of Texas System (Austin, TX) Patent Number: 6,455,541 Date filed: May 8, 2000 Abstract: The present invention focuses upon a method for inhibiting bone resorption. This method involves administering a 5-lipoxygenase inhibitor to a subject in an amount inhibiting the effects of an osteoclast-stimulating factor. When the production of the osteoclast-stimulating factors such as PTH, PTHrp, IL-1, TNF, LT, 1,25(OH).sub.2 D.sub.3 or other factors which may stimulate the production of 5-LO metabolites via the 5-lipoxygenase pathway is inhibited, bone resorption markedly declines. The direct osteoclast-stimulating factors include leukotriene, peptidoleukotriene and 5-
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hydroxyeicosatetraenoic acid. Other factors yet to be identified or previously known may also be 5-lipoxygenase metabolites that stimulate bone resorption. While 5lipoxygenase inhibitors may be substrate analogs or allosteric inhibitors, a substance which inhibits the activity of this enzyme may utilize other mechanisms (e.g., inhibition of 5-LO biosynthesis) and nevertheless function to inhibit bone resorption. Preferred inhibitors included NGDA, MK886 and ZM230,487. The best inhibitor thus far noted is ZM230,487. The inhibition of bone resorption is highly desirable with, for example, periodontal disease, osteoporosis, estrogen deficiency, Paget's disease, inflammatory bone loss, bone malignancy, hyperparathyroidism. Administering of a 5-lipoxygenase inhibitor may be enteral--when oral administration is desired, parenteral, when appropriate (preferably by vascular injection or infusion), or topical such as application to oral tissues to prevent bone loss due to periodontal disease. The preferred range of 5lipoxygenase inhibitors administered is from 0.1 to 10 mg/kg body weight/day. Excerpt(s): Diseases associated with bone loss are usually accompanied by increased osteoclast activation. Such diseases include estrogen deficiency after the menopause osteoporosis, primary hyperparathyroidism, malignancy, Paget's disease of bone and periodontal disease. The bone loss is caused by osteoclast activity. Osteoclasts are unique multinucleated cells within bone that are responsible for bone degradation. These are the only cells in the body known to be capable of resorbing bone. Since diseases of bone loss are associated with increased activity of these cells, it is important to understand the mechanisms by which osteoclasts are activated in these disease states, and to devise rational and therapeutic means to inhibit this activation. The molecular mechanisms by which osteoclasts are activated are unknown. In vitro data indicate cytokines and systemic hormones with bone resorbing effects do not act directly on osteoclasts, but rather act on accessory cells in the bone marrow microenvironment and that these cells in turn are responsible for osteoclast activation (Rodan & Martin 1981, Mcsheehy & Chambers 1986). This activation may be mediated either by cell-cell contact or by locally active soluble factors. In a search for cell sources of such soluble factors, the present inventors found that a stromal cell line (C433) derived from a giant cell tumor of bone produced prodigious amounts of osteoclast-stimulating activity greater than any we found in conditioned media from cells with osteoblast characteristics (Oreffo et al., 1993). Human giant cell tumors of bone comprise heterogeneous cell populations, including giant cells with many of the phenotypic and functional characteristics of osteoclasts as well as mononuclear cells. The multinucleated cells are positive for osteoclast surface antigens (Davies et al, 1989), for tartrate-resistant acid phosphatase (TRAP),.sup.1 possess receptors for calcitonin (Komiya et al., 1990) and lack monocytemacrophage surface antigens (Goldring et al., 1986). The mononuclear cells comprise two distinct populations. One population does not persist in culture and is positive for Ia and monocyte-macrophage antigens (Ling et al., 1988). Another population persists in culture and resembles connective tissue stromal cells, produces Types I and III collagen, and has receptors for parathyroid hormone (Goldring et al., 1986). These latter cells can be readily established in cell culture. One cell line (C433) derived from stomal cells from a giant cell tumor is shown herein to cause greater increases in osteoclast activity as measured by accumulation of TRAP activity than any of the known osteoblast-like cell lines. This study concerns characterizing the osteoclast stimulating activity produced by this cell line. This activity is ascribed to 5-hydroxyeicosanoids, which are 5-lipoxygenase metabolites of arachidonic acid. Web site: http://www.delphion.com/details?pn=US06455541__
Patents 169
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Surface acoustic wave periodontal probe and method of detecting periodontal disease Inventor(s): Rose; Emery S. (31-77 32th St., Astoria, Queens, NY 11106) Assignee(s): none reported Patent Number: 6,413,220 Date filed: November 8, 2000 Abstract: An ultrasonic probe (10) for measuring the depth of detachment between a tooth (30) and the tooth's supporting tissue includes a probe head (12) having an ultrasonic transducer (35). An incident acoustic wave pulse (50) is transmitted through a coupling medium at a critical angle of incidence for refraction at the interface between the coupling medium and the tooth surface (29, 31) to effect modal conversion to a surface acoustic wave pulse along the surface of the tooth (30). The critical angle of incidence is established by means of an angular setting of the ultrasonic transducer (35) in the probe head (12), a combination of the aforementioned angular setting with the ability to rock the probe head (12) to find the critical angle of incidence, and/or a phased array implementation. The disclosure also includes an algorithm for determining the depth of detachment based on the time lapse between transmission and detection of the reflection of the acoustic wave pulses. Excerpt(s): This disclosure relates to diagnostic probes and methods of incorporating diagnostic probes for detecting periodontal disease. More particularly, the present disclosure relates to a non-invasive diagnostic probe which emits and analyzes surface acoustic waves to detect and diagnose periodontal disease. The instrument and method disclosed herein is directed to the non-invasive detection and measurement of periodontal disease by means of measuring the depth of detachment of a tooth from its supporting tissue or cementum. Since the crown of a tooth comprises enamel and the root of a tooth comprises dentin, the acoustic impedances of these various tooth elements differ. From the cementoenamel junction (a well defined boundary between the crown and the root) down towards the root, the tooth, under healthy conditions, is attached to supporting tissue by cementum. In the presence of periodontal disease, a portion of the root is detached from the supporting tissue thus forming a gap from the crown and root boundary downwardly into the gum. The depth and width of the gap differs depending on the extent of disease progression. Web site: http://www.delphion.com/details?pn=US06413220__
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Therapy with coenzyme Q10 to reduce subgingival microorganisms in patients with periodontal disease Inventor(s): Folkers; Karl (Austin, TX), Hanioka; Takashi (Suita-Osaka, JP), McRee; Judson T. (Lockhart, TX) Assignee(s): Biomedical and Clinical Research (Austin, TX) Patent Number: 6,461,593 Date filed: February 19, 1992 Abstract: The presence of diverse microorganisms in the gingiva of patients having periodontal disease is very well known to be deleterious to gingival health, and particularly to facilitate the appearance and development of dental cavities. Such microorganisms are always associated with periodontal disease, and if such microorganisms remain unchecked or uncontrolled, extraction of teeth are likely to
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occur.In the past, the presence of microorganisms in the gingiva of patients with periodontal disease has been periodically and erratically treated with anti-microbial agents, including antibiotics. For anti-microbial agents and antibiotics to be effective in the gingiva, such agents and antibiotics must come into direct contact with microorganisms, and such contact is known to be incomplete, partly because there may be barriers of fluid and tissue which prevent direct contact between the agents and antibiotics with the microorganisms. Also, such agents can be inactive for certain microorganisms and even when there is activity, such microorganisms can become metabolically resistant to the agents and antibiotics.A more effective way to reduce and to control microorganisms in the gingiva of patients with periodontal disease is to increase the efficacy of the immune system of the host. Coenzyme Q.sub.10 (CoQ.sub.10) has been known to increase the immune system, but previously it was unknown that CoQ.sub.10 could be a very effective mechanism to reduce and to eliminate microorganisms in the gingiva of patients with periodontal disease. Excerpt(s): This invention relates to a new and very safe therapy which involves treatment with coenzyme Q.sub.10 (CoQ.sub.10) of patients in the normal practice of dentistry who have periodontal disease. The gingiva of these patients with periodontal disease are afflicted with diverse microorganisms which are the primary cause of the initiation and development of dental caries and loss of bone support. There has never been a completely effective and safe therapy to diminish or eradicate microorganisms in periodontal disease. Anti-microbial agents and antibiotics have been used but have never been totally effective, although they have been widely and commonly used in dental practice across the country. Many periodontal patients do not respond to treatment with such agents and antibiotics. Many or most patients with periodontal disease have depressed immune systems which allow the growth and presence of microorganisms in the diseased gingiva. A new and far better approach to reduce subgingival microorganisms of patients with periodontal disease is to rejuvenate the depleted immune system of patients. Web site: http://www.delphion.com/details?pn=US06461593__
Patent Applications on Periodontal Disease As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to periodontal disease: •
2-oxo-imidazolidine-4-carboxylic acid hydroxamide compounds that inhibit matrix metalloproteinases Inventor(s): Laird, Ellen R.; (Mystic, CT), Robinson, Ralph P.; (Gales Ferry, CT) Correspondence: Paul H. Ginsburg; Pfizer Inc; 20th Floor; 235 East 42nd Street; New York; NY; 10017-5755; US Patent Application Number: 20010041710 Date filed: December 5, 2000
10
This has been a common practice outside the United States prior to December 2000.
Patents 171
Abstract: The present invention relates to a compound of the formula 1wherein R.sup.1, R.sup.2, R.sup.3 and R.sup.4 are as defined above, and pharmaceutically acceptable salts and solvates thereof, that are useful, for example, as matrix metalloproteinase inhibitors. The present invention is also directed to pharmaceutical compositions comprising such compounds and methods of treatment for diseases such as osteoarthritis, rheumatoid arthritis, cancer, osteoporosis, tissue ulceration, restinosis, periodontal disease, inflammation, epidermolysis bullosa, scleritis, stroke, Alzheimer's disease, and the like, characterized by inappropriate matrix metalloproteinase activity. Processes for the synthesis of compounds of formula (I) are also disclosed. Excerpt(s): The present invention relates to 2-oxo-imidazolidine-4-carboxylic acid hydroxamide derivatives, and to pharmaceutical compositions comprising such derivatives, and to the use of such derivatives in the treatment of arthritis, inflammation, cancer, and other diseases as described below. The compounds of the present invention are inhibitors of zinc metalloendopeptidases, especially those belonging to the matrix metalloproteinase (also called MMP or matrixin) and reprolysin (also known as adamylsin) subfamilies of the metzincins (Rawlings, et al., Methods in Enzymology, 248, 183-228 (1995) and Stocker, et al., Protein Science, 4, 823-840 (1995)). The MMP subfamily of enzymes, currently contains seventeen members (MMP-1, MMP2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-10, MMP-11, MMP-12, MMP-13, MMP-14, MMP-15, MMP-16, MMP-17, MMP-18, MMP-19, MMP-20). The MMPs are most well known for their role in regulating the turn-over of extracellular matrix proteins and as such play important roles in normal physiological processes such as reproduction, development and differentiation. In addition, the MMPs are expressed in many pathological situations in which abnormal connective tissue turnover is occurring. For example, MMP-13, an enzyme with potent activity at degrading type II collagen (the principal collagen in cartilage), has been demonstrated to be overexpressed in osteoarthritic cartilage (Mitchell, et al., J. Clin. Invest., 97, 761 (1996)). Other MMPs (MMP-2, MMP-3, MMP-8, MMP-9, MMP-12) are also overexpressed in osteoarthritic cartilage and inhibition of some or all of these MMP's is expected to slow or block the accelerated loss of cartilage typical of joint diseases such as osteoarthritis or rheumatoid arthritis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Alkynyl containing hydroxamic acid compounds as matrix metalloproteinase/tace inhibitors Inventor(s): Baker, Jannie L.; (White Plains, NY), Chen, James M.; (Stoddard Court, NJ), Du, Mila T.; (Suffern, NY), Levin, Jeremy I.; (New City, NY), Sandanayaka, Vincent P.; (Wesley Hills, NY), Venkatesan, Aranapakam M.; (Rekgo Park, NY), Zask, Arie; (New York, NY) Correspondence: American Home Products Corporation; Five Giralda Farms; Patent Law; Madison; NJ; 07940; US Patent Application Number: 20020086890 Date filed: December 21, 2001 Abstract: Compounds of the formula: 1useful in the treatment of arthritis, tumor metastasis, tissue ulceration, abnormal wound healing, periodontal disease, bone disease, diabetes (insulin resistance) and HIV infection.
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Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/155,184, filed Jan. 27, 1999. This invention relates to acetylenic hydroxamic acids which act as inhibitors of TNF-.alpha. converting enzyme (TACE). The compounds of the present invention are useful in disease conditions mediated by TNF-.alpha., such as rheumatoid arthritis, osteoarthritis, sepsis, AIDS, ulcerative colitis, multiple sclerosis, Crohn's disease and degenerative cartilage loss. Matrix metalloproteinases (MMPs) are a group of enzymes that have been implicated in the pathological destruction of connective tissue and basement membranes. These zinc containing endopeptidases consist of several subsets of enzymes including collagenases, stromelysins and gelatinases. Of these classes, the gelatinases have been shown to be the MMPs most intimately involved with the growth and spread of tumors. It is known that the level of expression of gelatinase is elevated in malignancies, and that gelatinase can degrade the basement membrane which leads to tumor metastasis. Angiogenesis, required for the growth of solid tumors, has also recently been shown to have a gelatinase component to its pathology. Furthermore, there is evidence to suggest that gelatinase is involved in plaque rupture associated with atherosclerosis. Other conditions mediated by MMPs are restenosis, MMP-mediated osteopenias, inflammatory diseases of the central nervous system, skin aging, tumor growth, osteoarthritis, rheumatoid arthritis, septic arthritis, corneal ulceration, abnormal wound healing, bone disease, proteinuria, aneurysmal aortic disease, degenerative cartilage loss following traumatic joint injury, demyelinating diseases of the nervous system, cirrhosis of the liver, glomerular disease of the kidney, premature rupture of fetal membranes, inflammatory bowel disease, periodontal disease, age related macular degeneration, diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, ocular inflammation, keratoconus, Sjogren's syndrome, myopia, ocular tumors, ocular angiogenesis/neovascularization and corneal graft rejection. For recent reviews, see: (1) Recent Advances in Matrix Metalloproteinase Inhibitor Research, R. P. Beckett, A. H. Davidson, A. H. Drummond, P. Huxley and M. Whittaker, Research Focus, Vol. 1, 16-26, (1996), (2) Curr. Opin. Ther. Patents (1994) 4(1): 7-16, (3) Curr. Medicinal Chem. (1995) 2: 743-762, (4) Exp. Opin. Ther. Patents (1995) 5(2): 1087-110, (5) Exp. Opin. Ther. Patents (1995) 5(12): 1287-1196: (6) Exp. Opin. Ther. Patents (1998) 8(3): 281-259. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Androgen receptor modulators and methods for use thereof Inventor(s): Breslin, Michael J.; (Drexel Hill, PA), Duggan, Mark E.; (Schwenksville, PA), Halczenko, Wasyl; (Lansdale, PA), Harada, Shun-Ichi; (Ambler, PA), Hutchinson, John H.; (La Jolla, CA), Rodan, Gideon A.; (Bryn Mawr, PA), Sahoo, Soumya P.; (Old Bridge, NJ), Schmidt, Azriel; (Bryn Mawr, PA), Towler, Dwight A.; (Brentwood, MO) Correspondence: Merck And CO Inc; P O Box 2000; Rahway; NJ; 070650907 Patent Application Number: 20030065004 Date filed: July 25, 2002 Abstract: Compounds of structural formula (I) as herein defined are disclosed as useful in a method for modulating the androgen receptor in a tissue selective manner in a patient in need of such modulation, as well as in a method of agonizing the androgen receptor in a patient, and in particular the method wherein the androgen receptor is antagonized in the prostate of a male patient or in the uterus of a female patient and agonized in bone and/or muscle tissue. These compounds are useful in the treatment of conditions caused by androgen deficiency or which can be ameliorated by androgen
Patents 173
administration, including: osteoporosis, periodontal disease, bone fracture, bone damage following bone reconstructive surgery, sarcopenia, frailty, aging skin, male hypogonadism, post-menopausal symptoms in women, atherosclerosis, hypercholesterolemia, hyperlipidemia, aplastic anemia and other hematopoietic disorders, pancreatic cancer, renal cancer, arthritis and joint repair, alone or in combination with other active agents. In addition, these compounds are useful as pharmaceutical composition ingredients alone and in combination with other active agents. Excerpt(s): The present application claims priority of U.S. provisional application Serial No. 60/308,841, filed Jul. 31, 2001. Androgens play important roles in post-natal development that are most pronounced at adrenarche and pubarche. Androgen production promotes the musculoskeletal anabolism associated with the pubertal growth in both males and females. At puberty, ovarian and testicular androgens are responsible for pubertal hair, acne, and enhancement of libido. In males, exposure to 100-fold increased levels of endogenous androgens results in the gender dimorphism in bone mass, muscle mass (positive nitrogen balance), and upper body strength, and are required for normal sexual development (genitalia, spermatogenesis, prostate and seminal vesicle maturation). Delay in puberty decreases the peak bone mass achieved during adulthood. (Bhasin, S., et al., Eds. Pharmacology, Biology, and Clinical Applications of Androgens: Current Status and Future Prospects. Wiley-Liss, Inc.:New York, 1996). In women, natural menopause causes virtually complete loss of ovarian estrogen production and gradually reduces ovarian production of androgen by approximately 50%. The physiological consequences of reduced androgen production after menopause are evident in decreased energy and libido, and contribute significantly in many women to vasomotor symptoms. Decreased androgen output is also thought to contribute--along with declining pituitary growth hormone (GH) secretion and insulin derived growth factor 1 (IGF1) action--to age-dependent sarcopenia, negative nitrogen balance and loss of bone mass. (Vestergaard, et al., Effect of sex hormone replacement on the insulin-like growth factor system and bone mineral: a cross-sectional and longitudinal study in 595 perimenopausal women participating in the Danish Osteoporosis Prevention Study, J Clin Endocrinol Metab. 84:2286-90, 1999; and Bhasin, et al., Eds. Pharmacology, Biology, and Clinical Applications of Androgens: Current Status and Future Prospects, Wiley-Liss, Inc.:New York. 1996). Postmenopausal osteoporosis results mainly from estrogen deficiency. However, many women who received estrogen replacement therapy still lose bone with age and develop age--related osteoporotic fractures (albeit at a lower rate than those taking estrogens), indicating that both estrogens and androgens play important roles for bone health in both women and men. The simultaneous decreases in bone mass, muscle mass and muscle strength increase the risk of falls and especially of hip fractures in both men and women >65 years of age. In fact, one-third of all hip fractures occur in men. The androgen receptor (AR) belongs to the nuclear receptor superfamily and controls transcription in a ligand dependent manner (Brinkman, et al., Mechanisms of androgen receptor activation and function, J. Ster. Biochem. Mol. Biol. 69, 307-313, 1999). Upon androgen binding, AR binds directly to specific DNA sequences present in the promoter region of androgen responsive genes, termed androgen response elements (AREs), to stimulate transcription. Using ARE-dependent transcription as a criterion, agents that bind to AR and stimulate ARE-dependent transcription can be classified as agonists, and those that bind to AR and suppress ARE-dependent transcription are classified as antagonists. A number of natural or synthetic androgen agonists have been used for treatment of musculoskeletal or hematopoietic disorders and for hormone replacement therapy. In addition, AR antagonists, such as flutamide or bicalutamide, are used for treatment of
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prostate cancer. However, clinical use of these androgen agonists or antagonists have been limited because of undesirable effects, such as hirsutism and prostate enlargement for agonists, and bone loss, fracture, gynecomastia and sarcopenia for antagonists. It would be useful to have available androgens with tissue selective agonistic activity, which increase bone formation and muscle mass but do not induce the virilization. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Arylsulfonylamino hydroxamic acid derivatives Inventor(s): McClure, Kim Francis; (Mystic, CT), Robinson, Ralph Pelton JR.; (Gales Ferry, CT) Correspondence: Paul H. Ginsburg; Pfizer INC.; 20th Floor; 235 East 42nd Street; New York; NY; 10017-5755; US Patent Application Number: 20020006920 Date filed: July 18, 2001 Abstract: A compound of the formula 1wherein R.sup.1, R.sup.2 and Q are as defined above, useful in the treatment of a condition selected from the group consisting of arthritis, cancer, tissue ulceration, macular degeneration, restenosis, periodontal disease, epidermolysis bullosa, sceritis, and other diseases characterized by matrix metalloproteinase activity, AIDS, sepsis, septic shock and other diseases involving the production of TNF. In addition, the compounds of the present invention may be used in combination therapy with standard non-steroidal anti-inflammatory drugs (NSAID'S) and analgesics, and in combination with cytotoxic drugs such as adriamycin, daunomycin, cis-platinum, etoposide, taxol, taxotere and other alkaloids, such as vincristine, in the treatment of cancer. Excerpt(s): The present invention relates to arylsulfonylamino hydroxamic acid derivatives which are inhibitors of matrix metalloproteinases or the production of tumor necrosis factor (TNF) and as such are useful in the treatment of a condition selected from the group consisting of arthritis, cancer, tissue ulceration, restenosis, periodontal disease, epidermolysis bullosa, scleritis and other diseases characterized by matrix metalloproteinase activity, AIDS, sepsis, septic shock and other diseases involving the production of TNF. In addition, the compounds of the present invention may be used in combination therapy with standard non-steroidal anti-inflammatory drugs (hereinafter NSAID'S) and analgesics for the treatment of arthritis, and in combination with cytotoxic drugs such as adriamycin, daunomycin, cis-platinum, etoposide, taxol, taxotere and alkaloids, such as vincristine, in the treatment of cancer. This invention also relates to a method of using such compounds in the treatment of the above diseases in mammals, especially humans, and to pharmaceutical compositions useful therefor. There are a number of enzymes which effect the breakdown of structural proteins and which are structurally related metalloproteases. Matrix-degrading metalloproteinases, such as gelatinase, stromelysin and collagenase, are involved in tissue matrix degradation (e.g. collagen collapse) and have been implicated in many pathological conditions involving abnormal connective tissue and basement membrane matrix metabolism, such as arthritis (e.g. osteoarthritis and rheumatoid arthritis), tissue ulceration (e.g. corneal, epidermal and gastric ulceration), abnormal wound healing, periodontal disease, bone disease (e.g. Paget's disease and osteoporosis), tumor metastasis or invasion, as well as HIV-infection (J. Leuk. Biol., 52 (2): 244-248, 1992). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 175
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Biphenyl butyric metalloproteinases
acids
and
their
derivatives
as
inhibitors
of
matrix
Inventor(s): Purchase, Claude Forsey JR.; (Ann Arbor, MI), Roth, Bruce David; (Plymouth, MI), Schielke, Gerald Paul; (Ann Arbor, MI), Walker, Lary Craswell; (Ann Arbor, MI), White, Andrew David; (Pinckney, MI) Correspondence: Attention: Ronald A. Daignault; Merchant & Gould P.C.; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20010000513 Date filed: December 14, 2000 Abstract: Biphenyl butyric acid compounds and derivatives are described as well as acid methods for the preparation and pharmaceutical compositions of same, which are useful as inhibitors of matrix metalloproteinases, particularly gelatinase A (72 kD gelatinase) and stromelysin-1 and for the treatment of multiple sclerosis, atherosclerotic plaque rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, treatment of burns, decubital ulcers, wound healing, cancer, inflammation, pain, arthritis, or other autoimmune or inflammatory disorders dependent upon tissue invasion by leukocytes or other activated migrating cells. Excerpt(s): 1. The present invention relates to novel biphenyl butyric acid compounds and their derivatives useful as pharmaceutical agents, to methods for their production, to pharmaceutical compositions which include these compounds and a pharmaceutically acceptable carrier, and to pharmaceutical methods of treatment. The novel compounds of the present invention are inhibitors of matrix metalloproteinases, e.g., gelatinase A (72 kDa gelatinase) and stromelysin-1. More particularly, the novel compounds of the present invention are useful in the treatment of atherosclerotic plaque rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, treatment of bums, decubital ulcers, wound repair, cancer, inflammation, pain, arthritis, multiple sclerosis, and other autoimmune or inflammatory disorders dependent on the tissue invasion of leukocytes or other activated migrating cells. Additionally, the compounds of the present invention are useful in the treatment of acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. 3. The catalytic zinc in matrix metalloproteinases is a focal point for inhibitor design. The modification of substrates by introducing chelating groups has generated potent inhibitors such as peptide hydroxymates and thiol-containing peptides. Peptide hydroxamates and the natural endogenous inhibitors of MMPs (TIMPs) have been used successfully to treat animal models of cancer and inflammation. 4. The ability of the matrix metalloproteinases to degrade various components of connective tissue makes them potential targets for controlling pathological processes. For example, the rupture of an atherosclerotic plaque is the most common event initiating coronary thrombosis. Destabilization and degradation of the extracellular matrix surrounding these plaques by MMPs has been proposed as a cause of plaque fissuring. The shoulders and regions of foam cell accumulation in human atherosclerotic plaques show locally increased expression of gelatinase B, stromelysin-1, and interstitial collagenase. In situ zymography of this tissue revealed increased gelatinolytic and caseinolytic activity (Galis Z. S., Sukhova G. K., Lark M. W., and Libby P., "Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques", J. Clin. Invest., 1994;94:2494-2503). In addition, high levels of stromelysin RNA message
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have been found to be localized to individual cells in atherosclerotic plaques removed from heart transplant patients at the time of surgery (Henney A. M., Wakeley P. R., Davies M. J., Foster K., Hembry R., Murphy G., and Humphries S., "Localization of stromelysin gene expression in atherosclerotic plaques by in situ hybridization", Proc. Nat'l. Acad. Sci., 1991;88:8154-8158). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Composition for promoting regeneration of hard tissues comprising an extract of cortex eucommiae Inventor(s): Kim, Sung-Jin; (Dongdaemoon-Ku, KR) Correspondence: Bruce B. Brunda; Stetina Brunda Garred & Brucker; Suite 250; 75 Enterprise; Aliso Viego; CA; 92656; US Patent Application Number: 20020168435 Date filed: February 21, 2002 Abstract: The present invention discloses a composition for promoting regeneration of hard tissues comprising an extract of Cortex Eucommiae. It can be applied to prevent and treat hard tissue disorders such as osteoporosis and periodontal disease followed by alveolar bone destruction. It can also be used to stimulate growth of children. Excerpt(s): Hard tissues in humans are largely classified as bones and teeth. The representative diseases caused by hard tissue disorders are osteoporosis and periodontal diseases. Bones are essential for locomotion and play an important role in calcium metabolism. With age, incidences of bone fracture, osteoporosis, and severe periodontal disease accompanied by alveolar bone destruction increase significantly. Teeth, as major components of the digestive system, are essential for mastication. Maintaining teeth in good condition is essential for satisfaction in eating and enjoying the taste of food, thereby especially increasing the quality of life for the elderly. Thus, the prevention and treatment of these aging-related diseases draw tremendous attention from societies with high percentages of elderly people. Hard tissues undergo constant remodeling through bone formation (via osteoblast) and bone resorption (via osteoclast) and maintain homeostasis. Such metabolism is regulated by systemic hormones as well as local factors. When bone resorption rates surpass bone formation rates by a variety of factors and bone mass decreases below a critical level, bone-related diseases such as osteoporosis and periodontal disease occur. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions for regenerating tissue that has deteriorated, and methods for using such compositions Inventor(s): Boss, William K. JR.; (Essex Fells, NJ), Marko, Olga; (Paramus, NJ) Correspondence: Stuart Macphail, PH.D.; Fish & Richardson P.C.; Suite 2800; 45 Rockefeller Plaza; New York; NY; 10111; US Patent Application Number: 20020197241 Date filed: June 11, 2002 Abstract: A composition for promoting regeneration of tissue which has degenerated in a subject as a result of a disease or disorder and a method of using the composition is
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provided. The composition comprises a biodegradable acellular matrix, and passaged autologous fibroblasts substantially free of immunogenic proteins, e.g., culture medium serum-derived proteins, integrated within the matrix. The method of using the composition to promote regeneration of tissue involves placing the composition on a site of degenerated tissue in a subject so that the composition promotes tissue regeneration at the site. The composition and the method of its use have applications promoting regeneration of tissue (i) that has degenerated as a result of numerous diseases or disorders or (ii) that has a defect, including, but not limited to, defects of the oral mucosa, trauma to the oral mucosa (e.g., extraction of a tooth), periodontal disease, diabetes, cutaneous ulcers, venous stasis, scars of the skin, or wrinkles of the skin. Also provided is an injectable composition comprising any type of collagen and passaged autologous fibroblasts substantially free of immunogenic proteins, e.g., culture medium serum-derived proteins, for correcting defects in skin, such as wrinkles or scars, and for augmenting tissue in the subject, particularly facial tissue. Excerpt(s): This application is a continuation-in part and claims priority of U.S. application Ser. No. 09/316,245, filed May 21, 1999, which is a continuation-in-part and claims priority of U.S. application Ser. No. 09/083,618, filed May 22, 1998. U.S. application Ser. Nos. 09/316,245 and 09/083,618 are incorporated herein by reference in their entirety. The present invention concerns the regeneration of tissues in a subject that have degenerated as a result of a disease or disorder in the subject. More particularly, the present invention concerns novel compositions for use in surgical and nonsurgical techniques that promote regeneration of tissue whose mass has been diminished due to a disease or disorder in a subject, correct defects in the skin of subjects, or augment tissue in subjects. Also disclosed is the use of a novel composition in conjunction with a biodegradable acellular matrix for ameliorating defects in the tissues, and methods for using the novel composition. "Periodontal disease" is the term commonly used to describe inflammatory disease of the periodontium, i.e., the tissue surrounding and securing teeth to the jawbone. The condition is characterized by inflammatory and degenerative processes that develop at the gingival margin (gingivitis) and lead to a progressive breakdown and resorption of the periodontal ligament and bone (periodontitis), oftentimes resulting in severe diminution of the periodontium. Periodontal disease is the leading cause of tooth loss in adults after middle age. [Anderson's Pathology, p. 2000, John M. Kissane ed., 9th ed. (1992)]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Diagnostics and treatments of periodontal disease Inventor(s): Bhogal, Peter Singh; (Victoria, AU), Reynolds, Eric Charles; (Victoria, AU), Slakeski, Nada; (Victoria, AU) Correspondence: Nixon & Vanderhye P.C.; 1100 North Glebe Road, 8th Floor; Arlington; VA; 22201-4714; US Patent Application Number: 20030157637 Date filed: August 28, 2002 Abstract: This invention relates to the PrtR-PrtK cell surface protein of Porphyromonas gingivalis and in particular a multimeric cell associated protein complex comprising the PrtR and PrtK proteins. Accordingly the invention provides a substantially purified antigenic complex for use in raising an antibody response directed against Porphyromonas gingivalis. The complex comprises at least one multimeric protein complex of arginine-specific and lysine-specific thiol endopeptidases each containing at
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least one adhesin domain, the complex having a molecular weight of greater than about 200 kDa. The invention also relates to pharmaceutical compositions and associated agents based on said complex for the detection, prevention and treatment of Periodontal disease associated with P. gingivalis. Excerpt(s): This invention relates to the PrtR-PrtK cell surface protein of Porphyromonas gingivalis and in particular a multimeric cell associated protein complex comprising the PrtR and PrtK proteins. The invention also relates to pharmaceutical compositions and associated agents based on said complex for the detection, prevention and treatment of Periodontal disease associated with P. gingivalis. Periodontal diseases are bacterialassociated inflammatory diseases of the supporting tissues of the teeth and range from the relatively mild form of gingivitis, the non-specific, reversible inflammation of gingival tissue to the more aggressive forms of periodontitis which are characterised by the destruction of the tooth's supporting structures. Periodontitis is associated with a subgingival infection of a consortium of specific Gram-negative bacteria that leads to the destruction of the periodontium and is a major public health problem. One bacterium that has attracted considerable interest is P. gingivalis as the recovery of this microorganism from adult periodontitis lesions can be up to 50% of the subgingival anaerobically cultivable flora, whereas P. gingivalis is rarely recovered, and then in low numbers, from healthy sites. A proportional increase in the level of P. gingivalis in subgingival plaque has been associated with an increased severity of periodontitis and eradication of the microorganism from the cultivable subgingival microbial population is accompanied by resolution of the disease. The progression of periodontitis lesions in non-human primates has been demonstrated with the subgingival implantation of P. gingivalis. These findings in both animals and humans suggest a major role for P. gingivalis in the development of adult periodontitis. P. gingivalis is a black-pigmented, anaerobic, asaccharolytic, proteolytic Gram-negative rod that obtains energy from the metabolism of specific amino acids. The microorganism has an absolute growth requirement for iron, preferentially in the form of haeme or its Fe(III) oxidation product haemin and when grown under conditions of excess haemin is highly virulent in experimental animals. A number of virulence factors have been implicated in the pathogenicity of P. gingivalis including the capsule, adhesins, cytotoxins and extracellular hydrolytic enzymes. In particular, proteases have received a great deal of attention for their ability to degrade a broad range of host proteins including structural proteins and others involved in defence. The proteins that have been shown to be substrates for P. gingivalis proteolytic activity include collagen types I and IV, fibronectin, fibrinogen, laminin, complement and plasma clotting cascade proteins,.alpha.sub.1-antitrypsin,.alpha.sub.2-macroglobulin antichymotrypsin, antithrombin III, antiplasmin, cystatin C, IgG and IgA. The major proteolytic activities associated with this organism have been defined by substrate specificity and are "trypsin-like", that is cleavage on the carboxyl side of arginyl and lysyl residues and collagenolytic although other minor activities have been reported. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Dispensing apparatus and cartridge Inventor(s): Bates, Mark; (Westwood, MA), Hunter, Gregory H.; (Dover, MA), Lanzilotti, Michael G.; (Newtown, PA), Lawter, James R.; (Yardley, PA) Correspondence: Patrea L. Pabst; Holland & Knight Llp; Suite 2000, One Atlantic Center; 1201 West Peachtree Street, N.E.; Atlanta; GA; 30309-3400; US Patent Application Number: 20030186191 Date filed: March 29, 2002 Abstract: A device for the treatment of periodontal disease includes a handle that has a configuration familiar to dental professionals, and a cartridge, that is locked into the handle when use, typically delivery of a composition to a periodontal pocket is desired. The cartridge provides for effective delivery of compositions, such as agents, as its tip is deformable, typically from a circular to an oval shape so as to flatten. The deformation may be made, either manually, by the dental professional, or upon contact with teeth or other tissues, whereby this flattened tip can penetrate deeply into periodontal pockets for quick and direct application of the composition, for example, therapeutic agents. Excerpt(s): The present disclosure is directed to apparatus, components, and methods of treatment for periodontal disease. Periodontal disease is an umbrella term for a variety of dental conditions associated with either gingivitis or periodontitis. Gingivitis is an inflammation of the gingiva, commonly known as gums, that is commonly associated with poor oral hygiene and/or the hormonal state of the patient. If left untreated, gingivitis may develop into periodontitis. Periodontitis is a bacterial disease in which the infection has progressed to involve the oral tissues that retain the teeth in the jawbone. With this disease the gums become red and inflamed. This condition, if untreated, results in damage to the ligaments and bone holding the teeth in place, and formation of pockets around the teeth. As the pockets become deeper, teeth loosen, to a point where they may fall out. The severity of periodontitis is determined by dentists and other dental practitioners, by measuring the depth of these pockets and reviewing x-rays of the teeth and jawbone. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Inhibition of matrix metalloproteases by substituted biaryl oxobutyric acids Inventor(s): Brittelli, David R.; (Branford, CT), Dixon, Brian R.; (Woodbridge, CT), VanZandt, Michael C.; (Guilford, CT) Correspondence: Jeffrey M. Greenman; Vice President, Patents And Licensing; Bayer Corporation; 400 Morgan Lane; West Haven; CT; 06516; US Patent Application Number: 20020042417 Date filed: April 30, 2001 Abstract: Matrix metalloprotease inhibiting compounds, pharmaceutical compositions thereof and a method of disease treatment using such compounds are presented. The compounds of the invention have the generalized formulas: 1wherein r is 0-2, T is selected from 2and R.sup.40 is a mono- or bi-heterocyclic structure.These compounds are useful for inhibiting matrix metalloproteases and, therefore, combating conditions to which MMP's contribute, such as osteoarthritis, rheumatoid arthritis, septic arthritis, periodontal disease, corneal ulceration, proteinuria, aneurysmal aortic disease, dystrophobic epidermolysis, bullosa, conditions leading to inflammatory responses,
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osteopenias mediated by MMP activity, tempero mandibular joint disease, demyelating diseases of the nervous system, tumor metastasis or degenerative cartilage loss following traumatic joint injury, and coronary thrombosis from athrosclerotic plaque rupture. The present invention also provides pharmaceutical compositions and methods for treating such conditions. Excerpt(s): This invention relates to enzyme inhibitors, and more particularly, to novel substituted biaryl oxobutyric acid compounds or derivatives thereof useful for inhibiting matrix metalloproteases. The matrix metalloproteases (a.k.a. matrix metalloendo-proteinases or MMPs) are a family of zinc endoproteinases which include, but are not limited to, interstitial collagenase (a.k.a. MMP-1), stromelysin (a.k.a. proteoglycanase, transin, or MMP-3), gelatinase A (a.k.a. 72 kDa-gelatinase or MMP-2) and gelatinase B (a.k.a. 95 kDa-gelatinase or MMP-9). These MMPs are secreted by a variety of cells including fibroblasts and chondrocytes, along with natural proteinaceous inhibitors known as TIMPs (Tissue Inhibitor of MetalloProteinase). All of these MMPs are capable of destroying a variety of connective tissue components of articular cartilage or basement membranes. Each MMP is secreted as an inactive proenzyme which must be cleaved in a subsequent step before it is able to exert its own proteolytic activity. In addition to the matrix destroying effect, certain of these MMPs such as MMP-3 have been implemented as the in vivo activator for other MMPs such as MMP-1 and MMP-9 (Ito, et al., Arch Biochem Biophys. 267, 211 (1988); Ogata, et al., J. Biol. Chem. 267, 3581 (1992)). Thus, a cascade of proteolytic activity can be initiated by an excess of MMP-3. It follows that specific MMP-3 inhibitors should limit the activity of other MMPs that are not directly inhibited by such inhibitors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Inhibitors of proteasomal activity for stimulating bone and hair growth Inventor(s): Garrett, Ross I.; (San Antonio, TX), Mundy, Gregory R.; (San Antonio, TX), Rossini, G.; (San Antonio, TX) Correspondence: Morrison & Foerster Llp; 3811 Valley Centre Drive; Suite 500; San Diego; CA; 92130-2332; US Patent Application Number: 20020107203 Date filed: January 15, 2002 Abstract: Compounds that inhibit the activity of NF-.kappa.B or inhibit the activity of the proteasome or both promote bone formation and hair growth and are thus useful in treating osteoporosis, bone fracture or deficiency, primary or secondary hyperparathyroidism, periodontal disease or defect, metastatic bone disease, osteolytic bone disease, post-plastic surgery, post-prosthetic joint surgery, and post-dental implantation; they also stimulate the production of hair follicles and are thus useful in stimulating hair growth, including hair density, in subject where this is desirable. Excerpt(s): This application is a continuation-in-part of U.S. Ser. No. 09/421,545, filed Oct. 20, 1999, now pending, which is a continuation-in-part of U.S. Ser. No. 09/361,775, filed Jul. 27, 1999, now pending, which is a continuation-in-part of U.S. Ser. No. 09/113,947, filed Jul. 10, 1998, now pending. The contents of these applications are incorporated herein by reference. The invention relates to compositions and methods for use in treating skeletal system disorders in a vertebrate at risk for bone loss, and in treating conditions that are characterized by the need for bone growth, in treating fractures, and in treating cartilage disorders. The invention also relates to enhancing hair
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density and growth. More specifically, the invention concerns the use of inhibitors of proteasomal activity, e.g., inhibitors of the chymotrypsin-like activity, and inhibitors of NF-.kappa.B activity for enhancing hair growth. Inhibitors of proteasomal activity, and to some extent inhibitors of NF-.kappa.B activity, have two important physiological effects. First, proteasome inhibitors are able to enhance bone formation and are thus useful for treating various bone disorders. Second, both of these inhibitors stimulate the production of hair follicles and are thus useful in stimulating hair growth, including hair density, in subject where this is desirable. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Isoprenoid pathway inhibitors for stimulating bone growth Inventor(s): Baindur, Nand; (Edmonds, WA), Gasper, Shirley R.; (Seattle, WA), Labroo, Virender M.; (Bangalore, IN), Martinez, Theresa; (Greenback, WA), McKernan, Patricia A.; (Woodinville, WA), Mundy, Gregory R.; (San Antonio, WA), Robbins, Kirk G.; (Renton, WA), West, Robert R.; (Seattle, WA) Correspondence: Kate H. Murashige; Morrison & Foerster Llp; Suite 500; 3811 Valley Centre Drive; San Diego; CA; 92130-2332; US Patent Application Number: 20010034364 Date filed: May 3, 2001 Abstract: Compounds of the formula 1wherein X in each of formulas (1) and (2) represents a substituted or unsubstituted alkylene, alkenylene, or alkynylene linker of 26C;Y is of the formula 2or a stereoisomer thereof,wherein R' is substituted or unsubstituted alkyl;each R.sup.2 is independently H, hydroxy, alkoxy (1-6C) or lower alkyl (1-4C);R.sup.3 is H, hydroxy, or alkoxy (1-6C); orY is of the formula 3wherein each n is 1,Z is N,K comprises a substituted or unsubstituted aromatic carbocyclic or heterocyclic ring system which may optionally be spaced from the linkage position shown in formula (7) by a linker of 1-2C, or in formula (7), Z may be spaced from the carbon bonded to X by.dbd.CR.sup.6-- wherein R.sup.6 is H or linear, branded or cyclic alkyl (1-6C),R.sup.5 is H or linear, branched or cyclic alkyl, andR' represents a cation, H or a substituted or unsubstituted alkyl group of 1-6C,promote bone formation and are thus useful in treating osteoporosis, bone fracture or deficiency, primary or secondary hyperparathyroidism, periodontal disease or defect, metastatic bone disease, osteolytic bone disease, post-plastic surgery, post-prosthetic joint surgery, and post-dental implantation.Also disclosed is a method to identify additional compounds which are inhibitors of enzymes in the isoprenoid scheme especially of HMG-CoA reductase which results in prenylation of proteins and in the synthesis of steroids or of inhibitors of their production which are useful in treating bone disorders. Excerpt(s): This application claims priority under 35 U.S.C.sctn.119 from provisional application Ser. No. 60/032,893 filed Dec. 13, 1996. It is also a continuation-in-part of U.S. Ser. No. 09/096,631 filed Jun. 12, 1998 which is a continuation-in-part of U.S. Ser. No. 08/989,862 filed Dec. 12, 1997 claiming benefit under 35 U.S.C.sctn.120. The entire contents of these documents are incorporated herein by reference. The invention relates to screening methods for compositions and to methods to use these compositions in treating bone disorders in vertebrates including fractures and cartilage disorders. More specifically, the invention concerns a method to identify agents that will be useful in treating bone disorders by assessing their ability to inhibit enzymes in the isoprenoid synthesis pathway and in particular, to inhibit HMG-CoA reductase, and to methods and compositions useful in treating bone disorders which contain the identified active
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ingredients as essential components. Bone is subject to constant breakdown and resynthesis in a complex process mediated by osteoblasts, which produce new bone, and osteoclasts, which destroy bone. The activities of these cells are regulated by a large number of cytokines and growth factors, many of which have now been identified and cloned. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Isoxazolone compounds useful in treating diseases associated with unwanted cytokine activity Inventor(s): Clark, Michael Philip; (Loveland, OH), De, Biswanath; (Cincinnati, OH), Djung, Jane Far-Jine; (Mason, OH), Laughlin, Steven Karl; (Taylor Mill, KY), Natchus, Michael George; (Alpharetta, GA), Tullis, Joshua Spector; (Broomfield, CO) Correspondence: The Procter & Gamble Company; Intellectual Property Division; Winton Hill Technical Center - Box 161; 6110 Center Hill Avenue; Cincinnati; OH; 45224; US Patent Application Number: 20030096814 Date filed: May 7, 2002 Abstract: Isoxazolone compounds having the generic structure: 1are used to treat disease associated with unwanted cytokine activity, including rheumatoid arthritis, osteoarthritis, diabetes, HIV/AIDS, inflammatory bowel disease, Crohn's disease, ulcerative colitis, congestive heart, hypertension, chronic obstructive pulmonary disease, septic shock syndrome, tuberculosis, adult respiratory distress, asthma, atherosclerosis, muscle degeneration, periodontal disease, cachexia, Reiter's syndrome, gout, acute synovitis, anorexia and bulimia nervosa fever, malaise, myalgia and headaches. Excerpt(s): This application claims priority under Title 35, United States Code 119(e) from Provisional Application Serial No. 60/293,889, filed May 24, 2001. The present invention is directed to certain isoxazolone compounds that inhibit the release of inflammatory cytokines such as interleukin-1 (1L-1) and tumor necrosis factor (TNF) from cells. The compounds of the invention, therefore, are useful in treating diseases involving unwanted cytokine activity. Many cytokine-mediated diseases and conditions are associated with excessive or unregulated production or activity of one or more cytokines such as interleukin 1 (IL-1), tumor necrosis factor (TNF), interleukin 6 (IL-6) and interleukin 8 (IL-8). IL-1 and TNF are important proinflammatory cytokines, which along with several other related molecules, mediate inflammatory cellular response in a wide variety of diseases and conditions. Proinflammatory cytokines such as IL-1 and TNF stimulate other inflammatory mediators such as nitric oxide, cyclooxygenase-2, matrix metalloproteinases. The inhibition of these cytokines is consequently both directly and indirectly beneficial in controlling, reducing and alleviating many of these disease states. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Liquid bisphosphonate formulations for bone disorders Inventor(s): Bergquist, Paul A.; (Collegeville, PA), Daifotis, Anastasia G.; (Westfield, NJ), Denker, Andrew E.; (Hoboken, NJ), Leung, Albert T.; (Ringoes, NJ) Correspondence: Merck And CO Inc; P O Box 2000; Rahway; NJ; 070650907 Patent Application Number: 20030139378 Date filed: November 26, 2002 Excerpt(s): The present invention relates to high dose oral liquid formulations of bisphosphonate and their methods of use to treat/prevent diseases related to bone remodeling or bone disorders, such as for example, Paget's disease, osteoporosis, metastatic bone disease, hypercalcemia of malignancy, periprosthetic osteolysis, periodontal disease, arthritic conditions, and the like, while minimizing the potential for esophageal irritation and other adverse gastrointestinal effects. These methods comprise orally administering to a mammal in need thereof a pharmaceutically effective amount of the liquid pharmaceutical composition of at least one bisphosphonate, or a pharmaceutically acceptable salt thereof, as a unit dosage according to a continuous schedule having a once-weekly, twice-weekly, biweekly, twice-monthly, or monthly dosing interval. The present invention also relates to liquid pharmaceutical compositions of the bisphosphonate for carrying out these methods. Paget's disease, osteoporosis, metastatic bone disease, hypercalcemia of malignancy, periprosthetic osteolysis, periodontal disease, and arthritic conditions constitute bone disorders in humans and other mammals that are characterized by abnormal bone remodeling. Because these bone disorders are chronic conditions, appropriate therapy generally requires long-term treatment. Paget's disease of bone is a chronic progressive skeletal bone disorder in which giant multinucleated cells called osteoclasts dramatically activate bone resorption which is followed by excessive bone formation. This accelerated bone resorption/bone formation cycle results in increased and disordered bone remodeling, bone hypertrophy, abnormal and weakened bone structure, and abnormal mechanical properties. Clinical consequences include severe bone pain, bone enlargement, bone deformity, and increased blood flow. Other complications can include bone pain due to deformity of bones adjacent to joints, entrapment of nerves, especially if the spine or the base of the skull is affected, and fractures [see W. D. Fraser et al., "Paget's disease of bone," Current Opinion in Rheumatology, 9: 347-354 (1997)]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Local delivery of agents for disruption and inhibition of bacterial biofilm for treatment of periodontal disease Inventor(s): Jernberg, Gary R.; (Mankato, MN) Correspondence: Merchant & Gould PC; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20030219387 Date filed: June 6, 2003 Abstract: The present invention relates to compositions and methods of treating periodontal disease and related disorders utilizing a sustained, controlled release targeted delivery method to effectively disrupt and inhibit bacterial biofilms at periodontal treatment sites.
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Excerpt(s): The present application is a continuation in part of U.S. patent application Ser. No. 09/715,514, filed Nov. 17, 2000, and issued Jun. 10, 2003 as U.S. Pat. No. 6,576,226, which application and patent are incorporated herein by reference. Periodontal diseases are a major affliction to mankind. Gingivitis, inflammation of gingival (gum) tissue, and periodontitis, inflammation and progressive loss of ligament and alveolar (socket) bone support to teeth, are caused by bacteria which colonize tooth surfaces and occupy the gingival crevice area. These are major periodontal disease afflictions worldwide. Bacterial plaque is the principal causative agent of these periodontal diseases. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Matrix metalloproteinase inhibitors Inventor(s): Quirk, Stephen; (Alpharetta, GA) Correspondence: John S. Pratt, Esq; Kilpatrick Stockton, Llp; 1100 Peachtree Street; Suite 2800; Atlanta; GA; 30309; US Patent Application Number: 20020086877 Date filed: December 29, 2000 Abstract: The present invention provides compounds that are effective in treating disorders caused by the enzymatic activity of matrix metalloproteinases. These disorders include, but are not limited to, rheumatoid arthritis, osteoarthritis, periodontal disease, aberrant angiogenesis, tumor invasion and metastasis, corneal ulceration, and in complications of diabetes. The present invention is also is useful for treating wounds. Excerpt(s): The present invention is directed to compounds and their pharmaceutically acceptable salts, which inhibit matrix metalloproteinases, and are therefore useful in the treatment of mammals having disease-states alleviated by the inhibition of such matrix metalloproteinases. Matrix metalloproteinases ("MMPs)" are a family of proteinases (enzymes) involved in the degradation and remodeling of connective tissues. Members of this family of endopeptidase enzymes are present in various cell types that reside in or are associated with connective tissue, such as fibroblasts, monocytes, macrophages, endothelial cells, and invasive or metastatic tumor cells. MMP expression is stimulated by growth factors and cytokines in the local tissue environment, where these enzymes act to specifically degrade protein components of the extracellular matrix, such as collagen, proteoglycans (protein core), fibronectin and laminin. These ubiquitous extracellular matrix components are present in the linings of joints, interstitial connective tissues, basement membranes, and cartilage. Excessive degradation of extracellular matrix by MMPs is implicated in the pathogenesis of many diseases, including rheumatoid arthritis, osteoarthritis, periodontal disease, aberrant angiogenesis, tumor invasion and metastasis, corneal ulceration, and in complications of diabetes. Another disorder wherein MMPs play a major role is in chronic wounds. Chronic wounds that are refractive to normal healing processes are characterized by an increase in the activity of matrix metalloproteinases. MMP inhibition is, therefore, recognized as a good target for therapeutic intervention. In normal tissues, cellular connective tissue synthesis is offset by extracellular matrix degradation, the two opposing effects existing in dynamic equilibrium. Degradation of the matrix is brought about by the action of MMPs released from resident connective tissue cells and invading inflammatory cells. Normally these catabolic enzymes are tightly regulated at the level of their synthesis and secretion and also at the level of their extracellular activity, the
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latter through the action of specific regulators, such as TIMPs (tissue inhibitors of metalloproteinases), which form inactive complexes with MMPs, and more general proteinase regulators which form complexes with MMPs. These complexes prevent MMP action. Cellular level control of MMP activity occurs primarily by regulating MMP gene expression and by down regulating the expression of the membrane bound MMPs (MT-MMP) that activate the excreted proenzyme form of the MMP. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for the treatment of periodontal disease Inventor(s): Crooks, Stephen L.; (St. Paul, MN), Merrill, Bryon A.; (St. Paul, MN) Correspondence: Ted K. Ringsred; Office OF Intellectual Property Counsel; 3M Innovative Properties Company; P.O. Box 33427; ST. Paul; MN; 55133-3427; US Patent Application Number: 20030130299 Date filed: June 15, 2001 Abstract: The disclosure provides methods for the treatment and prevention of periodontal disease. In preferred embodiments, the invention provides for local treatment of periodontal tissues with a pharmaceutical composition including an immune response modifier (IRM) selected from the group of immune response modifiers comprising imidazoquinoline amines, imidazopyridine amines, 6,7-fused cycloalkylimidazopyridine amines, imidazonaphthyridine amines, oxazoloquinoline amines, thiazoloquinoline amines and 1,2-bridged imidazoquinoline amines. Excerpt(s): The invention is directed to methods for the treatment or prevention of periodontal conditions. Specifically the invention includes the novel use of immune response modifier compounds to treat or prevent periodontal disease. Preferred immune response modifiers are selected from the group of immune response modifiers comprising imidazoquinoline amines, imidazopyridine amines, 6,7-fused cycloalkylimidazopyridine amines, imidazonaphthyridine amines, oxazoloquinoline amines, thiazoloquinoline amines and 1,2-bridged imidazoquinoline amines. Periodontal disease or periodontitis is an inflammatory disease that results in the destruction of both the hard and soft tissues supporting the teeth and has recently been hypothesized as a risk factor for cardiovascular disease. Beck et al. "Dental Infections and atherosclerosis, "American Heart Journal, 13:S528-533 (1999). It is estimated that over 10 million people in the United States are currently being treated for the more serious forms of this disease, with approximately 8 billion dollars spent for treatment each year. Clinically, periodontitis is an inflammation of the periodontium that results in inflammation of the gingiva and may result in resorption of alveolar bone and recession of the gingiva. Recession of the gingiva can lead to exposure of the periodontal ligament allowing microorganisms to invade and destroy the ligament. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of collecting data for estimation of susceptibility to periodontal disease Inventor(s): Abiko, Yoshihiro; (Sapporo-shi, JP), Arakawa, Toshiya; (Sapporo-shi, JP), Kaku, Tohru; (Sapporo-shi, JP), Kusano, Kaoru; (Sapporo-shi, JP), Nishimura, Michiko; (Ebetsu-shi, JP), Takuma, Taishin; (Sapporo-shi, JP) Correspondence: Sherman & Shalloway; 413 N. Washington Street; Alexandria; VA; 22314; US Patent Application Number: 20030175755 Date filed: November 21, 2002 Abstract: A method is provided, which comprises examining the regulating activity of a defensin gene promoter closely associated with the expression activity of defensin, an antibacterial peptide, on the basis of the detection of a gene mutation, and estimating future susceptibility to periodontal disease. The sequence homology between DNA derived from a defensin gene promoter existing in a sample obtained from the gingival tissues of a subject and a nucleotide sequence comprising a mutation site in the promoter region, and/or compatibility in PCR amplification, are determined. Thereby a gene mutation is detected and then the site of the gene mutation is determined, so that data for the estimation can be collected. Excerpt(s): The present invention relates to a method of collecting data for estimating susceptibility to periodontal disease and nucleotide sequences used in the data collection. Specifically, the present invention relates to nucleotide sequences comprising mutant sequence portions in a defensin gene promoter region that regulates the expression of defensin, an antibacterial peptide; and a method of collecting data for estimating susceptibility to periodontal disease wherein the variations of the promoter activity of regulating the expression activity of the defensin gene are examined using the above nucleotide sequences so as to obtain the above data. Periodontal disease is a chronic inflammatory disease of periodontal tissues caused by dental plaque bacteria. A number of periodontal disease-related bacteria have been specified, which are directly or indirectly associated with that disease. When periodontitis is developed, factors 2 associated with the innate immunity of gingival epithelial cells exerting a protective function such as cytokines, adhesive factors and antibacterial substances, intervene in the activity of the periodontal disease-related bacteria. Defensin is a microbicidal peptide known as such an antimicrobial substance. Defensins are peptides having an antimicrobial activity against Gram-positive bacteria, Gram-negative bacteria, fungi and envelope viruses, and these are classified into.alpha. type and.beta. type. Examples of.alpha. type defensins, which have been reported, include a total 6 types such as HNP1 to -4 localized in azurophilic granules of human neutrophil and human defensin-5 and -6 localized in Paneth cells in human small intestine. Examples of.beta. type include LAP (lingual antimicrobial peptide) and TAP (trancheal antimicrobial peptide), which are localized in bovine tongue and trachea, and these act as epithelium-derived protective factors against infection. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of treating periodontal disease Inventor(s): Basara, Michael; (Hugo, MN) Correspondence: Schwegman, Lundberg, Woessner & Kluth, P.A.; P.O. Box 2938; Minneapolis; MN; 55402; US Patent Application Number: 20030185768 Date filed: April 2, 2003 Abstract: The present invention includes a method for treating periodontal disease. The method comprises delivering to a pocket of a tooth with periodontal disease, a viscous, reddish-brown solution comprising sulfuric acid and sulphonated phenolic compounds. The method also comprises retaining the reddish-brown solution in the pocket for t time ranging from about 5 seconds to about 60 seconds. Excerpt(s): This application is a continuation application of Ser. No.: 09/575,297, filed May 19, 2000, entitled: METHOD OF TREATING PERIODONTAL DISEASE. The present invention relates to a method for treating periodontal disease. Periodontal disease is characterized by a loss of supporting tissues of the teeth. In particular, periodontitis includes a loss of the periodontal ligament and a disruption of the ligament attachments to cementum, as well as reabsorption of alveola and bone. Along with a loss of tissue attachments, periodontal disease produces a migration of the epithelial attachments along the root surface and reabsorption of bone. It is widely accepted that an initiation and progression of periodontal disease is dependent upon the presence of micro-organisms which are capable of causing the disease. At least three characteristics of periodontal micro-organisms have been identified which contribute to the ability of microbes to act as pathogens. A first characteristic is a capacity of the microbes to colonize. A second characteristic is an ability of the microbes to evade antibacterial host defense mechanisms. A third characteristic is an ability of the microbes to produce substances which directly initiate tissue destruction. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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METHODS FOR TREATING PERIODONTAL DISEASE Inventor(s): Andersen, Scot N.; (Draper, UT), Wilson, Jimmy B.; (Draper, UT) Correspondence: Rick D. Nydegger; Workman, Nydegger & Seeley; 1000 Eagle Gate Tower; 60 East South Temple; Salt Lake City; UT; 84111; US Patent Application Number: 20030059379 Date filed: September 19, 2001 Abstract: Methods for treating periodontal disease and other diseased tissues that utilize a dye composition and laser energy. The laser energy (typically about 450 nm to about 600 nm) heats and destroys the diseased tissue and bacteria, while the dye composition causes the laser energy to be selectively absorbed by the targeted tissue. An argon gas laser that emits blue-green light may be used in conjunction with a red-orange dye that strongly absorbs light energy emitted by the argon gas laser. An 810 diode laser may be used in conjunction with the argon laser in order to provide additional heating properties. Excerpt(s): The present invention relates generally to methods for treating periodontal disease, particularly to methods that utilize laser energy to destroy necrotic tissue and bacteria that have been stained with an appropriate dye. It is well known that
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periodontal disease is caused by bacteria that grows and festers within the periodontal pocket. Porphyromonas gingivalis and other bacteria host not only in the soft tissue around the periodontal pocket, but also in plaque that is formed on the surface of the tooth. If left untreated, such bacteria can cause swelling of the gingiva, pain and possible loss of the tooth. Surrounding gums and teeth can also become infected. In the conventional treatment of periodontal disease, instruments are inserted into the periodontal pocket to mechanically debride the plaque from the tooth and also to remove the necrotic soft tissue by curettage. Antibiotics may also be conventionally placed in the periodontal pocket following such conventional treatment to ensure complete eradication of the infection and to combat reinfection. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods of treating periodontal disease Inventor(s): Daluge, Susan Mary; (Chapel Hill, NC), Jurgensen, Cynthia Holder; (Raleigh, NC), Martin, Michael Tolar; (Durham, NC), Osterhout, Martin Howard; (Raleigh, NC) Correspondence: David J Levy, Corporate Intellectual Property; Glaxosmithkline; Five Moore DR.; PO Box 13398; Durham; NC; 27709-3398; US Patent Application Number: 20030032804 Date filed: March 26, 2002 Abstract: The present invention relates to novel compounds of formula (I): processes for their preparation, pharmaceutical formulations containing them, and their use in medicine, particularly in the prophylaxis and treatment of inflammatory conditions, immune disorders, septic shock circulatory disorders, and gastrointestinal inflammation and disorders. Excerpt(s): The present invention relates to glycol derivatives of xanthines, processes for their preparation, pharmaceutical formulations comprising them, and their use in medicine, particularly in the treatment and prophylaxis of inflammatory conditions, immune disorders, septic shock, circulatory disorders and gastrointestinal inflammation, infection or damage. Leukocyte adhesion to vascular endothelium plays a critical role in the pathogenesis of various diseases. This adhesion is an early and requisite step in the migration of leukocytes into surrounding tissues, and is essential for the initiation and perpetuation of inflammatory and immune disorders. The adhesion process is dependent on the induction or upregulation of adhesion molecules on the endothelium, thereby representing an important target for diseases in which leukocytes contribute significantly to vascular and tissue damage. The discovery and development of small molecules which specifically block or inhibit the adhesive interactions of leukocytes and the endothelium is an attractive area of therapeutic intervention, particularly for inflammatory diseases. Current antiiflammatory-treatment- s have limited efficacy, often accompanied by severe side-effects. We here describe the discovery of a series of complex esters and amides of selected phenyl xanthine derivatives which, at low concentrations, inhibits the expression of adhesion molecules on cultured human umbilical vein endothelial cells. These compounds are therefore indicated for the treatment of inflammatory conditions, immune disorders, infectious diseases, circulatory disorders, and a number of other conditions in which the adhesion between leukocytes and endothelium plays a major role. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 189
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N-hydroxy-2-(alkyl, aryl, or heteroaryl sulfanyl, sulfinyl or sulfonyl)-3-substituted alkyl, aryl or heteroarylamides as matrix metalloproteinase inhibitors Inventor(s): Baker, Jannie Lea; (White Plains, NY), Davis, Jamie Marie; (Nyack, NY), Grosu, George Theodore; (Pearl River, NY), Levin, Jeremy Ian; (New City, NY), Venkatesan, Aranapakam Mudumbai; (Rego Park, NY) Correspondence: American Home Products Corporation; Patent Section; Five Giralda Farms; Madison; NJ; 07940-0874; US Patent Application Number: 20020006922 Date filed: July 5, 2001 Excerpt(s): This application is a continuation in part of U.S. patent application Ser. No. 09/026,372, filed on Feb. 19, 1998 which claims the benefit of priority of U.S. Provisional Application No. 60/038,899 filed on Feb. 27, 1997. Matrix metalloproteinases (MMPs) are a group of enzymes that have been implicated in the pathological destruction of connective tissue and basement membranes. These zinc containing endopeptidases consist of several subsets of enzymes including collagenases, stromelysins and gelatinases. Of these classes, the gelatinases have been shown to be the MMPs most intimately involved with the growth and spread of tumors. It is known that the level of expression of gelatinase is elevated in malignancies, and that gelatinase can degrade the basement membrane which leads to tumor metastasis. Angiogenesis, required for the growth of solid tumors, has also recently been shown to have a gelatinase component to its pathology. Furthermore, there is evidence to suggest that gelatinase is involved in plaque rupture associated with atherosclerosis. Other conditions mediated by MMPs are restenosis, MMP-mediated osteopenias, inflammatory diseases of the central nervous system, skin aging, tumor growth, osteoarthritis, rheumatoid arthritis, septic arthritis, corneal ulceration, abnormal wound healing, bone disease, proteinuria, aneurysmal aortic disease, degenerative cartilage loss following traumatic joint injury, demyelinating diseases of the nervous system, scirrhosis of the liver, glomerular disease of the kidney, premature rupture of fetal membranes, inflammatory bowel disease, periodontal disease, age related macular degeneration, diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, ocular inflammation, keratoconus, Sjogren's syndrome, myopia, ocular tumors, ocular angiogenesis/neovascularization and corneal graft rejection. For recent reviews, see: (1g) Recent Advances in Matrix Metalloproteinase Inhibitor Research, R. P. Beckett, A. H. Davidson, A. H. Drummond, P. Huxley and M. Whittaker, Research Focus, Vol. 1, 1626, (1996), (2) Curr. Opin. Ther. Patents (1994) 4(1): 7-16, (3) Curr. Medicinal Chem. (1995) 2: 743-762, (4) Exp. Opin. Ther. Patents (1995) 5(2): 1087-110, (5) Exp. Opin. Ther. Patents (1995) 5(12): 1287-1196. TNF-.alpha. converting enzyme (TACE) catalyzes the formation of TNF-.alpha. from membrane bound TNF-.alpha. precursor protein. TNF.alpha. is a pro-inflammatory cytokine that is now thought to have a role in rheumatoid artritis, septic shock, graft rejection, cachexia, anorexia, inflammation, congestive heart failure, inflammatory disease of the central nervous system, inflammatory bowel disease, insulin resistance and HIV infection in addition to its well documented antitumor properties. For example, research with anti- TNF antibodies and tralsgenic animals has demonstrated that blocking the formation of TNFc inhibits the progression of arthritis. This observation has recently been extended to humans as well. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Novel bisphosphonates and uses thereof Inventor(s): Blackburn, George M.; (Sheffield, GB), Holick, Michael F.; (Sudbury, MA), Ramanathan, Halasya; (Worcester, MA) Correspondence: Sterne, Kessler, Goldstein & Fox Pllc; 1100 New York Avenue, N.W., Suite 600; Washington; DC; 20005-3934; US Patent Application Number: 20020002140 Date filed: January 16, 2001 Abstract: Glycosides and orthoester glyco side derivatives of bisphosphonate compounds useful for treating and/or preventing hypercalcaemia of malignancy, Paget's disease, osteoporosis, metastatic cancer in bone and soft tissue and periodontal disease have markedly enhanced intestinal absorption and enhanced bioavailability. Excerpt(s): This claims priority to U.S. Provisional Application Nos. 60/176,006, filed Jan. 14, 2000, and 60/210,021, filed Jun. 8, 2000, the contents of each of which are fully incorporated by reference herein. The present invention relates to novel derivatives of bisphosphonate compounds, and to their use in the treatment and/or prevention of such conditions as hypercalcaemia of malignancy, Paget's disease, osteoporosis, metastatic cancer in bone and soft tissue, and periodontal disease. Bisphosphonates are synthetic compounds, structurally related to pyrophosphate, in that two phosphonates are attached to a common atom. More specifically, bisphosphonates of particular interest contain a P--C--P bond, whereas pyrophosphate has a P--O--P bond. The difference in the two chemical bonding schemes means that bisphosphonates are resistant to enzymatic hydrolysis in osseous tissue, for example. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Oral care compositions comprising chlorite and methods Inventor(s): Wimalasena, Rohan Lalith; (Liberty Township, OH), Witt, Jonathan James; (Cincinnati, OH), Wong, Andrew Lee; (West Chester, OH) Correspondence: Emelyn L. Hiland; The Procter & Gamble Company; Health Care Research Center (box 1050); P.O. Box 8006; Mason; OH; 45040-8006; US Patent Application Number: 20010006624 Date filed: January 30, 2001 Abstract: The present invention relates to oral care compositions, including therapeutic rinses, especially mouth rinses, as well as toothpastes, gels, tooth powders, chewing gums, mouth sprays, and lozenges (including breath mints), comprising at least a minimally effective amount of chlorite ion, wherein preferably the pH of the final composition is greater than 7 and level of chlorine dioxide or chlorous acid is less than about 50 ppm, preferably is essentially free of chlorine dioxide or chlorous acid. This invention fuirther relates to a method for treating or preventing gingivitis, plaque, periodontal disease, and/or breath malodor, and/or for the whitening of teeth, in humans or other animals, by applying a safe and effective amount of the chlorite ion composition to the oral cavity. Excerpt(s): The present invention relates to oral care compositions, including therapeutic rinses, especially mouth rinses, as well as toothpastes, tooth gels, tooth powders, chewing gums, mouth sprays, and lozenges (including breath mints), comprising an effective amount of chlorite ion. This invention further relates to a method for treating
Patents 191
or preventing conditions of the oral cavity, such as gingivitis, plaque, periodontal disease, and/or breath malodor, as well as to a method for whitening teeth, in humans or other animals. Oral malodor, plaque, gingivitis, periodontal disease, and discoloration of the teeth, are all undesirable conditions that affect many people. First malodor of the oral cavity is also known as halitosis or bad breath. It is broadly estimated in the US. that 20-90 million individuals have oral malodor. It is generally believed that the cause of this condition is due to the presence of anaerobic bacteria, especially gram-negative anaerobic bacteria, in the mouth. These bacteria will generate volatile sulfur compounds (VSC) which are known to cause breath malodor. It is recognized in the art that some breath malodor is caused by three chemical compounds. Specifically, these compounds are hydrogen sulfide (H--S--H), methyl mercaptan (CH.sub.3--S--H) and dimethyl sulfide (CH.sub.2--S--CH.sub.3). These compounds result from the degradation of epithelial cells and bacteria in the oral cavity. Specifically, the polypeptide chains of the epithelial cell walls, are composed of a series of amino acids including cysteine and methionine which contain sulfur side chains. The death of microorganisms or epithelial cells results in degradation of the polypeptide chains into their amino acid components, especially cysteine and methionine. Cysteine and methionine are precursors to the formation of VSC. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Oral therapeutic delivery appliance Inventor(s): Zegarelli, Peter J.; (Sleepy Hollow, NY) Correspondence: Fish & Neave; 1251 Avenue OF The Americas; 50th Floor; New York; NY; 10020-1105; US Patent Application Number: 20020110780 Date filed: April 15, 2002 Abstract: This invention relates to an oral therapeutic delivery appliance. Using this oral therapeutic delivery appliance medicaments may be delivered to oral soft tissues, where medicaments are easily absorbed. To aide the delivery of medicaments to oral soft tissues the oral therapeutic delivery appliance contains a therapeutic pooling reservoir where the medicaments may be placed. The oral therapeutic delivery appliance may be used to treat or aide in the treatment of various oral maladies such as periodontal disease (i.e., gum disease) as well as treating or aiding the treatment of other physical ailments and systemic diseases (e.g., diabetes and other chronic diseases which require either single, intermittent or constant dosing of medicament). Excerpt(s): This invention relates to a dental medical oral appliance, and more specifically a drug delivery device for the administration of medicaments orally by means of this appliance. This invention also relates to the methods for treating various oral maladies such as periodontal disease (i.e., gum disease) as well as treating other physical ailments and systemic diseases (e.g., diabetes and other chronic diseases which require either single, intermittent or constant dosing of medicament). Dental appliances or dental trays have been used in various dental procedures for many years. For example, dental appliances have been used to whiten teeth (See U.S. Pat. No. Re. 34,196 to Munro). Or, dental appliances (referred to as night guards)have been used to prevent patients from grinding their teeth while asleep. They have also been used in conjunction with fluoride as a caries (cavity) preventative. And, dental appliances in conjunction with medication have been used to treat oral pain. (See M. Padilla, C. T. Glenn and M. L. Robert, Topical medications for orofacial neuropathic pain: a review, 131 Journal of the
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American Dental Association 185 (February 2000). A general process for preparing these dental appliances is by forming an alginate impression which registers all teeth surfaces in a jaw. Next, a stone cast model is made using the alginate impression of the mouth. In the case of tooth whitening agents, the reservoirs for holding whitening agents are formed by building a layer of rigid material on the teeth surface(s) to be treated of the stone cast (See U.S. Pat. No. 5,985,249). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
PAI-2 AND T-PA AS DIAGNOSTIC MARKERS OF PERIODONTAL DISEASE Inventor(s): BARTOLD, PETER M.; (ROSEVILLE, AU), BUNN, CLIVE L.; (ROSEVILLE, AU), XIAO, YIN; (ROSEVILLE, AU) Correspondence: Foley & Lardner; 3000 K Street NW; Suite 500 P O Box 25696; Washington; DC; 200078696 Patent Application Number: 20020012944 Date filed: January 26, 1999 Abstract: The existence and the extent of periodontal disease can be diagnosed by measuring plasminogen activator inhibitor 2 (PAI-2) and/or tissue plasminogen activator (t-PA) levels in gingival crevicular fluid (GCF). Levels of PAI-2 and t-PA in GCF rise sharply in the context of periodontal disease, and they also correlate with the severity of disease at different sites in the same patient. Excerpt(s): Periodontal disease is possibly the most common disease known to man, and is said to affect three-quarters of the adult population. Loss of periodontal tissue due to periodontal disease is the principal cause of tooth loss in adulthood. Periodontal tissue loss may result from infectious disease (e.g., bacterially-induced gingivitis), nutritional disease, (e.g., scurvy), or neoplastic conditions. Typically, tissue loss is accompanied by inflammation, bleeding and ulceration. Without treatment, periodontal tissue loss loosens the tooth and ultimately may cause loss of the tooth and the alveolar bone tissue (periodontitis). Gingivitis and periodontal disease cause enlargement of the periodontal pocket (gingival sulcus) of the affected tooth. The pocket observed in diseased gingiva is much deeper than the normal sulcus. This enlarged pocket is difficult to clean with either a tooth brush or floss and, consequently, bacteria and plaque accumulate within the pocket, causing further enlargement of the pocket. Eventually, the periodontal ligament and supporting alveolar bone are destroyed, leading to loss of the tooth. To permit effective treatment of periodontitis, it is essential to identify the presence and severity of active periodontal disease within a periodontal pocket. Even deep periodontal pockets do not necessarily correlate with the presence of active periodontal disease and, accordingly, traditional methods of measuring pocket depth may not provide an accurate indicator of the progression of the disease. Clearly, a more accurate means of determining the presence and extent of active periodontal disease is greatly to be desired. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Peptoid and nonpeptoid containing alpha-keto oxadiazoles as serine protease inhibitors Inventor(s): Gyorkos, Albert; (Westminster, CO), Kawabata, Kazuhito; (Osaka, JP), Ohmoto, Kazuyuki; (Osaka, JP), Spruce, Lyle; (Chula Vista, CA) Correspondence: Dechert; P.O. Box 5218; Princeton; NJ; 08543; US Patent Application Number: 20020010315 Date filed: April 26, 2001 Abstract: The present invention relates to certain substituted oxadiazole peptoids and nonpeptoids useful as inhibitors of serine proteases, especially human neutophil elastase (HNE). Compounds of the present invention are useful for the treatment or amelioration of symptoms of adult respiratory distress syndrome, septic shock, and multiple organ failure. Processes mediated by HNE are also implicated in conditions such as arthritis, periodontal disease, glomerulonephritis, and cystic fibrosis. Excerpt(s): This application is a continuation in part of U.S. Ser. No. 09/090,046, filed Jun. 3, 1998, an U.S. Ser. No. 09/090,274, filed Jun. 3, 1998; both of which are incorporated herein by reference. The serine proteases are a class of enzymes, which includes elastase, chymotrypsin, cathepsin G, trypsin and thrombin. These proteases have in common a catalytic triad consisting of Serine-195, Histidine-57 and Aspartic acid-102(chymotrypsin numbering system). Human neutrophil elastase (HNE) is a proteolytic enzyme secreted by polymorphonuclear leukocytes (PMNs) in response to a variety of inflammatory stimuli. This release of HNE and its extracellular proteolytic activity are highly regulated and are normal, beneficial functions of PMNs. The degradative capacity of HNE, under normal circumstances, is modulated by relatively high plasma concentrations of.alpha.sub.1-proteinase inhibitor (.alpha.-PI). However, stimulated PMNs produce a burst of active oxygen metabolites, some of which (hypochlorous acid for example) are capable of oxidizing a critical methionine residue in.alpha.-PI. Oxidized.alpha.-PI has been shown to have limited potency as an HNE inhibitor and it has been proposed that alteration of this protease/antiprotease balance permits HNE to perform its degradative functions in localized and controlled environments. Despite this balance of protease/antiprotease activity, there are several human disease states in which a breakdown of this control mechanism is implicated in the pathogenesis of the condition. Improper modulation of HNE activity has been suggested as a contributing factor in adult respiratory distress syndrome, septic shock and multiple organ failure. A series of studies also have indicated the involvement of PMNs and neutrophil elastase in myocardial ischemia-reperfusion injury. Humans with below-normal levels of.alpha.sub.1-PI have an increased probability of developing emphysema. HNE-mediated processes are implicated in other conditions such as arthritis, periodontal disease, glomerulonephritis, dermatitis, psoriasis, cystic fibrosis, chronic bronchitis, atherosclerosis, Alzheimer's disease, organ transplantation, corneal ulcers, and invasion behavior of malignant tumors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Periodontal regeneration composition and method of using same Inventor(s): Szymaitis, Dennis W.; (Pittsburgh, PA) Correspondence: Buchanan Ingersoll, P.C.; One Oxford Centre, 301 Grant Street; 20th Floor; Pittsburgh; PA; 15219; US Patent Application Number: 20030026770 Date filed: July 25, 2001 Abstract: A periodontal structure regeneration composition for treatment of periodontal disease is a mixture of particles of a bone growth material and collagen. All particles are sized to be less than 1 mm in diameter. The periodontal regeneration composition is injected into the periodontal pocket through an 18 gauge needle. The composition is available in pre-filled syringes offered in a kit that may also contain strips of surgical sponge or gauze that are sized to fit within a periodontal pocket, a tube of adhesive, a dental bur, a probe, a gauze placement tool, gauze counter and a brush for cleaning the dental bur. Excerpt(s): The invention relates to a bone growth and periodontal structure regeneration material, and method for treating periodontal disease. Periodontal disease occurs when bacteria colonize the sulcus space between the teeth and gingiva. The bacteria cause inflammation. The inflammation destroys the gingival epithelial lining and epithelial attachment to the tooth. The inflammation then progresses down the tooth root toward the apex of the root and destroys periodontal structure and bone. As periodontal disease progresses open pockets develop between the tooth and the gingiva. A dentist can determine the presence and extent of periodontal disease using a probe to measure the depth of pockets between each tooth and gingiva. X rays can reveal the extent of any bone loss. Consequently, there is also a need for a procedure for reversing bone loss and periodontal structure damage caused by periodontal disease. There is also a need for a regeneration material that could be used without incisions to regenerate bone and periodontal structure lost to periodontal disease. Periodontal therapy without incisions, eliminates discomfort, pain, swelling, gingival recession, sensitive teeth, greatly shortens healing time, and greatly decreases potential for infections. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Preparation and use of ortho-sulfonamido heteroaryl hydroxamic acids as matrix metalloproteinase and TACE inhibitors Inventor(s): Levin, Jeremy Ian; (Nanuet, NY), Nelson, Frances Christy; (Wyckoff, NJ) Correspondence: American Home Products Corporation; Patent Section; Five Giralda Farms; Madison; NJ; 07940-0874; US Patent Application Number: 20010051614 Date filed: November 29, 2000 Abstract: The present invention relates to the discovery of novel, low molecular weight, non-peptide inhibitors of matrix metalloproteinases (e.g. gelatinases, stromelysins and collagenases) and TNF-.alpha. converting enzyme (TACE, tumor necrosis factor-.alpha. converting enzyme) which are useful for the treatment of diseases in which these enzymes are implicated such as arthritis, tumor growth and metastasis, angiogenesis, tissue ulceration, abnormal wound healing, periodontal disease, bone disease,
Patents 195
proteinuria, aneurysmal aortic disease, degenerative cartilage loss following traumatic joint injury, demyelinating diseases of the nervous system, graft rejection, cachexia, anorexia, inflammation, fever, insulin resistance, septic shock, congestive heart failure, inflammatory disease of the central nervous system, inflammatory bowel disease, HIV infection, age related macular degeneration, diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, ocular inflammation, keratoconus, Sjogren's syndrome, myopia, ocular tumors, ocular angiogenesis/neovascularization.The TACE and MMP inhibiting ortho-sulfonamido aryl hydroxamic acids of the present invention are represented by the formula 1where the hydroxamic acid moiety and the sulfonamido moiety are bonded to adjacent carbons on group A where A is defined as:a 5-6 membered heteroaryl having from 1 to 3 heteroatoms independently selected from N, O, and S and optionally substituted by R.sup.1, R.sup.2 and R.sup.3;and Z, R.sup.1, R.sup.2, R.sup.3, R.sup.4, R.sup.5, R.sup.6, R.sup.7, R.sup.8 and R.sup.9 are described in the specification,and the pharmaceutically acceptable salts thereof and the optical isomers and diastereomers thereof. Excerpt(s): Matrix metalloproteinases (MMPs) are a group of enzymes that have been implicated in the pathological destruction of connective tissue and basement membranes [Woessner, J. F., Jr. FASEB J. 1991, 5, 2145; Birkedal-Hansen, H.; Moore, W. G. I.; Bodden, M. K.; Windsor, L. J.; Birkedal-Hansen, B.; DeCarlo, A.; Engler, J. A. Crit. Rev. Oral Biol. Med. 1993, 4, 197; Cawston, T. E. Pharmacol. Ther. 1996, 70, 163; Powell, W. C.; Matrisian, L. M. Cur. Top. Microbiol. and Immunol. 1996, 213, 1]. These zinc containing endopeptidases consist of several subsets of enzymes including collagenases, stromelysins and gelatinases. Of these classes, the gelatinases have been shown to be the MMPs most intimately involved with the growth and spread of tumors, while the collagenases have been associated with the pathogenesis of osteoarthritis [Howell, D. S.; Pelletier, J.-P. In Arthritis and Allied Conditions; McCarthy, D. J.; Koopman, W. J., Eds.; Lea and Febiger: Philadelphia, 1993; 12th Edition Vol. 2, pp. 1723; Dean, D. D. Sem. Arthritis Rheun. 1991, 20, 2; Crawford, H. C; Matrisian, L. M. Invasion Metast. 1994-95, 14, 234; Ray, J. M.; Stetler-Stevenson, W. G. Exp. Opin. Invest. Drugs, 1996, 5, 323]. It is known that the level of expression of gelatinase is elevated in malignancies, and that gelatinase can degrade the basement membrane which may lead to tumor metastasis [Powell, W. C.; Matrisian, L. M. Cur. Top. Microbiol. and Immunol. 1996, 213, 1; Crawford, H. C; Matrisian, L. M. Invasion Metast. 1994-95, 14, 234; Ray, J. M.; StetlerStevenson, W. G. Exp. Opin. Invest. Drugs, 1996, 5, 323; Himelstein, B. P.; Canete-Soler, R.; Bernhard, E. J.; Dilks, D. W.; Muschel, R. J. Invasion Metast. 1994-95, 14, 246; Nuovo, G. J.; MacConnell, P. B.; Simsir, A.; Valea, F.; French, D. L. Cancer Res. 1995,55, 267-275; Walther, M. M.; Levy, A.; Hurley, K.; Venzon, D.; Linehen, W. M.; Stetler-Stevenson, W. J. Urol. 1995, 153 (Suppl. 4), 403A; Tokuraku, M; Sato, H.; Murakami, S.; Okada, Y.; Watanabe, Y.; Seiki, M. Int. J. Cancer, 1995, 64, 355; Himelstein, B.; Hua, J.; Bernhard, E.; Muschel, R. J. Proc. Am. Assoc. Cancer Res. Ann. Meet. 1996, 37, 632; Ueda, Y.; Imai, K.; Tsuchiya, H.; Fujimoto, N.; Nakanishi, I.; Katsuda, S.; Seiki, M.; Okada, Y. Am. J. Pathol. 1996, 148, 611; Gress, T. M.; Mueller-Pillasch, F.; Lerch, M. M.; Friess, H.; Buechler, M.; Adler, G. Int. J. Cancer, 1995, 62, 407; Kawashima, A.; Nakanishi, I.; Tsuchiya, H.; Roessner, A.; Obata, K.; Okada, Y. Virchows Arch., 1994, 424, 547-552.]. Angiogenesis, required for the growth of solid tumors, has also recently been shown to have a gelatinase component to its pathology [Crawford, H. C; Matrisian, L. M. Invasion Metast. 1994-95,14, 234; Ray, J. M.; Steder-Stevenson, W. G. Exp. Opin. Invest. Drugs, 1996, 5, 323.]. Furthermore, there is evidence to suggest that gelatinase is involved in plaque rupture associated with atherosclerosis [Dollery, C. M.; McEwan, J. R.; Henney, A. M. Circ. Res. 1995, 77, 863; Zempo, N.; Koyama, N.; Kenagy, R. D.; Lea, H. J.; Clowes, A. W. Arterioscler. Thromb. Vasc. Biol. 1996, 16, 28; Lee, R. T.; Schoen, F. J.; Loree, H. M.;
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Lark, M. W., Libby, P. Arterioscler. Thromb. Vasc. Biol. 1996, 16, 1070.]. Other conditions mediated by MMPs are restenosis, MMP-mediated osteopenias, inflammatory diseases of the central nervous system, skin aging, tumor growth, osteoarthnitis, rheumatoid arthritis, septic arthritis, corneal ulceration, abnormal wound healing, bone disease, proteinuria, aneurysmal aortic disease, degenerative cartilage loss following traumatic joint injury, demyelinating diseases of the nervous system, cirrhosis of the liver, glomerular disease of the kidney, premature rupture of fetal membranes, inflammatory bowel disease, periodontal disease, age related aacular degeneration, diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, ocular inflammation, keratoconus, Sjogren's syndrome, myopia, ocular tumors, ocular angiogenesis/neovascularization and corneal graft rejection. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Trace level detection of analytes using artificial olfactometry Inventor(s): Kelso, David; (Wilmette, IL), Lewis, Nathan; (La Canada, CA), Munoz, Beth; (Pasadena, CA), Severin, Erik; (Hayward, CA), Wong, Bernard; (Los Angeles, CA) Correspondence: Townsend And Townsend And Crew; Two Embarcadero Center; Eighth Floor; San Francisco; CA; 94111-3834; US Patent Application Number: 20010041366 Date filed: May 14, 2001 Abstract: The present invention provides methods for detecting the presence of an analyte indicative of various medical conditions, including halitosis, periodontal disease and other diseases are also disclosed. Excerpt(s): This application claims priority to U.S. Provisional Applications Ser. No. 60/090,012, filed Jun. 19, 1998, and Ser. No. 60/091,179, filed Jun. 30, 1998, the disclosures of which are incorporated herein by reference in their entirety. An artificial olfactory system is a device that is capable of detecting a wide variety of analytes in fluids such as vapors, gases and liquids. The device comprises an array of sensors that in the presence of an analyte produces a response. The device produces a unique signature output for a particular analyte. Using pattern recognition algorithms, the output signature, such as an electrical response, can be correlated and compared to a particular analyte or mixture of substances that are known. By comparing the unknown signature with the stored or known signatures, the analyte can be detected, identified and quantified. There are many instances where it is desirable to measure trace amounts of analytes. However, in certain instances, the analytes are found at levels that are too low to register a robust signal by direct exposure to currently available sensors. In headspace analysis of applications in agricultural, wine, tobacco, perfume, plastics, and the food industries, the detection and classification of trace levels of gases are present in the sub part per million (ppm) range, making detection difficult. Moreover, in residue analysis of pesticides on crops, the trace levels of certain herbicides must meet federal guidelines. For certain crops, these residues are present on the crops in the part per billion levels (ppb). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 197
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Tricyclic sulfonamides metalloproteinases
and
their
derivatives
as
inhibitors
of
matrix
Inventor(s): O'Brien, Patrick Michael; (Stockbridge, MI), Picard, Joseph Armand; (canton, MI), Sliskovic, Drago Robert; (Saline, MI) Correspondence: Attention OF Ronald A. Daignault; Merchant & Gould P.C.; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20020169164 Date filed: March 27, 2002 Abstract: Tricyclic sulfonamide compounds and derivatives are described as well as methods for the preparation and pharmaceutical compositions of same, which are useful as inhibitors of matrix metalloproteinases, particularly gelatinase A, collagenase-3, and stromelysin-1 and for the treatment of multiple sclerosis, atherosclerotic plaque rupture, aortic aneurysm, heart failure, left ventricular dilation, restenosis, periodontal disease, or other autoimmune or inflammatory disorders dependent upon tissue invasion by leukocytes or other activated migrating cells, acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. Excerpt(s): The present invention relates to novel tricyclic sulfonamide compounds and their derivatives useful as pharmaceutical agents, to methods for their production, to pharmaceutical compositions which include these compounds and a pharmaceutically acceptable carrier, and to pharmaceutical methods of treatment. The novel compounds of the present invention are inhibitors of matrix metalloproteinases, e.g., gelatinase A (MMP-2), collagenase-3 (MMP-13), and stromelysin-1 (MMP-3): More particularly, the novel compounds of the present invention are useful in the treatment of atherosclerotic plaque rupture, aortic aneurism, heart failure, left ventricular dilation, restenosis, periodontal disease, corneal ulceration, treatment of burns, decubital ulcers, wound repair, cancer, inflammation, pain, arthritis, osteoporosis, multiple sclerosis, renal disease, and other autoimmune or inflammatory disorders dependent on the tissue invasion of leukocytes or other activated migrating cells. Additionally, the compounds of the present invention are useful in the treatment of acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. Gelatinase A and stromelysin-1 are members of the matrix metalloproteinase (MMP) family (Woessner J. F., FASEB J., 1991;5:2145-2154). Other members include fibroblast collagenase, neutrophil collagenase, gelatinase B (92 kDa gelatinase), stromelysin-2, stromelysin-3, matrilysin, collagenase 3 (Freije J. M., Diez-Itza I., Balbin M., Sanchez L. M., Blasco R., Tolivia J., and Lopez-Otin C., J. Biol. Chem., 1994;269:16766-16773), and the newly discovered membrane-associated matrix metalloproteinases (Sato H., Takino T., Okada Y., Cao J., Shinagawa A., Yamamoto E., and Seiki M., Nature, 1994;370:61-65). The catalytic zinc in matrix metalloproteinases is a focal point for inhibitor design. The modification of substrates by introducing chelating groups has generated potent inhibitors such as peptide hydroxymates and thiolcontaining peptides. Peptide hydroxamates and the natural endogenous inhibitors of MMPs (TIMPs) have been used successfully to treat animal models of cancer and inflammation.
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Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with periodontal disease, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “periodontal disease” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on periodontal disease. You can also use this procedure to view pending patent applications concerning periodontal disease. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON PERIODONTAL DISEASE Overview This chapter provides bibliographic book references relating to periodontal disease. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on periodontal disease include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “periodontal disease” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on periodontal disease: •
Periodontal Diseases Source: Torrance, CA: Homestead Schools, Inc. 2001. 68 p. Contact: Available from Homestead Schools, Inc. 23844 Hawthorne Boulevard, Suite 200, Torrance, CA 90505. (310) 791-9975. Fax (310) 791-0135. E-mail:
[email protected]. Website: www.homesteadschools.com. PRICE: $48.00 plus shipping and handling. Course No. 6600. Summary: Periodontal disease is characterized by infection and inflammation of the gums and surrounding tissue resulting in the formation of periodontal pockets (spaces between the gum and tooth) and loss of supporting bone structure. Periodontal disease is recurring, progressive and episodic and, if not controlled, may lead to loss of teeth. This continuing education program for dentists focuses on periodontal diseases. Topics include the importance of identifying the specific genetic marker responsible for
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producing excess amount of the chemical that regulates the body's inflammatory response to bacteria; the two most common forms of periodontal diseases, gingivitis and periodontitis; the pathophysiology of periodontal disease; the symptoms of periodontal disease; the progression of periodontal disease; risk factors for periodontitis; prevention strategies; the link between periodontitis and other serious systemic disorders, such as heart disease, chronic pulmonary disease, and premature low birth weight babies; the effectiveness of antibiotics against bacteria that cause most gum disease; new approaches in the etiology, treatment and monitoring of periodontal disease; the body's host immune response system in initiating the destructive periodontal disease process; pharmaceutical and nonsurgical treatment options for periodontal disease; the application and benefits of PerioChip in the treatment of periodontal disease, particularly as it compares with scaling and root planing; the application of Atridox in the nonsurgical treatment of chronic periodontitis; the application of Periostat in fighting adult periodontitis; patient education concerns, including assessment, prevention, causes of periodontal diseases, and treatment; the various stages of periodontal disease; and the necessity and benefits of various treatments of periodontal disease, including pocket reduction, regeneration, crown lengthening, soft tissue grafts, and dental implants. The document includes a posttest with which readers can qualify for continuing education. 31 figures. 4 tables. 4 references. •
Diagnosis and Risk Prediction of Periodontal Diseases, Volume 3 Source: Chicago, IL: Quintessence Publishing Co, Inc. 2002. 463 p. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $156.00 plus shipping and handling. ISBN: 0867153636. Summary: The aim of this book, the third volume of a five volume series of textbooks and atlases, is to give the reader updated knowledge about the etiology, modifying factors, risk evaluation, pathogenesis, diagnosis, and epidemiology of periodontal diseases, as well as the relationship between periodontal diseases and other diseases. Specific topics include the formation of plaque, the oral environment, oral microbiology tests, the role of tobacco products, the role of low socioeconomic status, systemic diseases, patient compliance, dental care habits, genetic factors, risk groups, individual risk, the classification of periodontal diseases, factors affecting the rate of periodontal disease progression, diagnostic tests, and the prevalence and incidence of periodontal diseases. For each topic, detailed scientific backgrounds, well-illustrated guides to implementing recommendations, and conclusions and future directions are addressed. Black-and-white and full-color photographs and graphics illustrate the text. The volume concludes with a lengthy list of references, a list of abbreviations, and a detailed subject index.
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Management of HIV-Associated Periodontal Diseases Source: Perspectives on Oral Manifestations of AIDS: Diagnosis and Management of HIV-Associated Infections. San Diego, CA, January 18-20, 1988. Contact: PSG Publishing Company, 545 Great Rd, Littleton, MA, 01460, (508) 486-8971. Summary: These proceedings of the Conference Perspectives on Oral Manifestations of AIDS: Diagnosis and Management of HIV-Associated Infections held in San Diego, CA, on January 18-20, 1988. They describe some important concepts in periodontal research concerning the infectious nature of periodontal disease. It is suggested that periodontal
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diseases are caused by microorganisms in dental plaque, and that only a small number of bacterial species in dental plaque is responsible for the variety of periodontal disease. Periodontal pathogens named are Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, Bacteroides intermedius, and Wolinella recta. Initial studies of subgingival microflora in patients with Acquired immunodeficiency syndrome (AIDS) suggest that these periodontal pathogens as well as several microorganisms not usually associated with human periodontal disease, may be important in understanding the microbiology of periodontal diseases. •
Understanding Periodontal Diseases: Assessment and Diagnostic Procedures in Practice Source: Chicago, IL: Quintessence Publishing Co, Inc. 2002. 160 p. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $46.00 plus shipping and handling. ISBN: 185097053. Summary: This text is the first of five books that aim to provide the general dental practitioner with an illustrated practical and contemporary guide to the management of patients with gingival and periodontal diseases. The book aims to bridge the gulf between the complex pathobiology of periodontal diseases and their assessment and diagnosis in dental practice. The authors provide a visual tour of the periodontium, discuss how the host responds to periodontal pathogens, and reclassify the diseases. Risk-factor identification is introduced prior to a step-by-step guide to diagnosis, commencing with the patient's first visit. Ten chapters cover the anatomy and physiology of the periodontium, how plaque causes disease, the role of the host response, risk assessment, the natural history and clinical signs of periodontal disease, the classification of periodontal diseases, the initial consultation, the detailed clinical periodontal examination, radiographic examinations and special tests, and periodontal diagnosis and prognosis. Each chapter includes aims, anticipated outcomes, full-color and black-and-white illustrations to complement the text, and suggestions for further reading. A detailed subject index concludes the text.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “periodontal disease” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “periodontal disease” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “periodontal disease” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
A Patient Guide to Periodontal Disease: Dentistry Explained by Shannon Nanne (2003); ISBN: 1591950694; http://www.amazon.com/exec/obidos/ASIN/1591950694/icongroupinterna
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Atlas of the Surgical Management of Periodontal Disease by Henry M. Goldman, et al (1982); ISBN: 0931386411; http://www.amazon.com/exec/obidos/ASIN/0931386411/icongroupinterna
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Brushing up on gum disease (SuDoc HE 20.4010/a:G 95) by Steven Shepherd; ISBN: B000106YHM; http://www.amazon.com/exec/obidos/ASIN/B000106YHM/icongroupinterna
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Clinical periodontology; prevention, diagnosis, and treatment of periodontal disease in the practice of general dentistry by Irving Glickman; ISBN: 0721641377; http://www.amazon.com/exec/obidos/ASIN/0721641377/icongroupinterna
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Dental Maintenance for Patients With Periodontal Diseases by Thomas G., Jr, Dds Wilson (1989); ISBN: 0867152095; http://www.amazon.com/exec/obidos/ASIN/0867152095/icongroupinterna
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Diabetes & periodontal disease : a guide for patients (SuDoc HE 20.3408:D 54/997) by U.S. Dept of Health and Human Services; ISBN: B00010STG6; http://www.amazon.com/exec/obidos/ASIN/B00010STG6/icongroupinterna
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Diabetes, periodontal disease : a guide for patients (SuDoc HE 20.3408:D 54) by U.S. Dept of Health and Human Services; ISBN: B00010LCD8; http://www.amazon.com/exec/obidos/ASIN/B00010LCD8/icongroupinterna
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Diagnosis and Risk Prediction of Periodontal Diseases (Axelsson, Per, Axelsson Series on Preventive Dentistry, V. 3.) by Per, Dds Axelsson (2002); ISBN: 0867153636; http://www.amazon.com/exec/obidos/ASIN/0867153636/icongroupinterna
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Glickman's Clinical periodontology : prevention, diagnosis, and treatment of periodontal disease in the practice of general dentistry by Irving Glickman; ISBN: 0721624405; http://www.amazon.com/exec/obidos/ASIN/0721624405/icongroupinterna
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Host-Parasite Interactions in Periodontal Diseases: Proceedings of a Symposium Held at Buffalo, New York, 4-6 May, 1981 by Robert Genco, Stephen Mergenhagen; ISBN: 0914826379; http://www.amazon.com/exec/obidos/ASIN/0914826379/icongroupinterna
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Ignore Your Teeth and They'll Go Away: The Complete Guide to Gum Disease by Sheldon D. Sydney; ISBN: 0960749829; http://www.amazon.com/exec/obidos/ASIN/0960749829/icongroupinterna
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Inflammation and Immunology in Chronic Inflammatory Periodontal Disease (1992); ISBN: 9992296267; http://www.amazon.com/exec/obidos/ASIN/9992296267/icongroupinterna
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Inflammation and Immunology in Chronic Inflammatory Periodontal Disease: Proceedings of the 11th Meeting of the British Inflammation Research Associa by Hubert N. Newman, David M. Williams (Editor); ISBN: 0905927885; http://www.amazon.com/exec/obidos/ASIN/0905927885/icongroupinterna
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Molecular Pathogenesis of Periodontal Disease by Robert Genco (Editor), et al; ISBN: 1555810756; http://www.amazon.com/exec/obidos/ASIN/1555810756/icongroupinterna
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Pathology of Periodontal Disease (Oxford Medical Publications) by David M. Williams, et al (1992); ISBN: 0192621203; http://www.amazon.com/exec/obidos/ASIN/0192621203/icongroupinterna
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Periodontal Disease by Michael Kowolik; ISBN: 0948269847; http://www.amazon.com/exec/obidos/ASIN/0948269847/icongroupinterna
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Periodontal disease : basic phenomena, clinical management, and occlusal and restorative interrelationships by Saul Schluger; ISBN: 0812105583; http://www.amazon.com/exec/obidos/ASIN/0812105583/icongroupinterna
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Periodontal disease among youth 12-17 years, United States (SuDoc HE 20.2210:11/141.) by Marcus J. Sanchez; ISBN: 0840600070; http://www.amazon.com/exec/obidos/ASIN/0840600070/icongroupinterna
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Periodontal disease in children and adolescents by Paul N. Baer; ISBN: 0397502974; http://www.amazon.com/exec/obidos/ASIN/0397502974/icongroupinterna
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Periodontal Disease Management: A New Educational Opportunity Designed Specifically for 3 Distinct Dental Teams by M. McGuire (Editor), C. Townsend (Editor) (1994); ISBN: 0962469955; http://www.amazon.com/exec/obidos/ASIN/0962469955/icongroupinterna
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Periodontal Disease: Immunological Factors by Irving Glickman (1972); ISBN: 0842270612; http://www.amazon.com/exec/obidos/ASIN/0842270612/icongroupinterna
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Periodontal Disease: Recognition, Interception and Prevention by S. Cripps (1984); ISBN: 0867151188; http://www.amazon.com/exec/obidos/ASIN/0867151188/icongroupinterna
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Periodontal diseases & dentistry : subject analysis index with research bibliography by Virgil D. Hathawaye; ISBN: 0881643572; http://www.amazon.com/exec/obidos/ASIN/0881643572/icongroupinterna
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Periodontal Diseases: A Manual of Diagnosis, Treatment and Maintenance by Lars Laurell, Hans R. Preus (2003); ISBN: 1850970726; http://www.amazon.com/exec/obidos/ASIN/1850970726/icongroupinterna
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Periodontal Diseases: Basic Phenomena, Clinical Management, and Occlusal and Restorative Interrelationships by Saul Schluger (Editor), et al; ISBN: 0812110846; http://www.amazon.com/exec/obidos/ASIN/0812110846/icongroupinterna
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Periodontal Diseases: Pathogens and Host Immune Responses by Shigeyuki Hamada, et al; ISBN: 487417342X; http://www.amazon.com/exec/obidos/ASIN/487417342X/icongroupinterna
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Prevention of Periodontal Disease. Ed by Fermin A. Carranza, Tr. Proc of Symp Held in Santa Monica, Ca, April, May 1980 (97P) by International Symposium of Prevention of Periodontal Disease (1981); ISBN: 0931386519; http://www.amazon.com/exec/obidos/ASIN/0931386519/icongroupinterna
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Public Health Aspects of Periodontal Disease by A. Frandsen (Editor); ISBN: 0867151536; http://www.amazon.com/exec/obidos/ASIN/0867151536/icongroupinterna
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Reversing Gum Disease Naturally : A Holistic Home Care Program by Sandra Senzon (Author) (2003); ISBN: 0471222305; http://www.amazon.com/exec/obidos/ASIN/0471222305/icongroupinterna
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Risk Markers for Oral Diseases: Volume 3, Periodontal Diseases: Markers of Disease Susceptibility and Activity by N. W. Johnson (Editor); ISBN: 0521385660; http://www.amazon.com/exec/obidos/ASIN/0521385660/icongroupinterna
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The 2002 Official Patient's Sourcebook on Diabetes-Related Periodontal Disease by Icon Health Publications, et al (2002); ISBN: 0597831394; http://www.amazon.com/exec/obidos/ASIN/0597831394/icongroupinterna
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The Borderland between caries and periodontal disease : proceedings of a conference sponsored by the Royal Society of Medicine, 28 February 1977; ISBN: 0808910817; http://www.amazon.com/exec/obidos/ASIN/0808910817/icongroupinterna
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The Borderland Between Caries and Periodontal Disease II by T. Lehner, G. Cimasoni (Editor); ISBN: 0808913131; http://www.amazon.com/exec/obidos/ASIN/0808913131/icongroupinterna
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The Borderline Between Caries and Periodontal Disease II by G. and T. Lehner Cimasoni (1981); ISBN: 0127925066; http://www.amazon.com/exec/obidos/ASIN/0127925066/icongroupinterna
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The diagnosis and treatment of periodontal disease by John F. Prichard; ISBN: 0721673627; http://www.amazon.com/exec/obidos/ASIN/0721673627/icongroupinterna
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The Prevention of periodontal disease: proceedings of a European symposium held at the University of Sussex, 14th-18th September, 1970; ISBN: 0853137617; http://www.amazon.com/exec/obidos/ASIN/0853137617/icongroupinterna
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Understanding Periodontal Diseases (Educate Your Patients) by Joel M. Berns (1993); ISBN: 0867152397; http://www.amazon.com/exec/obidos/ASIN/0867152397/icongroupinterna
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Understanding Periodontal Diseases: Assessment and Diagnostic Procedures in Practice_(periodontology Vol. 1) by Iain L. C. Chapple, Angela Gilbert (2002); ISBN: 185097053X; http://www.amazon.com/exec/obidos/ASIN/185097053X/icongroupinterna
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What Is Periodontal Disease? by Joel M. Berns; ISBN: 0867151099; http://www.amazon.com/exec/obidos/ASIN/0867151099/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “periodontal disease” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
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A symposium on a new bone-grafting implant material for the treatment of periodontal disease: proceedings of a Periodontal Clinical Conference, Boca Raton,
In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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Florida, October 5 and 6, 1981 Author: World Health Information Services.; Year: 1982; Lawrenceville, NJ: Dental Learning Systems Co., c1982 •
A textbook of clinical periodontia; a study of the causes and pathology of periodontal disease and a consideration of its treatment, by Paul R. Stillman. and John Oppie McCall. with a chapter on Normal and abnormal occlusal relations by Egon Neustadt. Author: Stillman, Paul Roscoe,; Year: 1937; New York, The Macmillan company, 1937
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Advanced periodontal disease: surgical and prosthetic management. Author: Prichard, John F.; Year: 1972; Philadelphia, Saunders, 1972; ISBN: 072167366X
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Concomitant periodontal disease and dental caries in young adult males Author: Ainamo, Jukka.; Year: 1973; Turku [Finland: s.n.], 1970
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Evaluation of the NIDR periodontal disease research activity: report of the Ad Hoc Scientific Evaluation Panel to the Director of National Institute of Dental Research (NIDR). Author: National Institute of Dental Research (U.S.). Ad Hoc Scientific Evaluation Panel.; Year: 1976; [s.l.: s.n.], 1976
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Examination and diagnosis of periodontal disease Author: University of California, San Francisco. Division of Periodontology. Section on Instrumental System Design.; Year: 1982; Bethesda, Md.: U.S. Dept. of Health, Education, and Welfare, Public Health Service, Health Resources Administration, Bureau of Health Resources Development, Division of Dentistry, [1974?]-
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Hypersensitivity mechanisms in bacterial inflammation with special reference to periodontal disease. Author: Gustafson, Gunnar T.; Year: 1968; Copenhagen, Munksgaard, 1968
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International Conference on Research in the Biology of Periodontal Disease, Chicago, Illinois, June 12-15, 1977 Author: Klaven, Bennett.; Year: 1980; [Chicago?: s.n., 1977?]
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Ligatures, splints, bite planes and pyramids; adjuncts in the treatment of periodontal disease. Author: Berliner, Abraham.; Year: 1964; Philadelphia, Lippincott [c1964]
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Lymphocyte-mediated cellular immunity and the pathogenesis of periodontal disease. Author: Movius, David Lewis.; Year: 1975; [Minneapolis] 1975
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On the development and prevention of periodontal disease in the beagle dog Author: Hamp, Sven-Erik.; Year: 1976; Göteborg, Sweden: [s.n.], 1973; ISBN: 9173330325
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Periodontal disease and its treatment by ionic medication, by Ernest Sturridge. illustrated with 66 engravings. Author: Sturridge, Ernest,; Year: 1961; Philadelphia and New York, Lea; Febiger, 1919
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Periodontal disease and oral hygiene among children, United States; estimates of the periodontal index (PI) and the simplified oral hygiene index (OHI-S) for noninstitutionalized children aged 6-11 years in the United States, by age, sex, race, family income, education of the head of household, and geographic region, and a correlation analysis of the interrelation of the PI, OHI-S, and selected demographic characteristics. Author: National Center for Health Statistics (U.S.); Year: 1972; Rockville, Md., For sale by the Supt. of Docs., U. S. Govt. Print. Off., 1972
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Periodontal disease, assessing the effectiveness and costs of the Keyes technique Author: Scheffler, Richard M.; Year: 1981; Washington, D.C.: Congress of the United States, Office of Technology Assessment: For sale by the Supt. of Docs., U.S. G.P.O., 1981
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Periodontal disease, report. Author: World Health Organization. Expert Committee on Dental Health.; Year: 1961; Geneva, World Health Organization, 1961
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Periodontal disease: clinical, radiographic and histopathologic features [by] Irving Glickman [and] Jerome B. Smulow. Author: Glickman, Irving.; Year: 1974; Philadelphia, Saunders, 1974; ISBN: 0721641385
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http://www.amazon.com/exec/obidos/ASIN/0721641385/icongroupinterna •
Plaque control: a determining factor in the treatment of periodontal disease Author: Rosling, Bengt.; Year: 1974; Göteborg, Sweden: [s.n.], 1976
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Report on the proceedings of the Workshop on Diet, Nutrition, and Periodontal Disease Author: Hazen, Stanley P.; Year: 1975; Chicago: American Society for Preventive Dentistry, c1975
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Studies on periodontal disease; report of the co-operative research, Ministry of Education, Medicine. Author: Imagawa, Yoso,; Year: 1960; [Tokyo, Research Group of
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T and B lymphocyte distribution in periodontal disease Author: Pazandak, David Patrick.; Year: 1977; [Minneapolis?: s.n.], 1977
Chapters on Periodontal Disease In order to find chapters that specifically relate to periodontal disease, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and periodontal disease using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “periodontal disease” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on periodontal disease: •
Systemic Effects of Periodontal Diseases Source: in Wilson, T.G., Jr.; Kornman, K.S. Fundamentals of Periodontics. 2nd ed. Chicago, IL: Quintessence Publishing Co., Inc. 2003. p. 228-237. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $82.00 plus shipping and handling. ISBN: 0867154055. Summary: A healthy mouth is part of a healthy lifestyle and recent evidence suggests that poor oral health may be as detrimental to general health as other risk factors, such as smoking or high cholesterol levels. Although the beneficial systemic effects of oral therapy have not been demonstrated, the oral benefits clearly have a positive impact on the quality of life. This chapter on the systemic effects of periodontal diseases is from a periodontics textbook that focuses on diagnosis and clinical management. The authors discuss which systemic diseases are linked with periodontal disease, who is most at risk, how oral infection can affect overall health, the entry of periodontal pathogens into the bloodstream, systemic inflammation caused by periodontal pathogens, the evidence linking periodontal disease to heart disease, periodontal infection during pregnancy, the relationship among periodontitis, pneumonia and osteoporosis, the risks associated with periodontal disease in people with diabetes, animal models, and the potential impact on dentistry. The authors note that the recognition of the medical necessity for periodontal care will increase the perceived importance of dental services, and the demand for dental services will increase. 88 references.
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Gingivitis and Periodontal Disease Source: in McDonald, R.E. and Avery, D.A., eds. Dentistry for the Child and Adolescent. 7th ed. St. Louis, MO: Mosby, Inc. 2000. p. 440-484. Contact: Available from Harcourt Health Sciences. 11830 Westline Industrial Drive, St. Louis, MO 63146. (800) 325-4177. Fax (800) 874-6418. Website: www.harcourthealth.com. PRICE: $72.00 plus shipping and handling. ISBN: 0815190174. Summary: Gingivitis, a type of periodontal disease, is an inflammation involving only the gingival (gum) tissues next to the tooth. This chapter on gingivitis and periodontal disease is from a textbook on dentistry for the child and adolescent that is designed to help undergraduate dental students and postdoctoral pediatric dentistry students provide comprehensive oral health care for infants, children, teenagers, and individuals with various disabilities. The authors cover simple gingivitis, including eruption gingivitis, gingivitis associated with poor oral hygiene, and allergy and gingival inflammation; acute gingival disease, including that due to herpes simplex virus infection, recurrent aphthous ulcer (canker sore), acute necrotizing ulcerative gingivitis (ANUG), acute candidiasis (thrush, a fungal infection), and acute bacterial infections; chronic nonspecific gingivitis; chlorhexidine as a therapeutic plaque control agent; conditioned gingival enlargement, including puberty gingivitis, fibromatosis, and phenytoin (Dilantin) induced gingival overgrowth; scorbutic gingivitis (associated with vitamin C deficiency); periodontal diseases in children, including periodontitis, premature bone loss in primary dentition, Papillon Lefevre syndrome (precocious periodontosis), gingival recession, the differential diagnosis of self mutilation, abnormal frenum attachment, and frenectomy; the clinical assessment of oral cleanliness and periodontal disease; extrinsic stains and deposits on teeth; and dental calculus (seen with low frequency in children). 44 figures. 93 references.
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Review of Presentations on Periodontal Diseases and HIV Infection Source: in Greenspan, J.S.; Greenspan, D., eds. Oral Manifestations of HIV Infection: Proceedings of the Second International Workshop on the Oral Manifestations of HIV Infection. Carol Stream, IL: Quintessence Publishing Company, Inc. 1995. p. 289-291. Contact: Available from Quintessence Publishing Company, Inc. 551 North Kimberly Drive, Carol Stream, IL 60188-1881. (800) 621-0387 or (630) 682-3223; Fax (630) 682-3288; E-mail:
[email protected]; http://www.quintpub.com. PRICE: $64.00 plus shipping and handling. ISBN: 0867152869. Summary: In this chapter from the proceedings of the Second International Workshop on the Oral Manifestations of HIV Infection, held in February 1993, in San Francisco, California, the author reviews the presentations on periodontal diseases and HIV infection and extrapolates four areas for future research. The four areas include the prevalence or severity of periodontal diseases in HIV-infected patients compared with patients with other immunologic disease or patients who are otherwise healthy; the manifestations of HIV-associated periodontal diseases and how they differ from general periodontal diseases; the pathogenic mechanisms responsible for periodontal diseases in HIV-infected patients; and recommended treatment approaches and outcomes for HIVpositive patients and how they differ from those for HIV-negative patients.
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External Modifying Factors Involved in Periodontal Diseases Source: in Axelsson, P. Diagnosis and Risk Prediction of Periodontal Diseases. Chicago, IL: Quintessence Publishing Co, Inc. 2002. p. 95-143.
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Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $156.00 plus shipping and handling. ISBN: 0867153636. Summary: Many factors modify the prevalence, onset, and progression of periodontal diseases. These modifiers can be divided into external and internal factors; this chapter discusses external modifying factors. The chapter is from a textbook that gives the reader updated knowledge about the etiology, modifying factors, risk evaluation, pathogenesis, diagnosis, and epidemiology of periodontal diseases, as well as the relationship between periodontal diseases and other diseases. This chapter begins by defining relevant terms, then discusses the roles of tobacco products; low socioeconomic status; lifestyle, compliance, and dental care habits; and acquired systemic and infectious diseases. The authors offer a section of concluding thoughts on each of these topics. Black-and-white and full-color photographs and graphics illustrate the text. 25 figures. 13 tables. •
Classification and Pathogenesis of Periodontal Diseases Source: in Axelsson, P. Diagnosis and Risk Prediction of Periodontal Diseases. Chicago, IL: Quintessence Publishing Co, Inc. 2002. p. 237-315. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $156.00 plus shipping and handling. ISBN: 0867153636. Summary: Periodontal diseases range in severity from early inflammation of the gingival (gum) margin to advanced loss of periodontal support and tooth loss. The chapter on the classification and pathogenesis of periodontal diseases is from a textbook that gives the reader updated knowledge about the etiology, modifying factors, risk evaluation, pathogenesis, diagnosis, and epidemiology of periodontal diseases, as well as the relationship between periodontal diseases and other diseases. This chapter begins by defining classification categories, then discusses the pathogenesis of periodontal diseases at the clinical and cellular levels, and at the cellular and molecular levels; factors affecting rates of periodontal disease progression; and the arrest and control of periodontal diseases. The authors offer a section of concluding thoughts on each of these topics. Black-and-white and full-color photographs and graphics illustrate the text. 108 figures. 9 tables.
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Tobacco Use and Its Relation to Periodontal Diseases Source: in Wilson, T.G., Jr.; Kornman, K.S. Fundamentals of Periodontics. 2nd ed. Chicago, IL: Quintessence Publishing Co., Inc. 2003. p. 185-194. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $82.00 plus shipping and handling. ISBN: 0867154055. Summary: There is an increasing awareness of the role of tobacco use in the prevalence and severity of periodontal diseases and subsequent tooth loss. Cigarette smoking is one of the most important risk factors in the development of a variety of periodontal diseases, including various forms of chronic periodontitis, aggressive periodontitis, and necrotizing periodontal disease. This chapter on tobacco use is from a periodontics
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textbook that focuses on diagnosis and clinical management. The author discusses the effect of tobacco smoking on the prevalence and severity of periodontal diseases, alterations to periodontal treatment response in smokers, the underlying mechanisms of tobacco smoking in periodontal diseases, cigar smoking, pipe smoking, and smokeless tobacco products, and applications to clinical practice. The author concludes that cigarette smoking may play a harmful role in almost all forms of periodontal disease and adversely affect the outcomes of almost all forms of periodontal treatment. 4 figures. 126 references. •
Acquired Gingival and Periodontal Disease Source: in Scully, C., et al. Color Atlas of Orofacial Health and Disease in Children and Adolescents. London, England: Martin Dunitz Ltd. 2002. p.105-121. Contact: Available from Martin Dunitz Ltd, The Livery House. 7-9 Pratt Street, London, England NW1 0AE. 4404074822202. Website: www.dunitz.co.uk. Email:
[email protected]. PRICE: $125.00 plus shipping and handling. ISBN: 1841841021. Summary: This chapter on acquired gingival (gum) and periodontal disease is from a full-color atlas that covers the presentation of the common orofacial disorders and a wide range of less common and some rare disorders. The chapter begins with an overview of inflammatory gingival and periodontal disease, including common complaints, then covers acute necrotizing ulcerative gingivitis (ANUG, Vincent's disease), acute pericoronitis, Cancrum oris (noma), chronic hyperplastic gingivitis, chronic marginal gingivitis, drug-induced gingival overgrowth (hyperplasia), pyogenic granuloma, fibroepithelial polyps, giant cell granuloma, lateral periodontal abscess, early onset periodontitis, and trauma. Full-color photographs are accompanied by brief text entries describing each condition and noting diagnostic and management considerations for each. 33 figures. 4 tables.
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Aging and Periodontal Disease Source: in Allen, P.F. Teeth for Life for Older Adults. Chicago, IL: Quintessence Publishing Co, Inc. 2002. p.35-45. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $83.00 plus shipping and handling. ISBN: 185097056-4. Summary: This chapter on aging and periodontal disease is from a textbook that gives the general dental practitioner insight into the management of older adults. The author discusses the frequency with which periodontal diseases are seen in the older population, the biological age changes that take place in the periodontium, the older patient's attitude to periodontal diseases, and how these factors interrelate in the clinical management of periodontal disease in older patients. Although a large variety of age changes can be demonstrated in the periodontium, these appear to have a small impact on periodontal disease progression and therapeutic outcomes. Periodontal disease is not part of the aging process, but a consequence of disease progression in susceptible subjects over a number of years. In general, older patients will respond biologically to periodontal treatment as well as younger individuals, and thus the full range of periodontal therapies should be used in their treatment. 4 figures. 3 references.
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Necrotizing Periodontal Disease Source: in Lindhe, J.; Karring, T.; Lang, N.P., eds. Clinical Periodontology and Implant Dentistry. 3rd ed. Copenhagen, Denmark: Munksgaard International Publishers Ltd. 1997. p. 258-278. Contact: Available from Munksgaard International Publishers Ltd. 35 Norre Sogade, P.O. Box 2148, DK-1016 Copenhagen K, Denmark. Phone +45 33 12 70 30; Fax +45 33 12 93 87; E-mail:
[email protected]; http://www.munksgaard.dk. PRICE: $122.00 plus shipping and handling. ISBN: 8716120604. Summary: This chapter on necrotizing periodontal disease is from a textbook on clinical periodontology and implant dentistry. The authors discuss nomenclature, prevalence, clinical characteristics, diagnosis, histopathology, microbiology, host response and predisposing factors, and treatment. The authors use the term necrotizing periodontal disease (NPD) as a common denominator for necrotizing gingivitis, necrotizing periodontitis, and necrotizing stomatitis. Clinical characteristics discussed include the rapid development of painful lesions, interproximal craters, sequestrum formation, involvement of the alveolar mucosa, swelling of the lymph nodes, fever and malaise, and the role of oral hygiene. Host response and predisposing factors include systemic diseases (HIV and malnutrition), poor oral hygiene, pre-existing gingivitis, psychologic stress, inadequate sleep, smoking, alcohol use, Caucasian background, and young age. Full-color photographs illustrate many of the problems discussed. 17 figures. 1 table. 87 references. (AA-M).
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Clinical Manifestations and Management of HIV-Related Periodontal Disease Source: in Oral Health Care for Adults, Adolescents, and Children with HIV Infection. New York, NY: AIDS Institute, New York State Department of Health. 1998. p. 7-1 to 74. Contact: Available from New York State Department of Health. AIDS Institute, Director, HIV Educational Materials, 5 Penn Plaza, First Floor, New York, NY 10001. Fax (212) 613-4996. PRICE: Single copy free. Order number 9290. Summary: This chapter on the clinical manifestations and management of HIV related periodontal disease is from a handbook that assists dentists, dental hygienists, dental assistants, and primary care providers in providing patients with HIV infection with the most up to date care. The authors emphasize that oral health care is an important component of the overall management of patients with HIV infection. The chapter opens by discussing lineal gingival erythema and necrotizing ulcerative periodontitis, two types of periodontal disease associated with HIV; necrotizing ulcerative gingivitis is also mentioned. The chapter then offers specific recommendations and discusses their implementation. The recommendations are: the diagnosis of linear gingival erythema (LGE) and necrotizing ulcerative periodontitis (NUP) should be made on the basis of identification of their distinctive clinical characteristics; the most important component in the management of gingival and periodontal disease associated with HIV is the removal of such local irritants as plaque and calculus from the root surfaces, and debridement of necrotic tissues; systemic antibiotics should be combined with debridement of necrotic tissue; because systemic antibiotics increase the risk of developing candidiasis, concurrent administration of an antifungal agent should be considered; monthly dental visits should be scheduled for the first 3 to 4 months following an acute episode for HIV-associated periodontal disease; and a thorough periodontal examination should be performed at each recall session for any patient with a history of NUP. 5 references.
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Examination of Patients with Periodontal Disease Source: in Lindhe, J.; Karring, T.; Lang, N.P., eds. Clinical Periodontology and Implant Dentistry. 3rd ed. Copenhagen, Denmark: Munksgaard International Publishers Ltd. 1997. p. 383-395. Contact: Available from Munksgaard International Publishers Ltd. 35 Norre Sogade, P.O. Box 2148, DK-1016 Copenhagen K, Denmark. Phone +45 33 12 70 30; Fax +45 33 12 93 87; E-mail:
[email protected]; http://www.munksgaard.dk. PRICE: $122.00 plus shipping and handling. ISBN: 8716120604. Summary: This chapter on the examination of patients with periodontal disease is from a textbook on clinical periodontology and implant dentistry. The authors discuss symptoms of periodontal disease; the gingiva; the periodontal ligament (the root cementum), including assessment of pocket depth, assessment of attachment level, errors inherent in periodontal probing, assessment of furcation involvement, and assessment of tooth mobility; the alveolar bone, including radiographic analysis and sounding; the diagnosis of periodontal lesions; and oral hygiene status. The authors describe methods of patient examination that provide a thorough analysis of the presence, extent, and severity of the disease in the dentition. The correct diagnosis for each individual tooth should form the basis for treatment planning of the individual case. Full-color photographs and radiographs illustrate the chapter. 15 figures. 16 references. (AA-M).
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Natural History and Clinical Signs of Periodontal Diseases Source: in Chapple, I.L.C.; Gilbert, A.D. Understanding Periodontal Diseases: Assessment and Diagnostic Procedures in Practice. Chicago, IL: Quintessence Publishing Co, Inc. 2002. p.71-79. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail:
[email protected]. Website: www.quintpub.com. PRICE: $46.00 plus shipping and handling. ISBN: 185097053. Summary: This chapter on the natural history and clinical signs of periodontal diseases is from a book that aims to bridge the gulf between the complex pathobiology of periodontal diseases and their assessment and diagnosis in dental practice. The authors explain the changing paradigm of the natural history of periodontitis and help the reader visualize the important clinical features of periodontal health and disease. They discuss natural history studies, linear disease progression versus the burst theory, disease markers, the clinical signs of pristine periodontal health, clinical signs of gingivitis, clinical signs of periodontitis, historical versus active disease, and the concept of site-specificity. The chapter includes a list of aims, anticipated outcomes, full-color and black-and-white illustrations to complement the text, and suggestions for further reading. 8 figures. 4 references.
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Pathogenesis of HIV-Associated Periodontal Disease: What's Known and What Isn't Source: in Greenspan, J.S.; Greenspan, D., eds. Oral Manifestations of HIV Infection: Proceedings of the Second International Workshop on the Oral Manifestations of HIV Infection. Carol Stream, IL: Quintessence Publishing Company, Inc. 1995. p. 263-272. Contact: Available from Quintessence Publishing Company, Inc. 551 North Kimberly Drive, Carol Stream, IL 60188-1881. (800) 621-0387 or (630) 682-3223; Fax (630) 682-3288;
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E-mail:
[email protected]; http://www.quintpub.com. PRICE: $64.00 plus shipping and handling. ISBN: 0867152869. Summary: This chapter on the pathogenesis of HIV-associated periodontal disease is from the proceedings of the Second International Workshop on the Oral Manifestations of HIV Infection, held in February 1993 in San Francisco, California. The author stresses that it is necessary to discuss conventional periodontal lesions in order to appreciate the difficulties encountered in elucidating the pathogenesis of HIV-associated lesions. The chapter's topics include systemic disease and periodontal lesions; a description of periodontal disease, including classification and indices; the histology of periodontal diseases; the course of infection; periodontal destruction; and difficulties encountered by research in these areas. The author concludes with a call for a better set of clinical diagnostic criteria for the HIV-associated periodontal disease. 1 figure. 51 references. •
Pathology and Treatment of Periodontal Diseases in the Aging Individual Source: in Holm-Pedersen, P.; Loe, H., eds. Textbook of Geriatric Dentistry. 2nd ed. Copenhagen, Denmark: Munksgaard. 1996. p. 388-405. Contact: Available from Munksgaard. 35 Norre Sogade, P.O. Box 2148, DK-1016, Copenhagen K, Denmark. Telephone +45 33 12 70 30; Fax +45 33 12 93 87; E-mail:
[email protected]; http://www.munksgaard.dk/publishers/. PRICE: DKK 520,000; contact directly for current price in US dollars. ISBN: 8716105338. Summary: This chapter on the pathology and treatment of periodontal disease in the aging individual is from a comprehensive text on the processes of aging and their relevance to the delivery of dental health care. Topics include the etiology and pathogenesis of gingivitis and periodontitis; the prevalence and severity of periodontal disease in the aging population; susceptibility to periodontal disease; the prognosis for periodontal therapy; periodontal treatment and prophylaxis; treatment considerations for various populations of elderly people, from functionally independent elderly people living in their own home to frail elderly people to functionally dependent elderly people; and maintenance of good oral health after periodontal treatment. The author stresses that periodontal care for elderly people involves a complete analysis of the physical and emotional status of the patient. Age changes may affect the assessment of the periodontal problem, the treatment plan, its prognosis, and the risk for complications following therapy. Available evidence clearly demonstrates that periodontal diseases can be treated successfully in the elderly and that periodontal health can be sustained. 5 figures. 63 references. (AA-M).
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Are Unique Bacterial Pathogens Involved in HIV-Associated Periodontal Diseases? Source: in Greenspan, J.S.; Greenspan, D., eds. Oral Manifestations of HIV Infection: Proceedings of the Second International Workshop on the Oral Manifestations of HIV Infection. Carol Stream, IL: Quintessence Publishing Company, Inc. 1995. p. 257-262. Contact: Available from Quintessence Publishing Company, Inc. 551 North Kimberly Drive, Carol Stream, IL 60188-1881. (800) 621-0387 or (630) 682-3223; Fax (630) 682-3288; E-mail:
[email protected]; http://www.quintpub.com. PRICE: $64.00 plus shipping and handling. ISBN: 0867152869. Summary: This chapter, from the proceedings of the Second International Workshop on the Oral Manifestations of HIV Infection, held in February 1993 in San Francisco, California, addresses the role of unique bacterial pathogens involved in HIV-associated periodontal diseases. The authors review microbiologic studies of subgingival plaque
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and conclude that these studies support the concept that HIV-associated periodontal diseases are due to the same types of predominantly anaerobic bacteria as are associated with periodontal disease in otherwise healthy subjects. They briefly discuss the clinical implications of these findings. 2 tables. 17 references.
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CHAPTER 8. MULTIMEDIA ON PERIODONTAL DISEASE Overview In this chapter, we show you how to keep current on multimedia sources of information on periodontal disease. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on periodontal disease is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “periodontal disease” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “periodontal disease” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on periodontal disease: •
Etiology of Periodontal Disease and the Periodontal Examination Source: Chapel Hill, NC: Health Sciences Consortium. 1990. (videocassette). Contact: Available from Health Sciences Consortium. 201 Silver Cedar Court, Chapel Hill, NC 27514-1517. (919) 942-8731; Fax (919) 942-3689. PRICE: $276.50 for members; $395.00 for non-members. Rentals (per title) $80.00; HSC Members $55.00; plus shipping and handling. Previews (per title) $30.00; HSC members $20.00; plus shipping and handling. Order Number D900-VI-001. Summary: This videotape program describes the four foundations of correct diagnosis in periodontics. The author stresses that correct diagnosis in periodontics is possible only after the operator understands the etiology and process of periodontal disease and completes perioral, intraoral, and periodontic examinations. After studying this presentation, the viewer should be able to describe plaque formation, the roles of the dental team and the patient in preventing it, and the four classifications of periodontal
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disease. In addition, having prior experience conducting the hard and soft tissue exam and periodontal probing, the student will be able to demonstrate the routine, general patient examination, and the four main steps in the periodontal exam: gingival index, periodontal probing, tooth mobility, and plaque index. (AA-M). •
Periodontal Disease Source: Chicago, IL: American Dental Association (ADA). 1998. (videocassette). Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174. (800) 947-4746. Fax (888) 476-1880 or (630) 443-9970. Website: www.ada.org. PRICE: $40.00; nonmembers add 50 percent; bulk rates available. Item number X790. Summary: Three out of four adults will face periodontal disease at some time in their lives. This educational video from the American Dental Association (ADA) provides basic information about periodontal diseases. Topics include the causes of periodontal diseases, notably the bacteria in plaque; common symptoms, which include red, swollen gums that bleed easily and can culminate in tooth loss; treatment options, including thorough cleaning (scaling and planing), bite adjustment, antimicrobial rinses, and minor gum surgery; and prevention strategies to increase longterm retention of the teeth. These prevention strategies include regular dental care, daily brushing and flossing, and monitoring one's own oral health. The program reiterates the fact that periodontal disease, particularly in the early stages, is usually not accompanied by any pain. However, it is important that any problems are addressed as soon as possible, in order to prevent tooth loss. The program shows real patients and uses graphics to show the advancement of periodontal diseases and their treatment.
Bibliography: Multimedia on Periodontal Disease The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in periodontal disease (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on periodontal disease: •
Furcation involvement in periodontal disease [videorecording]: root amputation Source: Academy of Health Sciences; Year: 1975; Format: Videorecording; Fort Sam Houston, Tex.: The Academy: [for loan by its Health Sciences Media Division, 1975]
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Gum disease [videorecording] Source: a presentation of Films for the Humanities & Sciences; ITV, Information Television Network; Year: 2001; Format: Videorecording; Princeton, N.J.: Films for the Humanities & Sciences, c2001
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Ligatures and splints [motion picture]: adjuncts in the treatment of periodontal disease Source: produced and narrated by Abraham Berliner; Year: 1961; Format: Motion picture; United States: [A. Berliner, 1961]
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Microcosms of the mouth; part III, role in periodontal disease [motion picture] Source: Sumter S. Arnim; [made by] A-V Corporation; Year: 1965; Format: Motion picture; [Cincinnati: Procter & Gamble, Crest Professional Services Division; St. Petersburg, Fla.: for loan by Modern Talking Picture Service, inc., 1965]
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Periodontal disease [motion picture] Source: American Dental Association; Year: 1970; Format: Motion picture; [Houston, Tex.]: Teaching Films, c1970
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Periodontal disease [motion picture]: prevention and early treatment Source: produced by Low & Associates, Inc; Year: 1963; Format: Motion picture; United States: Dept. of the Navy, 1963
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Periodontal gum disease [videorecording] Source: presented by the Warren Magnuson Clinical Center, National Institutes of Health, Office of Clinical Reports & Inquiries; a production of AVP Inc; Year: 1985; Format: Videorecording; [Los Angeles, Calif.]: Hospital Satellite Network, c1985
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Pulp pathology and periodontal disease [slide] Source: produced by American Dental Association, Council on Dental Therapeutics; Year: 1966; Format: Slide; Chicago, Ill.: The Association, 1966
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Recognizing and describing gingival changes in chronic inflammatory periodontal disease [slide] Source: Theodosios G. Frantzis; produced by the Visual Education Dept., Virginia Commonwealth University, Medical College of Virginia Campus; Year: 1979; Format: Slide; Richmond: The College; [Chapel Hill, N.C.: for loan or sale by Health Sciences Consortium], 1979
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The bite plane [motion picture]: a selective adjunct in the treatment of periodontal disease Source: produced and narrated by Abraham Berliner; Year: 1955; Format: Motion picture; United States: A. Berliner, [1955]
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The Etiology of periodontal [videorecording] Source: produced conjunction with the Department of [Houston, Tex.]: University of Texas 1989
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Ultrasonic bactericidal curettage [videorecording]: effective antibacterial treatment for periodontal disease Source: University of Southern California 23rd Annual Periodontal Symposium, February 7 and 8, 1997, Los Angeles Omni Hotel; [presented by] A-V Healt; Year: 1997; Format: Videorecording; [La Jolla, Calif.]: A-V Health Promotions, c1997
disease and the periodontal examination by the Office of Instructional Development, in Periodontics; Year: 1989; Format: Videorecording; Health Science Center at Houston, Dental Branch,
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CHAPTER 9. PERIODICALS AND NEWS ON PERIODONTAL DISEASE Overview In this chapter, we suggest a number of news sources and present various periodicals that cover periodontal disease.
News Services and Press Releases One of the simplest ways of tracking press releases on periodontal disease is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “periodontal disease” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to periodontal disease. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “periodontal disease” (or synonyms). The following was recently listed in this archive for periodontal disease: •
Gum disease raises death risk in diabetics: study Source: Reuters Health eLine Date: July 04, 2003
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Obese young adults more likely to have gum disease Source: Reuters Health eLine Date: June 05, 2003
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Findings tie gum disease to mouth cancer Source: Reuters Health eLine Date: March 20, 2003
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Periodontal disease linked with left ventricular mass Source: Reuters Medical News Date: March 18, 2003
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Periodontal disease linked with oral cancer Source: Reuters Medical News Date: March 17, 2003
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Maternal periodontal disease, preeclampsia possibly linked Source: Reuters Medical News Date: February 17, 2003
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Gum disease tied to pregnancy complication Source: Reuters Health eLine Date: February 03, 2003
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Tooth loss, gum disease may up man's stroke risk Source: Reuters Health eLine Date: December 12, 2002
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Periodontal disease, tooth loss linked to risk of ischemic stroke Source: Reuters Medical News Date: December 12, 2002
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Periodontal disease linked to elevated CRP levels in hemodialysis patients Source: Reuters Medical News Date: November 29, 2002
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Gum disease linked to ulcer-causing bacteria Source: Reuters Health eLine Date: November 08, 2002
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Israel approves CollaGenex periodontal disease drug Source: Reuters Industry Breifing Date: May 06, 2002
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Maternal periodontal disease may impair fetal growth Source: Reuters Industry Breifing Date: March 11, 2002
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Mom's gum disease may impair fetal growth: study Source: Reuters Health eLine Date: March 08, 2002
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Gold teeth can worsen gum disease, dentists warn Source: Reuters Health eLine Date: March 07, 2002
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Diabetes linked to increased periodontal disease in pregnant women Source: Reuters Medical News Date: November 27, 2001
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Heart attack-related protein tied to gum disease Source: Reuters Health eLine Date: September 27, 2001
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Elevated C-reactive protein may explain link between MI, periodontal disease Source: Reuters Medical News Date: September 27, 2001
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Periodontal disease associated with premature birth Source: Reuters Medical News Date: July 25, 2001
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Scientists map genome of gum disease bacteria Source: Reuters Industry Breifing Date: June 13, 2001
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Gum disease linked to diabetes Source: Reuters Health eLine Date: April 24, 2001
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Teen smokers end up with gum disease in their 20s Source: Reuters Health eLine Date: March 20, 2001
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Long-term smoking predictive of periodontal disease in young adults Source: Reuters Medical News Date: March 16, 2001
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Periodontal disease contributes to premature birth risk Source: Reuters Medical News Date: March 12, 2001
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Gum disease can raise risk for premature birth Source: Reuters Health eLine Date: March 12, 2001
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Blood-clotting gene linked to gum disease Source: Reuters Health eLine Date: March 12, 2001
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FDA approves OraPharma's periodontal disease treatment Source: Reuters Industry Breifing Date: February 16, 2001
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Periodontal disease may not be a risk factor for cardiovascular disease Source: Reuters Medical News Date: February 07, 2001
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Periodontal disease activity may contribute to COPD Source: Reuters Medical News Date: February 02, 2001
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Gum disease may not boost heart disease risk Source: Reuters Health eLine Date: January 31, 2001
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Gum disease linked to heart attack risk Source: Reuters Health eLine Date: November 13, 2000
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Smoking may cause half of US gum disease cases Source: Reuters Health eLine Date: May 30, 2000
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Gum disease linked to premature delivery risk Source: Reuters Health eLine Date: May 08, 2000
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Gum disease linked to blood clotting factors Source: Reuters Health eLine Date: February 23, 2000
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Periodontal disease appears to increase risk of cardiovascular disease Source: Reuters Medical News Date: February 10, 2000
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Gene linked to rare disorder may help understanding of periodontal disease Source: Reuters Medical News Date: December 20, 1999
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Financial strain may raise gum disease risk Source: Reuters Health eLine Date: July 19, 1999
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Gum disease may boost stroke risk Source: Reuters Health eLine Date: April 22, 1999
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Periodontal disease linked to coronary heart disease Source: Reuters Medical News Date: January 27, 1999
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Gum disease linked to heart disease Source: Reuters Health eLine Date: January 26, 1999
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FDA approves low-dose doxycycline for gum disease Source: Reuters Medical News Date: October 02, 1998
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Birth control pills may up gum disease risk Source: Reuters Health eLine Date: September 10, 1998
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FDA Designates Periodontal Disease Treatment Approvable Source: Reuters Medical News Date: April 09, 1998
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Gum Disease Begins at Home Source: Reuters Health eLine Date: September 17, 1997
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Antibiotics May Obviate Surgery For Periodontal Disease Source: Reuters Medical News Date: May 15, 1996
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “periodontal disease” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “periodontal disease” (or synonyms). If you know the name of a company that is relevant to periodontal disease, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “periodontal disease” (or synonyms).
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Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “periodontal disease” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on periodontal disease: •
Smoking and Periodontal Disease, Tooth Loss, and Dental Caries Source: Oral Care Report. 13(1): 4,8. 2003. Contact: Available from Oral Care Report. c/o Dr. Chester W. Douglass, Department of Oral Health Policy, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115. Fax (617) 432-0047. E-mail:
[email protected]. Website: www.colgateprofessional.com (full-text available online). Summary: Apart from the established associations between smoking and serious illnesses such as cancer, heart disease and lung disease, oral health problems are also linked to smoking. Numerous studies report an increased risk for periodontal disease, tooth loss, and dental caries in smokers as compared to nonsmokers. This brief article explores this association, focusing on tooth loss, probing attachment loss, and dental caries in smokers. The authors consider the potential mechanisms by which smoking affects dental status, noting that said mechanisms are not well understood. 1 table. 3 references.
•
Dentistry's Challenge for the Future: Periodontal Disease in the Older Patient Source: Focus on Adult Oral Health. 1(3): 1-5. December 1993. Contact: Available from Colgate Oral Pharmaceuticals. Professional Relations, 1 Colgate Way, Canton, MA 02021. (800) 2-COLGATE or (617) 821-2880; Fax (617) 821-2187; http://www.colgate.com. PRICE: Single copy free; limited to dental professionals. Summary: This article describes the biological, psychological, and systemic factors that influence the diagnosis and treatment of periodontal disease in the elderly. The author addresses the myth that loss of teeth is an inexorable consequence of aging, and encourages the general practitioner to utilize practical therapies to maintain the existing dentition in older patients. Topics include age as a factor in periodontal disease, the incidence and prevalence of periodontal disease, plaque control, evaluation of risk factors, bone loss concerns, xerostomia, and gingival hyperplasia. The author emphasizes that in light of changing demographics, the need of older persons for dental care and periodontal care is already having a major impact upon the dental practice. 3 figures. 1 table. 29 references. (AA-M).
•
Periodontal Disease and Sjogren's Syndrome Source: Moisture Seekers Newsletter. p. 1-2. February 2000. Contact: Available from Sjogren's Syndrome Foundation, Inc. 8120 Woodmont Avenue, Suite 530, Bethesda MD 20814-1437. (301) 718-0300 or (800) 475-6473. Fax (301) 718-0322. Website: www.sjogrens.org.
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Summary: This newsletter article explores the problem of periodontal disease in individuals with Sjogren's syndrome (SS). The author first briefly reviews SS and its characteristics, noting that patients with SS have a 2.2 times higher risk of having periodontal disease than healthy subjects. The article then discusses the development of periodontal disease, explaining why the reduced saliva flow in patients with SS contributes to this problem. The author lists the more common symptoms of periodontal disease, reminds readers of the daily oral hygiene (brushing and flossing) strategies to prevent or control periodontal disease, and reviews the treatments for periodontal disease (the most common of which is scaling and root planing). The author concludes with a brief discussion of the destructive enzymes that are present in SS and the indications for drug therapy to block these destructive enzymes. In patients with SS who suffer from periodontal disease, the use of an enzyme inhibitor might not only help in the management of their periodontitis, but may also directly aid in slowing down the destruction of their salivary glands.
Academic Periodicals covering Periodontal Disease Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to periodontal disease. In addition to these sources, you can search for articles covering periodontal disease that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for periodontal disease. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a non-profit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with periodontal disease. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.).
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The following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to periodontal disease: Ascorbic Acid (Vitamin C) •
Systemic - U.S. Brands: Ascorbicap; Cecon; Cee-500; Cemill; Cenolate; Cetane; Cevi-Bid; Flavorcee; Ortho/CS; Sunkist http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202071.html
Chlorhexidine •
Implantation-Dental - U.S. Brands: PerioChip http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203651.html
Doxycycline •
Dental - U.S. Brands: Atridox http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203716.html
Doxycycline for Dental Use •
Systemic - U.S. Brands: Periostat http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203724.html
Tetracycline Periodontal Fibers •
Dental - U.S. Brands: Actisite http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202729.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html.
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Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13 Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “periodontal disease” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “periodontal disease” (or synonyms) into the “For these words:” box. The following is a sample result: •
Oral Malodor Source: JADA. Journal of the American Dental Association. 134(2): 209-214. February 2003. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2867. Website: www.ada.org. Summary: Oral malodor (bad breath, halitosis) is a common complaint among the general population. This article brings dentists and dental care professionals up to date on the current thinking about the diagnosis and treatment of oral malodor. Topics include prevalence, causes (etiology), diagnosis, patient assessment, and treatment. The role of periodontal disease in bad breath is uncertain, and more studies are needed on the various conditions that affect oral malodor. A thorough medical and dental history is necessary to evaluate oral malodor complaints. The primary reference standard for detection of oral malodor is the human nose (organoleptic assessment) because it provides an overall evaluation of the existing malodor condition. This could be supplemented with an instrumental method, such as evaluation by sulfide monitor or gas chromatographic (GC), for an objective malodor assessment. For the treatment of bad breath, improved oral hygiene, especially tongue cleaning, has been shown to reduce oral malodor significantly. The value of some oral care products in reducing bad breath, however, is less certain. 46 references.
•
Guidelines for Periodontal Therapy Source: Journal of Periodontology. 72(11): 1624-1628. November 2001. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: This article reprints the Guidelines for Periodontal Therapy as established by the American Academy of Periodontology. These guidelines are intended to fulfill the Academy's obligation to the public and to the dental profession. This article sets forth the clinical objectives and scope of periodontal therapy. The goals of periodontal therapy are to preserve the natural dentition (teeth), periodontium and peri-implant
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tissues; and to maintain and improve periodontal and peri-implant health, comfort, esthetics, and function. Currently accepted clinical signs of a healthy periodontium include the absence of inflammatory signs of disease such as redness, swelling, suppuration, and bleeding on probing; maintenance of a functional periodontal attachment level; minimal or no recession in the absence of interproximal bone loss; and functional dental implants. The guidelines summarize the scope of periodontics, the periodontal examination itself, establishing a diagnosis and prognosis, periodontal diseases and conditions, development of a treatment plan, informed consent and patient records, treatment procedures, periodontal maintenance therapy, factors modifying results, and the evaluation of therapy. These guidelines are designed to give guidance to state legislatures and agencies that regulate the practice of periodontology and should be considered in their entirety. 30 references. •
Improving women's health and perinatal outcomes: The impact of oral diseases Source: Baltimore, MD: Women's and Children's Health Policy Center, John Hopkins Bloomberg School of Public Health. 2002. 12 pp. Contact: Available from HRSA Information Center, 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. Telephone: (888) ASK-HRSA or (877) 474-4772 TTY / fax: (703) 821-2098 / e-mail:
[email protected] / Web site: http://www.ask.hrsa.gov. Available at no charge; also available from the Web site at no charge. Summary: This brief discusses the impact of oral diseases on women's health and perinatal outcomes. It is divided into the following sections: (1) oral health status of women in the United States; (2) determination of women's oral health status; (3) periodontal diseases and general health status; (4) maternal oral health status and perinatal outcomes; (5) addressing women's oral health needs; and (6) implications of current research for improving women's oral and general health status. References conclude the brief. [Funded by the Maternal and Child Health Bureau].
•
Oral health U.S., 2002 Source: Bethesda, MD: Dental, Oral, and Craniofacial Data Resource Center. 2002. 224 pp., (1 CD-ROM). Contact: Available from Dental, Oral and Craniofacial Data Resource Center, 1700 Research Boulevard, Suite 400, Rockville, MD 20850. Telephone: (301) 294-5634 Exec Dir or (301) 294-5594 Contact / fax: (301) 294-5401 / e-mail:
[email protected] / Web site: http://drc.nidcr.nih.gov. Available from the Web site at no charge. Summary: This first annual report summarizes the current state of oral health in the United States, using nationally representative data in the areas of oral health, disease, and oral health care practices. The goals of this report are to establish a baseline, identify trends, and provide a clearer picture of the presence and magnitude of disparities in oral health status. Topics include dental caries, preventive interventions, periodontal diseases, tooth loss, overall oral health, oral infections, delivery of dental services, surveillance systems, congenital craniofacial abnormalities, orofacial pain, injuries, tobacco, oral and pharyngeal cancer, xerostomia, links to systemic health and disease, workforce, costs, accessibility issues, and the social and economic impact of oral disease. The format for this report includes introductory text in each section followed by graphic displays. A discussion of the sources of data and methodologies used can be found at the end of the report. Extensive charts and tables present statistical data throughout the report.
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Operational Definitions for Year 2000 Objectives: Priority Area 13, Oral Health Source: Healthy People 2000. Statistical Notes. Number 12: 1-20. May 1997. Contact: Available from National Center for Health Statistics. Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Service, 6525 Belcrest Road, Hyattsville, MD 20782. (301) 436-8500; E-mail:
[email protected]; http://www.cdc.gov/nchswww/nchshome.htm. PRICE: Single copy free. DHHS Publication Number 97-1237. Summary: This issue of Statistical Notes provides definitions and data collection specifications for objectives in Priority Area 13: Oral Health, one of 22 priority areas of the Healthy People 2000 project. In this publication, the text and operational definitions of the objectives are presented, important data issues are discussed, and references are cited for expanded discussions of the data systems that provide data for the national objectives. Topics covered in the objectives include dental caries (in children and adolescents), untreated dental caries, no tooth loss (tooth retention), complete tooth loss, gingivitis, periodontal diseases, oral cancer deaths, protective sealants, water fluoridation, topical and systemic fluorides, baby bottle tooth decay, oral health screening (including referral and follow up), oral health care at institutional facilities, regular dental visits, oral health care for infants with cleft lip or palate, protective equipment in sporting and recreation events, and the reduction of smokeless tobacco (spit tobacco) use. One appendix lists the oral health objectives in total. One chart provides a data comparability worktable with objective definitions, data sources, and issues. This table presents the short text of each objective, the measure, the operational definition, the national data source, and a brief description of data issues. 8 figures. 1 table. (AA-M).
•
The oral-systemic health connection Source: Bethesda, MD: National Institute of Dental and Craniofacial Research. 1999. 15 pp. Contact: Available from National Institute of Dental and Craniofacial Research, Building 45, Room 4AS19, 9000 Rockville Pike, Bethesda, MD 20892-6400. Telephone: (301) 4964261 publications / fax: (301) 496- 9988 / Web site: http://www.nidcr.nih.gov. Available at no charge. Summary: This report describes the relationship between periodontal disease and other health problems such as chronic degenerative diseases, diabetes mellitus, heart diseases, low birth weight, AIDS, Sjogrens syndrome, and xerostomia. The report discusses current and projected research in the field.
•
Prevention on a shoestring: Case studies of three health center programs Source: Washington, DC: National Association of Community Health Centers. 1995. 82 pp. Contact: Available from National Association of Community Health Centers, 1330 New Hampshire Avenue, N.W., Suite 122, Washington, DC 20036. Telephone: (202) 659-8008 / fax: (202) 659-8519. $6.00 members, $7.50 nonmembers includes shipping and handling. Summary: This report evaluates the design, implementation, and results of three small preventive health education demonstration grants awarded to community health centers. The study reviewed the Pike Market Medical Clinic Nutrition Intervention
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Program in Seattle, Washington; the Adolescent Periodontal Disease Prevention Program, a Colorado migrant health program; and 'Great to Wait,' the adolescent pregnancy prevention program operated by Health Care Partners of South Carolina. The latter program was based on the adolescent abstinence training program 'Postponing Sexual Involvement,' developed by Dr. Marion Howard at Grady Memorial Hospital in Atlanta, with additional information from 'True Love Waits.' The 'Great to Wait' program targeted adolescents ages 11-14 in rural communities with a large African-American population. The report includes information on the design of each program, its organization and implementation, the outcomes, and the evaluation process. The report also includes examples of the training materials and evaluation instruments. •
Oral Health Care for Adults With HIV Infection Contact: New York State Department of Health, Statewide AIDS Service Delivery Consortium, AIDS Institute, 5 Penn Plz, New York, NY, 10001, (212) 268-6235, http://www.health.state.ny.us/. Summary: This report reviews the principles of, and considerations for, dentistry in patients with HIV. It explains that patients with HIV may have soft-tissue and periodontal disease requiring frequent evaluations. The report considers HIV and tuberculosis infection control in the dentistry setting and ethical and legal issues of interest to dentists caring for HIV-positive patients. Topics addressed include patient evaluation, treatment planning, diagnosis, and management of soft-tissue lesions and oral ulcers, hairy leukoplakia, papillomavirus infections, Kaposi's sarcoma, lymphoma, and mucosal melanin pigmentation. Gingival and periodontal disease, endodontic treatment, oral and maxillofacial surgery, and restorative and prosthetic dental care are also reviewed.
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “periodontal disease” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category.
15 16
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH).
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Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 44677 602 914 36 8 46237
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “periodontal disease” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
17
Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html.
18
The HSTAT URL is http://hstat.nlm.nih.gov/.
19
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21 The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on periodontal disease can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internetbased services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to periodontal disease. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to periodontal disease. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “periodontal disease”:
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Guides on periodontal disease Gum Disease http://www.nlm.nih.gov/medlineplus/gumdisease.html
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Other guides Child Dental Health http://www.nlm.nih.gov/medlineplus/childdentalhealth.html Cosmetic Dentistry http://www.nlm.nih.gov/medlineplus/cosmeticdentistry.html Dental Health http://www.nlm.nih.gov/medlineplus/dentalhealth.html Heart Diseases http://www.nlm.nih.gov/medlineplus/heartdiseases.html Tooth Disorders http://www.nlm.nih.gov/medlineplus/toothdisorders.html
Within the health topic page dedicated to periodontal disease, the following was listed: •
General/Overviews Fighting Gum Disease: How to Keep Your Teeth Source: Food and Drug Administration http://www.fda.gov/fdac/features/2002/302_gums.html General Periodontal Questions Source: American Academy of Periodontology http://www.perio.org/consumer/faq.htm What Are Periodontal Diseases? Source: American Academy of Periodontology http://www.perio.org/consumer/2a.html
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Diagnosis/Symptoms Tooth Problems: Self-Care Flowcharts Source: American Academy of Family Physicians http://familydoctor.org/flowcharts/511.html
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Treatment Blade-Free Radiosurgery Offers New Cosmetic and Surgery Source: Academy of General Dentistry http://www.agd.org/consumer/topics/technology/radiosurgery.html Periodontal Procedures Source: American Academy of Periodontology http://www.perio.org/consumer/procedures.htm
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Specific Conditions/Aspects Endocarditis Prophylaxis Information Source: American Heart Association http://www.americanheart.org/presenter.jhtml?identifier=11086 Facts and Fallacies About Periodontal Disease Source: American Academy of Periodontology http://www.perio.org/consumer/f1.html Mouth-Body Connection Source: American Academy of Periodontology http://www.perio.org/consumer/mbc.top2.htm Pericoronitis Source: InteliHealth, University of Pennsylvania, School of Dental Medicine http://www.simplestepsdental.com/SS/ihtSS/r.WSIHW000/st.32219/t.29748/pr.3 .html Periodontitis Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00369 Prevent Diabetes Problems: Keep Your Teeth and Gums Healthy Source: National Diabetes Information Clearinghouse http://diabetes.niddk.nih.gov/dm/pubs/complications_teeth/index.htm Tobacco Use and Periodontal Disease Source: American Academy of Periodontology http://www.perio.org/consumer/smoking.htm Trench Mouth Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00457 What is Gingivitis? Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00363
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Children Protecting Children's Oral Health Source: American Academy of Periodontology http://www.perio.org/consumer/children.htm
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From the National Institutes of Health Periodontal (Gum) Diseases Source: National Institute of Dental and Craniofacial Research http://www.nidcr.nih.gov/health/newsandhealth/gumDiseasesPub.asp Special Care in Oral Health Source: National Institute of Dental and Craniofacial Research http://www.nohic.nidcr.nih.gov/special_care.html
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Men Women and Periodontal Disease: Protecting Oral Health Throughout Your Life Source: American Academy of Periodontology http://www.perio.org/consumer/women.htm
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Organizations American Academy of Periodontology http://www.perio.org/ American Dental Association http://www.ada.org/ National Institute of Dental and Craniofacial Research http://www.nidcr.nih.gov/
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Prevention/Screening Oral Health: Preventing Cavities, Gum Disease, and Mouth and Throat Cancer Source: Centers for Disease Control and Prevention http://www.cdc.gov/nccdphp/aag/aag_oh.htm Preventing Periodontal Disease Source: American Dental Association http://www.ada.org/prof/resources/pubs/jada/patient/patient_08.pdf
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Research Periodontal Disease Increases Risk of Preeclampsia Source: American College of Obstetricians and Gynecologists http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZCKHVGSBD &sub_cat=2 Scientists Report Important Lead in Studying Possible Association Between Periodontal and Cardiovascular Disease Source: National Institute of Dental and Craniofacial Research http://www.nidcr.nih.gov/news/08042003.asp
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Statistics FASTATS: Oral Health Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/dental.htm National Oral Health Surveillance System Source: Centers for Disease Control and Prevention http://www.cdc.gov/nohss/
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Teenagers Gum Disease Source: Nemours Foundation http://kidshealth.org/teen/diseases_conditions/mouth/gum_disease.html
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Women Women and Periodontal Disease: Protecting Oral Health Throughout Your Life Source: American Academy of Periodontology http://www.perio.org/consumer/women.htm
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on periodontal disease. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
What You Need to Know About Gum Disease and Your Health Source: Phoenix, AZ: SmartPractice. 199x. [4 p.]. Contact: Available from SmartPractice. 3400 East McDowell, Phoenix, AZ 85008. (800) 522-0800. Fax (800) 522-8329. Website: www.smartpractice.com. PRICE: $34.00 for 100 brochures, plus shipping and handling. Summary: Good oral hygiene and regular professional care are the keys to preventing periodontal disease. This patient education brochure outlines facts about gum disease and general health. The brochure first describes gum disease and how it develops, then summarizes the impact of gum disease on general health, on the cardiovascular (heart) system, on patients with diabetes, on respiratory diseases, and specific concerns for women. Gum disease is caused by plaque, a colorless film of bacteria that forms on the teeth. Without daily removal, plaque hardens to form calculus (tartar) around the teeth. This process caused the gums to pull away from the teeth, creating pockets that become filled with plaque. These pockets may become deeper over time, destroying the bone structure that supports the teeth, thus resulting in tooth loss. The brochure notes that up to 90 percent of all systemic diseases including kidney disease, diabetes, and heart disease have links to oral health. For women, hormonal changes throughout life can affect many tissues in the body, including gum tissue; these changes call for special care of one's oral health. The brochure concludes by encouraging patients to work closely with their dentists to diagnose gum disease in its early stages or to prevent it altogether. A list of recommended oral hygiene strategies, including regular dental care, toothbrushing and flossing, and use of fluoride, is also provided. The brochure includes space for personalization by the dental office. The brochure is illustrated with full color graphics and photographs of smiling patients. 4 figures.
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Dealing with Gum Disease: A Life-Threatening Health Risk Source: Chicago, IL: American Dental Hygienists' Association. 2001. [2 p.]. Contact: American Dental Hygienists' Association. 444 North Michigan Avenue, Suite 3400, Chicago, IL 60611. (312) 440-8900. E-mail:
[email protected]. Website: www.adha.org. PRICE: $.75 for 24 fact sheets; $.50 for 25 plus fact sheets; $.25 for 100 plus fact sheets; plus shipping and handling. Summary: Nearly 75 percent of American adults have various forms of undiagnosed periodontal (gum) disease. Though reversible in its initial stages, mounting evidence of the relationship between oral bacteria and life threatening diseases makes it critical that the condition be prevented or treated aggressively. This consumer fact sheet from the American Dental Hygienists' Association (ADHA) explains the role of oral health in heart disease, diabetes, respiratory ailments, low birthweight, and other serious conditions. For each condition, the fact sheet offers statistics about incidence and complications, and briefly summarizes research on the relationship between that condition and oral health. The contact information for reaching the ADHA is provided (www.adha.org; 800-847-6718). The full color fact sheet is made possible by an educational grant from Procter and Gamble; the fact sheet uses the Crest logo. 3 figures.
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Preventing and Treating Periodontal Diseases Source: Chicago, IL: American Dental Association (ADA). 1998. [4 p.]. Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174. (800) 947-4746. Fax (888) 476-1880 or (630) 443-9970. Website: www.ada.org. PRICE: $19.00 for 50; nonmembers add 50 percent; bulk rates available. Item number W646. Summary: Periodontal (gum) disease is a condition in which bacteria attack the tissues that surround and support teeth. This brochure describes the use of scaling and root planing to prevent or treat the early stages of periodontal diseases. The brochure begins with a list of the common warning signs of periodontal diseases. The brochure then discusses the causes of periodontal diseases, how periodontal diseases are diagnosed, and prevention and treatment options. Scaling is used to remove plaque and tartar beneath the gumline with a small scaler or ultrasonic cleaner. The tooth's root surfaces are then smoothed or planed to allow the gum tissue to heal and reattach to the tooth. Once the scaling and root planing treatment is complete, another appointment will be made so the dentist can check how the gums have healed and how the periodontal pockets have decreased. When pockets greater than 3 mm persist after root planing and scaling, additional treatment may be needed. The brochure is illustrated with line drawings and full color photographs of gingivitis and of healthy gums. 10 figures.
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Ask Your Periodontist About Periodontal Disease and Heart Disease Source: Chicago, IL: American Academy of Periodontology. 1999. [5 p.]. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. Website: www.perio.org. PRICE: Single copy free. Summary: Periodontal disease (also known as gum disease) is a bacterial infection of the gums, bone and periodontal ligament (attachment fibers that support the teeth and hold them in the jaw). Recent research is showing a link between heart diseases and periodontal disease. This patient education brochure informs patients about these risks
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and encourages them to take precautions before dental treatment. The brochure emphasizes that taking care of one's periodontal health may be an important step toward prevention of heart disease, along with controlling the other well known risk factors for cardiovascular disease. The brochure describes the precautions that should be taken before dental treatment, to help limit the entry of bacteria into the blood stream during dental procedures. The brochure includes an insert that requests patients to list specific drugs that they are taking; the insert can then be given to the dentist or periodontist, who will work with the patient to minimize any potentially negative effects of the dental treatment. 1 figure. •
Orally Balanced Enzyme System For Reduction of Cavities, Plaque and Gum Disease Due to Xerostomia Source: Gardena, CA: Laclede Research Laboratories. 199x. 6 p. Contact: Available from Laclede Research Laboratories. 15011 Staff Court, Gardena, CA 90248. (800) 922-5856 or (310) 515-1430; Fax (310) 515-1154; E-mail:
[email protected]; http://www.laclede.com. PRICE: Single copy free. Summary: This brochure describes the Biotene system of oral care for reduction of cavities, plaque, and gum disease related to xerostomia (dry mouth). The Biotene products described include dry mouth toothpaste, a supersoft toothbrush, alcohol-free mouthwash, dental chewing gum, and a moisturizing gel. Each product (except the toothbrush) contains anti-bacterial enzymes to help prevent oral infections and gum disease. The products are sweetened with xylitol. The brochure describes each product and illustrates each with a full-color photograph. One figure shows the basic anatomy of the glands and another set of photographs shows the gum line of a patient before and after using Biotene toothpaste for two weeks. The brochure describes how the Biotene enzyme system enhances the mouth's natural defense mechanisms by supplementing the supply of key enzymes and substrates. A final section reminds readers of the importance of saliva in protecting the mouth and dentition. 5 figures. 1 table.
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Women and Gum Disease Source: Chicago, IL: American Dental Association (ADA). 1998. [4 p.]. Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174. (800) 947-4746. Fax (888) 476-1880 or (630) 443-9970. Website: www.ada.org. PRICE: $18.00 for 50; nonmembers add 50 percent; bulk rates available. Item number P081. Summary: This brochure discusses some of the special dental needs that women may face at different stages of life. Puberty, menstruation, pregnancy, and menopause can each influence oral health and the need for dental treatment. During these times, the body experiences hormonal changes that can make the gums sensitive and increase the risk for gum disease. The brochure describes gum disease (periodontal disease) and its causes, prevention, and treatment. The brochure then briefly reviews specific concerns for each of the stages of life noted above. The brochure concludes by reminding readers that it is dental plaque (not changing hormone levels) that is the major cause of periodontal disease. The brochure offers a list of strategies to prevent periodontal disease, noting that these techniques may be even more important during a woman's higher risk times. Understanding these unique dental needs can help promote good dental habits. 5 figures.
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Women and Gum Disease: Your Unique Oral Health Needs Source: Chicago, IL: American Academy of Periodontology. 1996. [4 p.]. Contact: Available from American Academy of Periodontology. Sales and Marketing Department, 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 5733253; Fax (312) 787-3670; E-mail:
[email protected]; http://www.perio.org. PRICE: $20.00 per 50 copies; bulk rates available. Summary: This brochure discusses the unique dental health needs and concerns of women, focusing on the prevention of gum disease. Topics include a definition of periodontal (gum) disease; the role of home oral care, including toothbrushing and flossing; and the physiological changes of each stage of a woman's life, including puberty, menstruation, pregnancy, and menopause. The brochure discusses the symptoms and changes of gums and gum disease during each stage. Specific topics covered include hormonal changes; gingivitis during menstruation; gingivitis, dental care, and tumors during pregnancy; oral contraceptives; and menopausal gingivostomatitis.
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Women and Periodontal Disease Source: Chicago, IL: American Academy of Periodontology. 1998. [4 p.]. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. Website: www.perio.org. PRICE: $39.00 for 100, plus shipping and handling. Summary: This brochure offers information for women about periodontal diseases (gum disease), chronic bacterial infections that can damage the gums and bone supporting the teeth. Left untreated, periodontal diseases can lead to tooth loss. The brochure describes how periodontal disease develops from plaque buildup, then notes that other factors can affect the health of the gums and the bone supporting the teeth. Smoking and tobacco use, stress, medications, diabetes and other systemic diseases, poor nutrition, clenching or grinding the teeth, and hormonal fluctuations are some of these factors. The brochure then outlines specific concerns for women during different times of life: puberty and menstruation, during pregnancy and during the use of oral contraceptives, and during menopause. The symptoms that a woman might experience during each of these times are outlined. The brochure focuses on the ongoing healthy mouth habits of good oral hygiene, brushing, and flossing, as well as the need for overall good health. Simple graphics illustrate the brochure.
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Periodontal Disease in Children: Healthy Gums Source: Chicago, IL: American Society of Dentistry for Children. 1990. [2 p.]. Contact: Available from American Society of Dentistry for Children. 875 North Michigan Avenue, Suite 4040, Chicago, IL 60611-1901. Voice (800) 637-ASDC; Fax (312) 943-5341. PRICE: $40.00 per 100 copies (nonmembers); $28.00 per 100 copies (members); shipping and handling additional. Item Number B1090. Summary: This brochure on gum disease in children is published by the American Society of Dentistry for Children as part of a series of 12 brochures on dental health for children. Topics covered include a description and definition of gum disease, signs of gum disease, the cause of gum disease, common conditions that can cause plaque to form, and the role of proper nutrition. The brochure includes a list of the other items in the series.
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Gum Disease: Are You At Risk? Source: Chicago, IL: American Dental Association (ADA). 1991. [4 p.]. Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174. (800) 947-4746; Fax (630) 443-9970; http://www.ada.org. PRICE: $19.00 for 50 copies; nonmembers add 50 percent; bulk orders available. Order Number W172. Summary: This brochure provides answers to some commonly asked questions about gum disease (periodontal disease). Topics include a description of periodontal disease, including gingivitis and periodontitis; the causes of gum disease; the symptoms of gum disease; times when gum disease is more likely to occur, such as puberty or pregnancy, and when certain lifestyle risks are present; how the dentist diagnoses gum disease; what patients can do to prevent gum disease; and how and by whom gum disease is treated. The brochure is illustrated with small photographs of patients representing various ethnic groups.
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Diabetes and Gum Disease Source: Chicago, IL: American Academy of Periodontology. 1995. 6 p. Contact: Available from American Academy of Periodontology. Sales and Marketing Department, Suite 800, 737 North Michigan Avenue, Chicago, IL 60611. (312) 573-3253. Fax (312) 787-3670. PRICE: $34 per 100 brochures, plus shipping and handling. Summary: This brochure provides readers with information about diabetes and gum disease. Topics include why oral health is so important to people who have diabetes; a definition of periodontal disease; oral conditions for which people with diabetes are at higher risk, including delayed wound healing, decreased or diminished flow of saliva, burning sensation in the mouth or on the tongue, and increased sugars in the gingival fluid; steps to take to prevent gum disease; managing periodontal disease; and monitoring oral health. The brochure concludes that, with careful attention to at-home oral hygiene and regular dental visits, periodontal infection should never play a major role in diabetes.
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Keep Your Teeth for Life: Prevent Gum Disease Source: Augusta, ME: Maine Department of Human Services, Bureau of Health, Division of Dental Health. 1992. 2 p. Contact: Available from Maine Department of Human Services, Bureau of Health, Division of Dental Health. State House Station 11, Augusta, ME 04333. (207) 287-2361 or (207) 287-3121. PRICE: Single copy free. Summary: This brochure reviews basic facts about gum disease and its prevention. The brochure describes the symptoms of gum disease; the causes of gum disease; and tips for preventing gum disease, including daily oral hygiene, toothbrushing, the use of dental floss, the use of fluoride toothpastes, and the role of regular dental care. The brochure is written in clear, easy-to-understand language and concludes with a summary of the concepts discussed.
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Periodontal Diseases: What You Need to Know Source: Chicago, IL: American Academy of Periodontology. 1996. 10 p.
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Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 787-5518. Fax (312) 787-3670. Website: www.perio.org. PRICE: Single copy free; bulk orders available. Summary: This brochure uses a question and answer format to provide information on periodontal diseases, which are bacterial gum infections that destroy the attachment fibers and supporting bone that hold the teeth in the mouth. The most common forms of periodontal disease are gingivitis, mild periodontitis, and moderate-advanced periodontitis. Although plaque is the main cause of periodontal disease, other factors such as smoking or tobacco use, pregnancy and puberty, stress, medications, clenching or grinding the teeth, diabetes, poor nutrition, and systemic diseases, can affect gum health. The brochure lists the symptoms of periodontal disease and discusses their prevention and treatment. It also includes four inserts that explain the relationship between periodontal disease and respiratory disease, pregnancy outcomes, diabetes, and heart disease. 6 figures. •
Periodontal Disease: Be Tested to See if You Have It Source: Chicago, IL: American Academy of Periodontology (AAP). 1996. [4 p.]. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 737, Chicago, IL 60611-2690. (312) 573-3253; Fax (312) 787-3670; E-mail:
[email protected]; http://www.perio.org. PRICE: $37.00 per 100 copies; bulk rates available. Summary: This brochure, from a series of patient education brochures produced by the American Academy of Periodontology, provides an introduction to periodontal disease and its detection. Written in question and answer format, the brochure covers the importance of testing for gum disease, the technique of periodontal probing, checking oneself for gum disease, the warning signs of gum disease, the causes of gum disease, and the prevention of gum disease. The brochure includes simple line drawings illustrating the concepts discussed.
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What You Should Know About Periodontal Disease Source: South Deerfield, MA: Channing L. Bete Co., Inc. 1997. 16 p. Contact: Available from Channing L. Bete Company, Inc. Dept. GSA, 200 State Road, South Deerfield, MA 01373-0200. (800) 628-7733; Fax (800) 499-6464; http://www.channing.bete.com. PRICE: $1.326 each for 1-24 copies; bulk pricing available. Booklet Number 12641. Summary: This dental health education brochure provides information about periodontal disease. Topics include how periodontal disease affects the gums and the underlying tissue and bone; how periodontal disease affects people in their teens, 20s, 30s, and after age 40; how periodontal disease progresses; the kinds of periodontal disease; the symptoms of periodontal disease; diagnostic tests used to confirm periodontal disease; treatment options for the various stages of periodontal disease; surgery and postoperative care; and the role of various health care providers in treating periodontal disease. The brochure concludes with a section reminding readers of the importance of preventing periodontal disease. The brochure is written in nontechnical language, with line drawings and cartoon figures illustrating most of the concepts presented.
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Preventing Periodontal Disease Source: JADA. Journal of the American Dental Association. 132(9): 1339. September 2001. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2867. Website: www.ada.org. Summary: This fact sheet on preventing periodontal disease is designed to be photocopied and distributed by dentists and dental care providers. The fact sheet notes that many adults develop some type of periodontal (the gums and other structures that hold the teeth) disease. There is some evidence that links periodontal diseases with other health concerns such as cardiovascular problems, stroke, bacterial pneumonia, and increased risk during pregnancy. The fact sheet reviews the known causes of gum disease, emphasizing the importance of daily removal of plaque (the sticky film of bacteria that constantly forms on teeth). If plaque is not removed with thorough daily brushing and cleaning between teeth, gums become irritated and inflamed (gingivitis). The irritated gum tissue can separate from the teeth and form spaces called pockets. Bacteria move into the pockets, where they continue to promote irritation. Left untreated, the process can continue until the bone and other tooth supporting tissues are destroyed. The early stage of periodontal disease is called gingivitis; this stage is usually reversible. The fact sheet emphasizes the importance of prevention through regular check ups and daily dental care. The fact sheet concludes with a list of the warning signs of gum disease, which include gums that bleed during brushing, red or swollen gums, gums that have pulled away from the teeth, persistent bad breath, pus between the teeth and gums, loose or separating teeth, a change in the way the teeth fit together when they are closed, a change in the fit of partial dentures.
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Know How to Detect and Prevent Gum Disease Source: Chicago, IL: American Dental Hygienists' Association (ADHA). 1995. 1 p. Contact: Available from American Dental Hygienists' Association (ADHA). 444 North Michigan Avenue, Chicago, IL 60611. (800) 243-2342 or (312) 440-8900; Fax (312) 4408929; E-mail:
[email protected]; http://www.adha.org. PRICE: $0.75 each for 1-24 copies; bulk orders available. Order Number 3506. Summary: This fact sheet provides patients with information about how to detect and prevent gum disease. Topics covered include a definition of periodontal disease, complications that can arise from gingivitis, the role of proper dental hygiene in preventing periodontal diseases, the warning signs of periodontal disease and what to do about them, conservative or nonsurgical periodontal therapy options, and surgical therapy options. The fact sheet includes a chart that lists ten warning signs of periodontal disease. The fact sheet is also available as a journal article in Access, a periodical published by the American Dental Hygienists' Association.
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Mouth: Owner's Manual: Preventing and Controlling Gum Disease Source: San Bruno, CA: Staywell Company. 1998. 16 p. Contact: Available from Staywell Company. Order Department, 1100 Grundy Lane, San Bruno, CA 94066-3030. (800) 333-3032. PRICE: $1.35 plus shipping and handling; quantity discounts available. Order Number 1315. Summary: This full-color, illustrated patient education brochure presents a guide to preventing and controlling periodontal (gum) disease. Topics covered include a guide to
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diagnosing gum disease, including a patient checklist of symptoms; the anatomy of the mouth and the physiology of bacteria, plaque, and periodontal disease; the three stages of gum disease: gingivitis, periodontitis, and advanced periodontitis; the full dental evaluation, including dental history, exam, and pocket charting; a how-to guide to selfcare, especially flossing and toothbrushing; and professional treatment options for periodontal disease. The brochure concludes with an overview of proper dental hygiene and a blank space for the dentist to record recommendations for the patient. •
Who Knows What Danger Lies Just Beneath the Surface: A Guide to Periodontal Disease Source: Sacramento, CA: California Dental Association (CDA). 1996. [6 p.]. Contact: Available from California Dental Association (CDA). P.O. Box 13749, Sacramento, CA 95853. (916) 443-0505; http://www.cda.org/cda. PRICE: Single copy free. Summary: This health education brochure familiarizes readers with periodontal disease and its prevention. Periodontal disease, also known as gum disease, is the major cause of tooth loss in adults. There are several types and stages of the disease, all of which start with a bacterial infection of the gums that can move into the bones and ligaments that support the teeth. Topics include the causes of periodontal disease, notably plaque, as well as food or chemical irritants, smoking or chewing tobacco, poorly fitting bridges, badly aligned teeth, defective fillings, clenching or grinding teeth, poor diet, pregnancy or oral contraceptives, systemic diseases, or certain medications; the stages of periodontal disease, including gingivitis, periodontitis, and advanced periodontitis; the symptoms of periodontal disease; treatment options, including professional cleaning, scaling, root planing, and surgery; and prevention considerations.
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Periodontal Diseases: A Major Cause of Tooth Loss Source: St. Charles, IL: American Dental Association (ADA). 1996. [6 p.]. Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174. (800) 947-4746; Fax (630) 443-9970; http://www.ada.org. PRICE: $21.00 per 50 copies; bulk orders available. Order Number W121. Summary: This lengthy brochure outlines the steps to take to prevent periodontal diseases. The brochure notes that periodontal diseases are caused by bacterial infections that attack gums, ligaments, and bones. Topics include the causes of periodontal disease; warning signs; types of periodontal diseases (gingivitis, periodontitis); and factors that can increase the risk of periodontal diseases, including smoking, misformed bridges, clenching the teeth, poor diet, pregnancy or use of oral contraceptives, systemic diseases, and medications. The brochure also discusses preventive measures, including toothbrushing, flossing, using an antimicrobial mouthrinse, eating a balanced diet, and scheduling regular dental checkups; screening tests for periodontal diseases; treatment options, including cleaning, scaling, antibiotics, and surgery; and maintenance. The brochure emphasizes the need for regular dental checkups, including a periodontal exam, in order to find problems before the gums and bone have been seriously compromised. Full-color photographs and line drawings illustrate the brochure. 13 figures.
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Gum Disease: The Warning Signs Source: Chicago, IL: American Dental Association (ADA). 1996. [2 p.].
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Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174. (800) 947-4746; Fax (630) 443-9970; http://www.ada.org. PRICE: Single copy free; bulk orders available. Order Number W105. Summary: This mini-brochure, from the American Dental Association, provides basic information about the warning signs of gum disease. Illustrated with colorful line drawings, the brochure discusses the forms of gum disease, including gingivitis, and periodontitis; the causes of gum disease; what happens during a dental care examination and how the dentist determines if gum disease is present; and the role of good oral hygiene in preventing gum disease. •
Mouth Care and Diabetes: Managing Periodontal Disease Source: San Bruno, CA: StayWell Company. 2000. [2 p.]. Contact: Available from StayWell Company. Order Department, 1100 Grundy Lane, San Bruno, CA 94066-9821. (800) 333-3032. Fax (650) 244-4512. E-mail:
[email protected]. Website: www.staywell.com. PRICE: $17.95 for a pack of 50; plus shipping and handling. Summary: This pamphlet provides people who have diabetes with tips for preventing and treating periodontal disease. People who have diabetes are at increased risk for periodontal disease. Periodontal disease occurs in three stages: gingivitis, periodontitis, and advanced periodontitis. Steps that people can take to prevent periodontal disease include using good oral hygiene, visiting the dentist every 3 to 4 months for examinations and cleanings, and keeping blood glucose at a healthy level. Treatment of periodontal disease involves scaling and root planing, taking antibiotics, and undergoing gum surgery. 13 figures.
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Taking Care of Your Teeth: Diabetes and Gum Disease Source: Albuquerque, NM: Indian Health Service Diabetes Program. 1992. 6 p. Contact: Available from IHS HQW Diabetes Program. 5300 Homestead Road, NE, Albuquerque, NM 78110. (505) 837-4182. Fax (505) 837-4188. PRICE: Materials are available only to health care professionals serving American Indian populations; contact the IHS Diabetes Program for list of currently available materials. Summary: This patient education booklet, written for the Native American population, describes the problem of diabetes and gum disease. Topics covered include the causes of gum disease, the problem of plaque build-up, the signs and symptoms of gum disease, and how to prevent gum disease. The brochure emphasizes the importance of the reader taking an active role in his or her own health care. Culturally-sensitive line drawings illustrate each of the concepts presented.
•
Periodontal Disease: More Than Bleeding Gums Source: Journal of Practical Hygiene. 12(2): 18. March-April 2003. Contact: Available from Montage Media Corporation. 1000 Wyckoff Avenue, Mahwah, NJ 07430-3164. (201) 891-3200. Summary: This patient education fact sheet reviews the problem of periodontal disease, an infection of the gums and bone supporting the teeth. Periodontal disease is caused by bacteria in plaque which makes the gums irritated. Untreated periodontal disease can lead to gum recession surrounding the teeth, exposing the roots of the teeth, and can even lead to tooth loss. The fact sheet reviews the epidemiology of periodontal disease
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(who gets it), the different types of periodontal disease, and how periodontal disease is treated and prevented. 4 figures. 2 references. The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “periodontal disease” (or synonyms). The following was recently posted: •
Parameter on acute periodontal diseases Source: American Academy of Periodontology - Professional Association; 1996 October (revised 2000 May); 4 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2329&nbr=1555&a mp;string=periodontal+AND+disease
•
Parameter on systemic conditions affected by periodontal diseases Source: American Academy of Periodontology - Professional Association; 2000 May; 4 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2334&nbr=1560&a mp;string=periodontal+AND+disease The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to periodontal disease. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
Patient Resources
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to periodontal disease. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with periodontal disease. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about periodontal disease. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “periodontal disease” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “periodontal disease”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “periodontal disease” (or synonyms) into the
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“For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “periodontal disease” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.23
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
23
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)24: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
•
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
•
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
24
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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•
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
•
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
•
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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•
South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
•
Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
•
Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
•
Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
•
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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PERIODONTAL DISEASE DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Accommodation: Adjustment, especially that of the eye for various distances. [EU] ACE: Angiotensin-coverting enzyme. A drug used to decrease pressure inside blood vessels. [NIH]
ACE Inhibitor: A type of drug used to lower blood pressure. Studies indicate that it may also help prevent or slow the progression of kidney disease in people with diabetes. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acetylgalactosamine: The N-acetyl derivative of galactosamine. [NIH] Acetylglucosamine: The N-acetyl derivative of glucosamine. [NIH] Acid Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.2. [NIH] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acoustic: Having to do with sound or hearing. [NIH] Actinomyces: A genus of gram-positive, rod-shaped bacteria whose organisms are nonmotile. Filaments that may be present in certain species are either straight or wavy and may have swollen or clubbed heads. [NIH] Acupuncture Therapy: Treatment of disease by inserting needles along specific pathways or meridians. The placement varies with the disease being treated. Heat or moxibustion and acupressure may be used in conjunction. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH]
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Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjunctive Therapy: Another treatment used together with the primary treatment. Its purpose is to assist the primary treatment. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Aged, 80 and Over: A person 80 years of age and older. [NIH] Agonists: Drugs that trigger an action from a cell or another drug. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure
Dictionary 269
and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Alendronate: A nonhormonal medication for the treatment of postmenopausal osteoporosis in women. This drug builds healthy bone, restoring some of the bone loss as a result of osteoporosis. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Allantois: An embryonic diverticulum of the hindgut of reptiles, birds, and mammals; in man its blood vessels give rise to those of the umbilical cord. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alpha-Defensins: Defensins found in azurophilic granules of neutrophils and in the secretory granules of intestinal paneth cells. [NIH] Alpha-helix: One of the secondary element of protein. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alveolar Bone Loss: The resorption of bone in the supporting structures of the maxilla or mandible as a result of periodontal disease. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amebiasis: Infection with any of various amebae. It is an asymptomatic carrier state in most individuals, but diseases ranging from chronic, mild diarrhea to fulminant dysentery may occur. [NIH] Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by
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posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]
Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to ampicillin except that its resistance to gastric acid permits higher serum levels with oral administration. [NIH] Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broadspectrum antibiotic. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Amputation: Surgery to remove part or all of a limb or appendage. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable. [NIH] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of
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the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Aneurism: A localized abnormal dilatation of a blood vessel filled with fluid or clotted blood, forming a pulsating tumor, and resulting from disease of the vessel wall. [NIH] Angina: Chest pain that originates in the heart. [NIH] Anginal: Pertaining to or characteristic of angina. [EU] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Anhydrous: Deprived or destitute of water. [EU] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]
Antiandrogens: Drugs used to block the production or interfere with the action of male sex hormones. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with
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specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiplasmin: A member of the serpin superfamily found in human plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin. [NIH] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [NIH] Aplastic anemia: A condition in which the bone marrow is unable to produce blood cells. [NIH]
Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH]
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Aqueous: Having to do with water. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Archaea: One of the three domains of life (the others being bacteria and Eucarya), formerly called Archaebacteria under the taxon Bacteria, but now considered separate and distinct. They are characterized by: 1) the presence of characteristic tRNAs and ribosomal RNAs; 2) the absence of peptidoglycan cell walls; 3) the presence of ether-linked lipids built from branched-chain subunits; and 4) their occurrence in unusual habitats. While archaea resemble bacteria in morphology and genomic organization, they resemble eukarya in their method of genomic replication. The domain contains at least three kingdoms: crenarchaeota, euryarchaeota, and korarchaeota. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Argon: A noble gas with the atomic symbol Ar, atomic number 18, and atomic weight 39.948. It is used in fluorescent tubes and wherever an inert atmosphere is desired and nitrogen cannot be used. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Articular: Of or pertaining to a joint. [EU] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aspartate: A synthetic amino acid. [NIH] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Endopeptidases: A sub-subclass of endopeptidases that depend on an aspartic acid residue for their activity. EC 3.4.23. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH]
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Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astigmatism: A condition in which the surface of the cornea is not spherical; causes a blurred image to be received at the retina. [NIH] Astringent: Causing contraction, usually locally after topical application. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Avian: A plasmodial infection in birds. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Backcross: A cross between a hybrid and either one of its parents. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bacterial Proteins: Proteins found in any species of bacterium. [NIH] Bacterial toxin: A toxic substance, made by bacteria, that can be modified to kill specific tumor cells without harming normal cells. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU]
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Base Sequence: The sequence of purines and pyrimidines in nucleic acids and polynucleotides. It is also called nucleotide or nucleoside sequence. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH] Beta 2-Microglobulin: An 11 kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants. [NIH] Beta-Defensins: Defensins found mainly in epithelial cells. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Bicalutamide: An anticancer drug that belongs to the family of drugs called antiandrogens. [NIH]
Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioassays: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biodegradation: The series of processes by which living organisms degrade pollutant chemicals, organic wastes, pesticides, and implantable materials. [NIH] Biofilms: Films of bacteria or other microbial organisms, usually embedded in extracellular polymers such as implanted medical devices, which adhere to surfaces submerged in, or subjected to, aquatic environments (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed). Biofilms consist of multilayers of microbial cells glued together to form microbial communities which are highly resistant to both phagocytes and antibiotics. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH]
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Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biomass: Total mass of all the organisms of a given type and/or in a given area. (From Concise Dictionary of Biology, 1990) It includes the yield of vegetative mass produced from any given crop. [NIH] Biometry: The use of statistical methods to analyze biological observations and phenomena. [NIH]
Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bolus: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus infusion. [NIH] Bolus infusion: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH] Bone Development: Gross development of bones from fetus to adult. It includes osteogenesis, which is restricted to formation and development of bone from the undifferentiated cells of the germ layers of the embryo. It does not include osseointegration. [NIH]
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Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone metastases: Cancer that has spread from the original (primary) tumor to the bone. [NIH]
Bone Morphogenetic Proteins: Bone-growth regulatory factors that are members of the transforming growth factor-beta superfamily of proteins. They are synthesized as large precursor molecules which are cleaved by proteolytic enzymes. The active form can consist of a dimer of two identical proteins or a heterodimer of two related bone morphogenetic proteins. [NIH] Bone Regeneration: Renewal or repair of lost bone tissue. It excludes bony callus formed after bone fracture but not yet replaced by hard bone. [NIH] Bone Remodeling: The continuous turnover of bone matrix and mineral that involves first, an increase in resorption (osteoclastic activity) and later, reactive bone formation (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium homeostasis. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as osteoporosis. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Bony Callus: The bony deposit formed between and around the broken ends of a fractured bone during normal healing. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchopulmonary: Pertaining to the lungs and their air passages; both bronchial and pulmonary. [EU] Bronchopulmonary Dysplasia: A chronic lung disease appearing in certain newborn infants
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treated for respiratory distress syndrome with mechanical ventilation and elevated concentration of inspired oxygen. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Budgets: Detailed financial plans for carrying out specific activities for a certain period of time. They include proposed income and expenditures. [NIH] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Butyric Acid: A four carbon acid, CH3CH2CH2COOH, with an unpleasant odor that occurs in butter and animal fat as the glycerol ester. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [NIH] Cadherins: A group of functionally related glycoproteins responsible for the calciumdependent cell-to-cell adhesion mechanism. They are divided into subclasses E-, P-, and Ncadherins, which are distinct in immunological specificity and tissue distribution. They promote cell adhesion via a homophilic mechanism. These compounds play a role in the construction of tissues and of the whole animal body. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcitonin: A peptide hormone that lowers calcium concentration in the blood. In humans, it is released by thyroid cells and acts to decrease the formation and absorptive activity of osteoclasts. Its role in regulating plasma calcium is much greater in children and in certain diseases than in normal adults. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Calculus I: An abnormal concretion occurring within the animal body and usually composed of mineral salts. [EU] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Candidiasis: Infection with a fungus of the genus Candida. It is usually a superficial infection of the moist cutaneous areas of the body, and is generally caused by C. albicans; it most commonly involves the skin (dermatocandidiasis), oral mucous membranes (thrush,
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def. 1), respiratory tract (bronchocandidiasis), and vagina (vaginitis). Rarely there is a systemic infection or endocarditis. Called also moniliasis, candidosis, oidiomycosis, and formerly blastodendriosis. [EU] Candidosis: An infection caused by an opportunistic yeasts that tends to proliferate and become pathologic when the environment is favorable and the host resistance is weakened. [NIH]
Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsular: Cataract which is initiated by an opacification at the surface of the lens. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbohydrate Sequence: The sequence of carbohydrates within polysaccharides, glycoproteins, and glycolipids. [NIH] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiac catheterization: A procedure in which a thin, hollow tube is inserted into a blood vessel. The tube is then advanced through the vessel into the heart, enabling a physician to study the heart and its pumping activity. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH]
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Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C
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(chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Chiropractic: A system of treating bodily disorders by manipulation of the spine and other parts, based on the belief that the cause is the abnormal functioning of a nerve. [NIH] Chlorhexidine: Disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque. [NIH] Chlorine: A greenish-yellow, diatomic gas that is a member of the halogen family of elements. It has the atomic symbol Cl, atomic number 17, and atomic weight 70.906. It is a powerful irritant that can cause fatal pulmonary edema. Chlorine is used in manufacturing, as a reagent in synthetic chemistry, for water purification, and in the production of chlorinated lime, which is used in fabric bleaching. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Chorion: The outermost extraembryonic membrane. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, chymotrypsinogen and carried in the pancreatic juice to the duodenum where it is activated by trypsin. It selectively cleaves aromatic amino acids on the carboxyl side. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and
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providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [NIH] Cleft Lip: Congenital defect in the upper lip where the maxillary prominence fails to merge with the merged medial nasal prominences. It is thought to be caused by faulty migration of the mesoderm in the head region. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clodronate: A drug used as treatment for hypercalcemia (abnormally high levels of calcium in the blood) and for cancer that has spread to the bone (bone metastases). It may decrease pain, the risk of fractures, and the development of new bone metastases. [NIH] Clodronic Acid: A diphosphonate which affects calcium metabolism. It is an effective inhibitor of bone resorption and soft tissue calcification. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coal: A natural fuel formed by partial decomposition of vegetable matter under certain environmental conditions. [NIH] Codons: Any triplet of nucleotides (coding unit) in DNA or RNA (if RNA is the carrier of primary genetic information as in some viruses) that codes for particular amino acid or signals the beginning or end of the message. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup
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characteristics. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Collagenases: Enzymes that catalyze the degradation of collagen by acting on the peptide bonds. EC 3.4.24.-. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colostrum: The thin, yellow, serous fluid secreted by the mammary glands during pregnancy and immediately postpartum before lactation begins. It consists of immunologically active substances, white blood cells, water, protein, fat, and carbohydrates. [NIH]
Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Commensal: 1. Living on or within another organism, and deriving benefit without injuring or benefiting the other individual. 2. An organism living on or within another, but not causing injury to the host. [EU] Community Health Centers: Facilities which administer the delivery of health care services to people living in a community or neighborhood. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the
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classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complement Activation: The sequential activation of serum components C1 through C9, initiated by an erythrocyte-antibody complex or by microbial polysaccharides and properdin, and producing an inflammatory response. [NIH] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Concretion: Minute, hard, yellow masses found in the palpebral conjunctivae of elderly people or following chronic conjunctivitis, composed of the products of cellular degeneration retained in the depressions and tubular recesses in the conjunctiva. [NIH] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [NIH] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH]
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Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] Conscious Sedation: An alternative to general anesthesia in patients for whom general anesthesia is refused or considered inadvisable. It involves the administering of an antianxiety drug (minor tranquilizer) and an analgesic or local anesthetic. This renders the patient free of anxiety and pain while allowing the patient to remain in verbal contact with the physician or dentist. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contraception: Use of agents, devices, methods, or procedures which diminish the likelihood of or prevent conception. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Corneal Ulcer: Loss of epithelial tissue from the surface of the cornea due to progressive erosion and necrosis of the tissue; usually caused by bacterial, fungal, or viral infection. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] Coronary Disease: Disorder of cardiac function due to an imbalance between myocardial function and the capacity of the coronary vessels to supply sufficient flow for normal function. It is a form of myocardial ischemia (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD
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results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Coronary Vessels: The veins and arteries of the heart. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cost Savings: Reductions in all or any portion of the costs of providing goods or services. Savings may be incurred by the provider or the consumer. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniofacial Abnormalities: Congenital structural deformities, malformations, or other abnormalities of the cranium and facial bones. [NIH] Criterion: A standard by which something may be judged. [EU] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Crown Lengthening: Technique combining controlled eruptive tooth movement and incision of the supracrestal gingival attachment to allow for proper restoration of a destroyed or damaged crown of a tooth. Controlled eruption of the tooth is obtained using orthodontic appliances. During this eruptive phase, repeated incisions are made at the junctional epithelium of the sulcus and the supracrestal connective tissue to prevent coronal displacement of the gingiva and of the attachment apparatus. [NIH] Crowns: A prosthetic restoration that reproduces the entire surface anatomy of the visible natural crown of a tooth. It may be partial (covering three or more surfaces of a tooth) or complete (covering all surfaces). It is made of gold or other metal, porcelain, or resin. [NIH] CSF: Cerebrospinal fluid. The fluid flowing around the brain and spinal cord. CSF is produced in the ventricles of the brain. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Curettage: Removal of tissue with a curette, a spoon-shaped instrument with a sharp edge. [NIH]
Curette: A spoon-shaped instrument with a sharp edge. [NIH] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyproterone: An anti-androgen that, in the form of its acetate, also has progestational properties. It is used in the treatment of hypersexuality in males, as a palliative in prostatic carcinoma, and, in combination with estrogen, for the therapy of severe acne and hirsutism in females. [NIH] Cysteine Endopeptidases: Endopeptidases which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH]
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Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytostatic: An agent that suppresses cell growth and multiplication. [EU] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Cytotoxins: Substances elaborated by microorganisms, plants or animals that are specifically toxic to individual cells; they may be involved in immunity or may be contained in venoms. [NIH]
Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] De novo: In cancer, the first occurrence of cancer in the body. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Defensins: Family of antimicrobial peptides that have been identified in humans, animals, and plants. They are thought to play a role in host defenses against infections, inflammation, wound repair, and acquired immunity. Based on the disulfide pairing of their characteristic six cysteine residues, they are divided into alpha-defensins and beta-defensins. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Demyelinating Diseases: Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Abutments: Natural teeth or teeth roots used as anchorage for a fixed or removable denture or other prosthesis (such as an implant) serving the same purpose. [NIH] Dental Assistants: Individuals who assist the dentist or the dental hygienist. [NIH] Dental Calculus: Abnormal concretion or calcified deposit that forms around the teeth or dental prostheses. [NIH]
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Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dental Care for Children: The giving of attention to the special dental needs of children, including the prevention of tooth diseases and instruction in dental hygiene and dental health. The dental care may include the services provided by dental specialists. [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Dental Hygienists: Persons trained in an accredited school or dental college and licensed by the state in which they reside to provide dental prophylaxis under the direction of a licensed dentist. [NIH] Dental implant: A small metal pin placed inside the jawbone to mimic the root of a tooth. Dental implants can be used to help anchor a false tooth or teeth, or a crown or bridge. [NIH] Dental Implantation: The grafting or inserting of a prosthetic device of alloplastic material into the oral tissue beneath the mucosal or periosteal layer or within the bone. Its purpose is to provide support and retention to a partial or complete denture. [NIH] Dental Plaque: A film that attaches to teeth, often causing dental caries and gingivitis. It is composed of mucins, secreted from salivary glands, and microorganisms. [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Dentition: The teeth in the dental arch; ordinarily used to designate the natural teeth in position in their alveoli. [EU] Dentures: An appliance used as an artificial or prosthetic replacement for missing teeth and adjacent tissues. It does not include crowns, dental abutments, nor artificial teeth. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Dermatitis: Any inflammation of the skin. [NIH] Desmosomes: Attachment bodies between cells such as in the corneal epithelium, which possibly allow tonofibrils to pass from cell to cell and which can degenerate to allow cells to migrate to cover a denuded area. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Dexterity: Ability to move the hands easily and skillfully. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous
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hemorrhage, and retinal detachment. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dilatation: The act of dilating. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases. [NIH] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Dispenser: Glass, metal or plastic shell fitted with valve from which a pressurized formulation is dispensed; an instrument for atomizing. [NIH] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Dosage Forms: Completed forms of the pharmaceutical preparation in which prescribed doses of medication are included. They are designed to resist action by gastric fluids, prevent vomiting and nausea, reduce or alleviate the undesirable taste and smells associated with oral administration, achieve a high concentration of drug at target site, or produce a delayed or long-acting drug effect. They include capsules, liniments, ointments, pharmaceutical solutions, powders, tablets, etc. [NIH] Doxycycline: A synthetic tetracycline derivative with a range of antimicrobial activity and mode of action similar to that of tetracycline, but more effective against many species. Animal studies suggest that it may cause less tooth staining than other tetracyclines. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given
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stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dysentery: Any of various disorders marked by inflammation of the intestines, especially of the colon, and attended by pain in the abdomen, tenesmus, and frequent stools containing blood and mucus. Causes include chemical irritants, bacteria, protozoa, or parasitic worms. [EU]
Dyspareunia: Painful sexual intercourse. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dystrophic: Pertaining to toxic habitats low in nutrients. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]
Ectopic: Pertaining to or characterized by ectopia. [EU] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Eicosanoids: A class of oxygenated, endogenous, unsaturated fatty acids derived from arachidonic acid. They include prostaglandins, leukotrienes, thromboxanes, and hydroxyeicosatetraenoic acid compounds (HETE). They are hormone-like substances that act near the site of synthesis without altering functions throughout the body. [NIH] Ejaculation: The release of semen through the penis during orgasm. [NIH] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU]
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Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Electroporation: A technique in which electric pulses of intensity in kilovolts per centimeter and of microsecond-to-millisecond duration cause a temporary loss of the semipermeability of cell membranes, thus leading to ion leakage, escape of metabolites, and increased uptake by cells of drugs, molecular probes, and DNA. Some applications of electroporation include introduction of plasmids or foreign DNA into living cells for transfection, fusion of cells to prepare hybridomas, and insertion of proteins into cell membranes. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endometriosis: A condition in which tissue more or less perfectly resembling the uterine mucous membrane (the endometrium) and containing typical endometrial granular and stromal elements occurs aberrantly in various locations in the pelvic cavity. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxemia: A condition characterized by the presence of endotoxins in the blood. If
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endotoxemia is the result of gram-negative rod-shaped bacteria, shock may occur. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [NIH] Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]
Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermolysis Bullosa: Group of genetically determined disorders characterized by the blistering of skin and mucosae. There are four major forms: acquired, simple, junctional, and dystrophic. Each of the latter three has several varieties. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Episcleritis: Inflammation of the episclera and/or the outer layers of the sclera itself. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH]
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Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal Ulcer: A sore in the esophagus. Caused by long-term inflammation or damage from the residue of pills. The ulcer may cause chest pain. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Estrogen: One of the two female sex hormones. [NIH] Estrogen Replacement Therapy: The use of hormonal agents with estrogen-like activity in postmenopausal or other estrogen-deficient women to alleviate effects of hormone deficiency, such as vasomotor symptoms, dyspareunia, and progressive development of osteoporosis. This may also include the use of progestational agents in combination therapy. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethmoid: An unpaired cranial bone which helps form the medial walls of the orbits and contains the themoidal air cells which drain into the nose. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Etidronate: A drug that belongs to the family of drugs called bisphosphonates. Bisphosphonates are used as treatment for hypercalcemia (abnormally high levels of calcium in the blood) and for cancer that has spread to the bone (bone metastases). [NIH] Etidronic Acid: A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover. [NIH] Etoposide: A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU]
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Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Facial: Of or pertaining to the face. [EU] Facial Expression: Observable changes of expression in the face in response to emotional stimuli. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femoral Neck Fractures: Fractures of the short, constricted portion of the thigh bone between the femur head and the trochanters. It excludes intertrochanteric fractures which are hip fractures. [NIH] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fertilizers: Substances or mixtures that are added to the soil to supply nutrients or to make available nutrients already present in the soil, in order to increase plant growth and productivity. [NIH] Fetal Membranes: Thin layers of tissue which surround the embryo or fetus and provide for its nutrition, respiration, excretion and protection; they are the yolk sac, allantois, amnion, and chorion. [NIH]
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Fetal Weight: The weight of the fetus in utero, which is usually estimated by various formulas based on measurements made during prenatal ultrasonography. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibronectins: Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fibula: The bone of the lower leg lateral to and smaller than the tibia. In proportion to its length, it is the most slender of the long bones. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatus: Gas passed through the rectum. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluoridation: The addition of fluorine usually as a fluoride to something, as the adding of a fluoride to drinking water or public water supplies for prevention of tooth decay in children. [NIH]
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Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH] Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species. [NIH] Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells. [NIH] Focus Groups: A method of data collection and a qualitative research tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Follicles: Shafts through which hair grows. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Frail Elderly: Older adults or aged individuals who are lacking in general strength and are unusually susceptible to disease or to other infirmity. [NIH] Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungistatic: Inhibiting the growth of fungi. [EU] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallium: A rare, metallic element designated by the symbol, Ga, atomic number 31, and atomic weight 69.72. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH]
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Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gasoline: Volative flammable fuel (liquid hydrocarbons) derived from crude petroleum by processes such as distillation reforming, polymerization, etc. [NIH] Gastric: Having to do with the stomach. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gelatinase A: A secreted endopeptidase homologous with interstitial collagenase, but which possesses an additional fibronectin-like domain. EC 3.4.24.24. [NIH] Gelatinases: A class of enzymes that catalyzes the degradation of gelatin by acting on the peptide bonds. EC 3.4.24.-. [NIH] Gels: Colloids with a solid continuous phase and liquid as the dispersed phase; gels may be unstable when, due to temperature or other cause, the solid phase liquifies; the resulting colloid is called a sol. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Library: A large collection of cloned DNA fragments from a given organism, tissue, organ, or cell type. It may contain complete genomic sequences (genomic library) or complementary DNA sequences, the latter being formed from messenger RNA and lacking intron sequences. [NIH] General practitioner: A medical practitioner who does not specialize in a particular branch of medicine or limit his practice to a specific class of diseases. [NIH] Genetic Counseling: Advising families of the risks involved pertaining to birth defects, in order that they may make an informed decision on current or future pregnancies. [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Screening: Searching a population or individuals for persons possessing certain genotypes or karyotypes that: (1) are already associated with disease or predispose to disease; (2) may lead to disease in their descendants; or (3) produce other variations not known to be associated with disease. Genetic screening may be directed toward identifying phenotypic expression of genetic traits. It includes prenatal genetic screening. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genomic Library: A form of gene library containing the complete DNA sequences present in the genome of a given organism. It contrasts with a cDNA library which contains only sequences utilized in protein coding (lacking introns). [NIH] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH]
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Geographic Locations: All of the continents and every country situated within, the United States and each of the constituent states arranged by region, Canada and each of its provinces, Australia and each of its states, the major bodies of water and major islands on both hemispheres, and selected major cities. Although the geographic locations are not printed in index medicus as main headings, in indexing they are significant in epidemiologic studies and historical articles and for locating administrative units in education and the delivery of health care. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germ Layers: The three layers of cells comprising the early embryo. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gestational Age: Age of the conceptus. In humans, this may be assessed by medical history, physical examination, early immunologic pregnancy tests, radiography, ultrasonography, and amniotic fluid analysis. [NIH] Giant Cell Tumors: Tumors of bone tissue or synovial or other soft tissue characterized by the presence of giant cells. The most common are giant cell tumor of tendon sheath and giant cell tumor of bone. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Giardiasis: An infection of the small intestine caused by the flagellated protozoan Giardia lamblia. It is spread via contaminated food and water and by direct person-to-person contact. [NIH] Gingival Hyperplasia: A pathological increase in the depth of the gingival crevice surrounding a tooth at the gum margin. [NIH] Gingival Recession: The exposure of root surface by an apical shift in the position of the gingiva. [NIH] Gingivitis: Inflammation of the gingivae. Gingivitis associated with bony changes is referred to as periodontitis. Called also oulitis and ulitis. [EU] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH]
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Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or Nacetylgalactosamine. [NIH] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH] Glycosylation: The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonads: The gamete-producing glands, ovary or testis. [NIH] Gonorrhea: Acute infectious disease characterized by primary invasion of the urogenital tract. The etiologic agent, Neisseria gonorrhoeae, was isolated by Neisser in 1879. [NIH] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the
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recipient. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-Negative Anaerobic Bacteria: A large group of anaerobic bacteria which show up as pink (negative) when treated by the Gram staining method. [NIH] Gram-Negative Bacteria: Bacteria which lose crystal violet stain but are stained pink when treated by Gram's method. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granuloma: A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Gravis: Eruption of watery blisters on the skin among those handling animals and animal products. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Guided Tissue Regeneration: The repopulating of the periodontium, after treatment for periodontal disease. Repopulation is achieved by guiding the periodontal ligament progenitor cells to reproduce in the desired location by blocking contact of epithelial and gingival connective tissues with the root during healing. This blocking is accomplished by using synthetic membranes or collagen membranes. [NIH] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Halitosis: An offensive, foul breath odor resulting from a variety of causes such as poor oral hygiene, dental or oral infections, or the ingestion of certain foods. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Behavior: Behaviors expressed by individuals to protect, maintain or promote their health status. For example, proper diet, and appropriate exercise are activities perceived to influence health status. Life style is closely associated with health behavior and factors
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influencing life style are socioeconomic, educational, and cultural. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Promotion: Encouraging consumer behaviors most likely to optimize health potentials (physical and psychosocial) through health information, preventive programs, and access to medical care. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Hemidesmosomes: An anchoring junction of the cell to a non-cellular substrate, similar in morphology to halves of desmosomes. They are composed of specialized areas of the plasma membrane where intermediate filaments bind on the cytoplasmic face to the transmembrane linkers, integrins, via intracellular attachment proteins, while the extracellular domain of the integrins binds to extracellular matrix proteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Heparin-binding: Protein that stimulates the proliferation of endothelial cells. [NIH] Herbicides: Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses, and woody plants. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes
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simplex or to herpes zoster. [EU] Herpes Zoster: Acute vesicular inflammation. [NIH] Heterodimer: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Hip Fractures: Fractures of the femur head, the femur neck, the trochanters, or the inter- or subtrochanteric region. Excludes fractures of the acetabulum and fractures of the femoral shaft below the subtrochanteric region. For the fractures of the femur neck the specific term femoral neck fractures is available. [NIH] Hirsutism: Excess hair in females and children with an adult male pattern of distribution. The concept does not include hypertrichosis, which is localized or generalized excess hair. [NIH]
Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone Replacement Therapy: Therapeutic use of hormones to alleviate the effects of hormone deficiency. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridoma: A hybrid cell resulting from the fusion of a specific antibody-producing spleen cell with a myeloma cell. [NIH] Hydrogel: A network of cross-linked hydrophilic macromolecules used in biomedical applications. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH]
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Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophilic: Readily absorbing moisture; hygroscopic; having strongly polar groups that readily interact with water. [EU] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxamic Acids: A class of weak acids with the general formula R-conhoh. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperopia: Farsightedness; ability to see distant objects more clearly than close objects; may be corrected with glasses or contact lenses. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrichosis: Localized or generalized excess hair. The concept does not include hirsutism, which is excess hair in females and children with an adult male pattern of distribution. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypochlorous Acid: HClO. An oxyacid of chlorine containing monovalent chlorine that acts as an oxidizing or reducing agent. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypogonadism: Condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. [NIH] Hypoxic: Having too little oxygen. [NIH] Ibuprofen: A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Ileostomy: Surgical creation of an external opening into the ileum for fecal diversion or drainage. Loop or tube procedures are most often employed. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH]
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Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunocompetence: The ability of lymphoid cells to mount a humoral or cellular immune response when challenged by antigen. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunodominant Epitopes: Subunits of the antigenic determinant that are most easily recognized by the immune system and thus most influence the specificity of the induced antibody. [NIH] Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunogen: A substance that is capable of causing antibody formation. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of
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neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incisor: Anything adapted for cutting; any one of the four front teeth in each jaw. [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infant, Newborn: An infant during the first month after birth. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infection Control: Programs of disease surveillance, generally within health care facilities, designed to investigate, prevent, and control the spread of infections and their causative microorganisms. [NIH] Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Informed Consent: Voluntary authorization, given to the physician by the patient, with full comprehension of the risks involved, for diagnostic or investigative procedures and medical and surgical treatment. [NIH]
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Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH]
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Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Intermediate Filaments: Cytoplasmic filaments intermediate in diameter (about 10 nanometers) between the microfilaments and the microtubules. They may be composed of any of a number of different proteins and form a ring around the cell nucleus. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Interstitial Collagenase: A member of the metalloproteinase family of enzymes that is principally responsible for cleaving fibrillar collagen. It can degrade interstitial collagens, types I, II and III. EC 3.4.24.7. [NIH] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intracellular: Inside a cell. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Introns: Non-coding, intervening sequences of DNA that are transcribed, but are removed from within the primary gene transcript and rapidly degraded during maturation of messenger RNA. Most genes in the nuclei of eukaryotes contain introns, as do mitochondrial and chloroplast genes. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Ion Transport: The movement of ions across energy-transducing cell membranes. Transport can be active or passive. Passive ion transport (facilitated diffusion) derives its energy from the concentration gradient of the ion itself and allows the transport of a single solute in one direction (uniport). Active ion transport is usually coupled to an energy-yielding chemical or photochemical reaction such as ATP hydrolysis. This form of primary active transport is called an ion pump. Secondary active transport utilizes the voltage and ion gradients produced by the primary transport to drive the cotransport of other ions or molecules. These may be transported in the same (symport) or opposite (antiport) direction. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irritants: Drugs that act locally on cutaneous or mucosal surfaces to produce inflammation; those that cause redness due to hyperemia are rubefacients; those that raise blisters are
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vesicants and those that penetrate sebaceous glands and cause abscesses are pustulants; tear gases and mustard gases are also irritants. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Isoelectric: Separation of amphoteric substances, dissolved in water, based on their isoelectric behavior. The amphoteric substances are a mixture of proteins to be separated and of auxiliary "carrier ampholytes". [NIH] Isoelectric Point: The pH in solutions of proteins and related compounds at which the dipolar ions are at a maximum. [NIH] Isoprenoid: Molecule that might anchor G protein to the cell membrane as it is hydrophobic. [NIH]
Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratoconus: A disorder characterized by an irregular corneal surface (cone-shaped) resulting in blurred and distorted images. [NIH] Keratolytic: An agent that promotes keratolysis. [EU] Keratosis: Any horny growth such as a wart or callus. [NIH] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketoprofen: An ibuprofen-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kinetics: The study of rate dynamics in chemical or physical systems. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU]
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Lactation: The period of the secretion of milk. [EU] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Laser Surgery: The use of a laser either to vaporize surface lesions or to make bloodless cuts in tissue. It does not include the coagulation of tissue by laser. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Leptospirosis: Infections with bacteria of the genus Leptospira. [NIH] Lethal: Deadly, fatal. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukoplakia: A white patch that may develop on mucous membranes such as the cheek, gums, or tongue and may become cancerous. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Levonorgestrel: A progestational hormone with actions similar to those of progesterone and about twice as potent as its racemic or (+-)-isomer (norgestrel). It is used for contraception,
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control of menstrual disorders, and treatment of endometriosis. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Likelihood Functions: Functions constructed from a statistical model and a set of observed data which give the probability of that data for various values of the unknown model parameters. Those parameter values that maximize the probability are the maximum likelihood estimates of the parameters. [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH] Lipid: Fat. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liposomes: Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins. [NIH] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lipoxygenase Inhibitors: Compounds or agents that combine with lipoxygenase and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of the eicosanoid products hydroxyeicosatetraenoic acid and various leukotrienes. [NIH] Liquor: 1. A liquid, especially an aqueous solution containing a medicinal substance. 2. A general term used in anatomical nomenclature for certain fluids of the body. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Localization: The process of determining or marking the location or site of a lesion or
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disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Logistic Models: Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor. [NIH] Longitudinal Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphokines: Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH]
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Macrophage Activation: The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants. [NIH] Macula: A stain, spot, or thickening. Often used alone to refer to the macula retinae. [EU] Macula Lutea: An oval area in the retina, 3 to 5 mm in diameter, usually located temporal to the superior pole of the eye and slightly below the level of the optic disk. [NIH] Macular Degeneration: Degenerative changes in the macula lutea of the retina. [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Malaise: A vague feeling of bodily discomfort. [EU] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports the lower teeth. [NIH] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Masticatory: 1. subserving or pertaining to mastication; affecting the muscles of mastication. 2. a remedy to be chewed but not swallowed. [EU] Matrilysin: The smallest member of the matrix metalloproteinases. It plays a role in tumor progression. EC 3.4.24.23. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Melanin: The substance that gives the skin its color. [NIH]
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Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Menarche: The establishment or beginning of the menstrual function. [EU] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Menthol: An alcohol produced from mint oils or prepared synthetically. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesoderm: The middle germ layer of the embryo. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metalloendopeptidases: Endopeptidases which use a metal, normally zinc, in the catalytic mechanism. This group of enzymes is inactivated by metal chelators. EC 3.4.24. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH]
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Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Metastatic cancer: Cancer that has spread from the place in which it started to other parts of the body. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Metronidazole: Antiprotozoal used in amebiasis, trichomoniasis, giardiasis, and as treponemacide in livestock. It has also been proposed as a radiation sensitizer for hypoxic cells. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985, p133), this substance may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [NIH] Mineralization: The action of mineralizing; the state of being mineralized. [EU] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitotic: Cell resulting from mitosis. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mode of Transmission: Hepatitis A [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU]
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Molecular Probes: A group of atoms or molecules attached to other molecules or cellular structures and used in studying the properties of these molecules and structures. Radioactive DNA or RNA sequences are used in molecular genetics to detect the presence of a complementary sequence by molecular hybridization. [NIH] Molecular Structure: The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Moths: Insects of the suborder Heterocera of the order Lepidoptera. [NIH] Motility: The ability to move spontaneously. [EU] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucositis: A complication of some cancer therapies in which the lining of the digestive system becomes inflamed. Often seen as sores in the mouth. [NIH] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Multiple Organ Failure: A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [NIH] Muscle relaxant: An agent that specifically aids in reducing muscle tension, as those acting at the polysynaptic neurons of motor nerves (e.g. meprobamate) or at the myoneural junction (curare and related compounds). [EU]
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Muscle Spindles: Mechanoreceptors found between skeletal muscle fibers. Muscle spindles are arranged in parallel with muscle fibers and respond to the passive stretch of the muscle, but cease to discharge if the muscle contracts isotonically, thus signaling muscle length. The muscle spindles are the receptors responsible for the stretch or myotactic reflex. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH] Myalgia: Pain in a muscle or muscles. [EU] Myasthenia: Muscular debility; any constitutional anomaly of muscle. [EU] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopia: That error of refraction in which rays of light entering the eye parallel to the optic axis are brought to a focus in front of the retina, as a result of the eyeball being too long from front to back (axial m.) or of an increased strength in refractive power of the media of the eye (index m.). Called also nearsightedness, because the near point is less distant than it is in emmetropia with an equal amplitude of accommodation. [EU]
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Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Nasal Septum: The partition separating the two nasal cavities in the midplane, composed of cartilaginous, membranous and bony parts. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Nearsightedness: The common term for myopia. [NIH] Necrotizing Enterocolitis: A condition in which part of the tissue in the intestines is destroyed. Occurs mainly in under-weight newborn babies. A temporary ileostomy may be necessary. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephropathy: Disease of the kidneys. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutrophil: A type of white blood cell. [NIH] Neutrophil Collagenase: A member of the matrix metalloproteinases that cleaves triplehelical collagens types I, II, and III. EC 3.4.24.34. [NIH]
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Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Norgestrel: (+-)-13-Ethyl-17-hydroxy-18,19-dinorpregn-4-en-20-yn-3-one. A progestational agent with actions similar to those of progesterone. This racemic or (+-)-form has about half the potency of the levo form (levonorgestrel). Norgestrel is used as a contraceptive and ovulation inhibitor and for the control of menstrual disorders and endometriosis. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Oligosaccharides: Carbohydrates consisting of between two and ten monosaccharides connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form. [NIH]
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Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve. [NIH]
Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Oral Hygiene: The practice of personal hygiene of the mouth. It includes the maintenance of oral cleanliness, tissue tone, and general preservation of oral health. [NIH] Oral Hygiene Index: A combination of the debris index and the dental calculus index to determine the status of oral hygiene. [NIH] Oral Manifestations: Disorders of the mouth attendant upon non-oral disease or injury. [NIH]
Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Organoleptic: Of, relating to, or involving the employment of the sense organs; used especially of subjective testing (as of flavor, odor, appearance) of food and drug products. [NIH]
Ornithine: An amino acid produced in the urea cycle by the splitting off of urea from arginine. [NIH] Orofacial: Of or relating to the mouth and face. [EU] Osseointegration: The growth action of bone tissue, as it assimilates surgically implanted devices or prostheses to be used as either replacement parts (e.g., hip) or as anchors (e.g., endosseous dental implants). [NIH] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoblasts: Bone-forming cells which secrete an extracellular matrix. Hydroxyapatite crystals are then deposited into the matrix to form bone. [NIH] Osteoclasts: A large multinuclear cell associated with the absorption and removal of bone. An odontoclast, also called cementoclast, is cytomorphologically the same as an osteoclast and is involved in cementum resorption. [NIH] Osteogenesis: The histogenesis of bone including ossification. It occurs continuously but particularly in the embryo and child and during fracture repair. [NIH] Osteolysis: Dissolution of bone that particularly involves the removal or loss of calcium. [NIH]
Osteolytic: Causing the breakdown of bone. [NIH] Osteomalacia: A condition marked by softening of the bones (due to impaired mineralization, with excess accumulation of osteoid), with pain, tenderness, muscular
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weakness, anorexia, and loss of weight, resulting from deficiency of vitamin D and calcium. [EU]
Osteopetrosis: Excessive formation of dense trabecular bone leading to pathological fractures, osteitis, splenomegaly with infarct, anemia, and extramedullary hemopoiesis. [NIH]
Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]
Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pamidronate: A drug that belongs to the family of drugs called bisphosphonates. Pamidronate is used as treatment for abnormally high levels of calcium in the blood. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in
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response to food in the duodenum. [NIH] Pancreatic Neoplasms: Tumors or cancer of the pancreas. [NIH] Papilla: A small nipple-shaped elevation. [NIH] Papillomavirus: A genus of Papovaviridae causing proliferation of the epithelium, which may lead to malignancy. A wide range of animals are infected including humans, chimpanzees, cattle, rabbits, dogs, and horses. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]
Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Compliance: Voluntary cooperation of the patient in following a prescribed regimen. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Pediatric Dentistry: The practice of dentistry concerned with the dental problems of children, proper maintenance, and treatment. The dental care may include the services provided by dental specialists. [NIH]
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Pelvic: Pertaining to the pelvis. [EU] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Penicillin Resistance: Nonsusceptibility of an organism to the action of penicillins. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins. [NIH] Peptide Hydrolases: A subclass of enzymes from the hydrolase class that catalyze the hydrolysis of peptide bonds. Exopeptidases and endopeptidases make up the sub-subclasses for this group. EC 3.4. [NIH] Peptide Library: A collection of cloned peptides, or chemically synthesized peptides, frequently consisting of all possible combinations of amino acids making up an n-amino acid peptide. [NIH] Pericoronitis: Inflammation of the gingiva surrounding the crown of a tooth. [NIH] Perimenopausal: The time of a woman's life when menstrual periods become irregular. Refers to the time near menopause. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Periodontal Abscess: Localized circumscribed purulent area of inflammation in the periodontal tissue. It is a derivative of marginal periodontitis and commonly associated with suprabony and infrabony pockets and interradicular involvements, in contrast to periapical abscess which is attributable to pulp necrosis. [NIH] Periodontal Attachment Loss: Loss or destruction of periodontal tissue caused by periodontitis or other destructive periodontal diseases or by injury during instrumentation. Attachment refers to the periodontal ligament which attaches to the alveolar bone. It has been hypothesized that treatment of the underlying periodontal disease and the seeding of periodontal ligament cells enable the creating of new attachment. [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontal Index: A numerical rating scale for classifying the periodontal status of a person or population with a single figure which takes into consideration prevalence as well as severity of the condition. It is based upon probe measurement of periodontal pockets and on gingival tissue status. [NIH] Periodontal Ligament: Fibrous connective tissue surrounding the root of a tooth that separates it from and attaches it to the alveolar bone. [NIH] Periodontal Pocket: An abnormal extension of a gingival sulcus accompanied by the apical migration of the epithelial attachment and bone resorption. [NIH] Periodontics: A dental specialty concerned with the histology, physiology, and pathology of the tissues that support, attach, and surround the teeth, and of the treatment and prevention of disease affecting these tissues. [NIH] Periodontist: A specialist in the treatment of diseases of the gums. [NIH] Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex.
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[NIH]
Perioperative: Around the time of surgery; usually lasts from the time of going into the hospital or doctor's office for surgery until the time the patient goes home. [NIH] Perioral: Situated or occurring around the mouth. [EU] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Periventricular Leukomalacia: Rare form of epilepsy. [NIH] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Pharmaceutical Solutions: Homogeneous liquid preparations that contain one or more chemical substances dissolved, i.e., molecularly dispersed, in a suitable solvent or mixture of mutually miscible solvents. For reasons of their ingredients, method of preparation, or use, they do not fall into another group of products. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phenytoin: An anticonvulsant that is used in a wide variety of seizures. It is also an antiarrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant
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effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators.
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It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activator Inhibitor 2: Member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Podophyllotoxin: The main active constituent of the resin from the roots of may apple or mandrake (Podophyllum peltatum and P. emodi). It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] Polylysine: A peptide which is a homopolymer of lysine. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH]
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Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Popliteal: Compression of the nerve at the neck of the fibula. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postoperative: After surgery. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predictive factor: A situation or condition that may increase a person's risk of developing a certain disease or disorder. [NIH] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Pregnancy Complications: The co-occurrence of pregnancy and a disease. The disease may precede or follow conception and it may or may not have a deleterious effect on the pregnant woman or fetus. [NIH] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Pregnancy Tests: Tests to determine whether or not an individual is pregnant. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prenatal Care: Care provided the pregnant woman in order to prevent complications, and decrease the incidence of maternal and prenatal mortality. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases
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in the population at a given time. [NIH] Prickle: Several layers of the epidermis where the individual cells are connected by cell bridges. [NIH] Prion: Small proteinaceous infectious particles that resist inactivation by procedures modifying nucleic acids and contain an abnormal isoform of a cellular protein which is a major and necessary component. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Proenzyme: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va
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and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [NIH]
Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia. [NIH]
Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right
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ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pyogenic: Producing pus; pyopoietic (= liquid inflammation product made up of cells and a thin fluid called liquor puris). [EU] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that
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the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recur: To occur again. Recurrence is the return of cancer, at the same site as the original (primary) tumor or in another location, after the tumor had disappeared. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Reentry: Reexcitation caused by continuous propagation of the same impulse for one or more cycles. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractive Power: The ability of an object, such as the eye, to bend light as light passes through it. [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see linear models) the relationship is constrained to be a straight line and least-squares analysis is used to determine the best fit. In logistic regression (see logistic models) the dependent variable is qualitative rather than continuously variable and likelihood functions are used to find the best relationship. In multiple regression the dependent variable is considered to depend on more than a single independent variable. [NIH]
Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Reinfection: A second infection by the same pathogenic agent, or a second infection of an organ such as the kidney by a different pathogenic agent. [EU] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the
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cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Replicon: In order to be replicated, DNA molecules must contain an origin of duplication and in bacteria and viruses there is usually only one per genome. Such molecules are called replicons. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Reproduction Techniques: Methods pertaining to the generation of new individuals. [NIH] Reproductive History: An important aggregate factor in epidemiological studies of women's health. The concept usually includes the number and timing of pregnancies and their outcomes, the incidence of breast feeding, and may include age of menarche and menopause, regularity of menstruation, fertility, gynecological or obstetric problems, or contraceptive usage. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]
Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH]
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Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rheology: The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and viscosity. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Ribonuclease: RNA-digesting enzyme. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Ristocetin: An antibiotic mixture of two components, A and B, obtained from Nocardia lurida (or the same substance produced by any other means). It is no longer used clinically because of its toxicity. It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]
Root Caries: Dental caries involving the tooth root, cementum, or cervical area of the tooth. [NIH]
Root Planing: A procedure for smoothing of the roughened root surface or cementum of a tooth after subgingival curettage or scaling, as part of periodontal therapy. [NIH] Rural Population: The inhabitants of rural areas or of small towns classified as rural. [NIH]
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Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Salivary Proteins: Proteins found in saliva and the salivary glands. These proteins show some enzymatic activity, but their composition varies in different individuals. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Scleritis: Refers to any inflammation of the sclera including episcleritis, a benign condition affecting only the episclera, which is generally short-lived and easily treated. Classic scleritis, on the other hand, affects deeper tissue and is characterized by higher rates of visual acuity loss and even mortality, particularly in necrotizing form. Its characteristic symptom is severe and general head pain. Scleritis has also been associated with systemic collagen disease. Etiology is unknown but is thought to involve a local immune response. Treatment is difficult and includes administration of anti-inflammatory and immunosuppressive agents such as corticosteroids. Inflammation of the sclera may also be secondary to inflammation of adjacent tissues, such as the conjunctiva. [NIH] Scleroproteins: Simple proteins characterized by their insolubility and fibrous structure. Within the body, they perform a supportive or protective function. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Scurvy: A deficiency disease due to lack of vitamin C in the diet. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes
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through the body. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Self Mutilation: The act of injuring one's own body to the extent of cutting off or permanently destroying a limb or other essential part of a body. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] Sequence Homology: The degree of similarity between sequences. Studies of amino acid and nucleotide sequences provide useful information about the genetic relatedness of certain species. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Sequestrum: A piece of dead bone that has become separated during the process of necrosis from the sound bone. [EU] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Seroconversion: The change of a serologic test from negative to positive, indicating the development of antibodies in response to infection or immunization. [EU] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Shedding: Release of infectious particles (e. g., bacteria, viruses) into the environment, for example by sneezing, by fecal excretion, or from an open lesion. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock.
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[NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Sinusitis: An inflammatory process of the mucous membranes of the paranasal sinuses that occurs in three stages: acute, subacute, and chronic. Sinusitis results from any condition causing ostial obstruction or from pathophysiologic changes in the mucociliary transport mechanism. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin Aging: The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smiling: A facial expression which may denote feelings of pleasure, affection, amusement, etc. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol
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Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Soybean Oil: Oil from soybean or soybean plant. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermatogenesis: Process of formation and development of spermatozoa, including spermatocytogenesis and spermiogenesis. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spirochete: Lyme disease. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splenomegaly: Enlargement of the spleen. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Spotting: A slight discharge of blood via the vagina, especially as a side-effect of oral contraceptives. [EU] Stabilization: The creation of a stable state. [EU]
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Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Steady state: Dynamic equilibrium. [EU] Stenosis: Narrowing or stricture of a duct or canal. [EU] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulants: Any drug or agent which causes stimulation. [NIH] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stomatitis: Inflammation of the oral mucosa, due to local or systemic factors which may involve the buccal and labial mucosa, palate, tongue, floor of the mouth, and the gingivae. [EU]
Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Structure-Activity Relationship: The relationship between the chemical structure of a
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compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups. Other factors contributing to structure-activity relationship include chemical reactivity, electronic effects, resonance, and inductive effects. [NIH] Students, Dental: Individuals enrolled a school of dentistry or a formal educational program in leading to a degree in dentistry. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts. [NIH] Subtrochanteric: Below a trochanter. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Sulfur Compounds: Inorganic or organic compounds that contain sulfur as an integral part of the molecule. [NIH] Sulfuric acid: A strong acid that, when concentrated is extemely corrosive to the skin and mucous membranes. It is used in making fertilizers, dyes, electroplating, and industrial explosives. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppuration: A pathologic process consisting in the formation of pus. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but,
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according to the general view, there is no direct contiguity. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Syncytium: A living nucleated tissue without apparent cellular structure; a tissue composed of a mass of nucleated protoplasm without cell boundaries. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synovial: Of pertaining to, or secreting synovia. [EU] Synovial Membrane: The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes synovial fluid. [NIH] Synovitis: Inflammation of a synovial membrane. It is usually painful, particularly on motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac. Synovitis is qualified as fibrinous, gonorrhoeal, hyperplastic, lipomatous, metritic, puerperal, rheumatic, scarlatinal, syphilitic, tuberculous, urethral, etc. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Tartar: A mass of calcium and magnesium salts deposited around the teeth and upon artificial dentures. [NIH] Tear Gases: Gases that irritate the eyes, throat, or skin. Severe lacrimation develops upon irritation of the eyes. [NIH] Technetium: The first artificially produced element and a radioactive fission product of uranium. The stablest isotope has a mass number 99 and is used diagnostically as a radioactive imaging agent. Technetium has the atomic symbol Tc, atomic number 43, and atomic weight 98.91. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH] Tenesmus: Straining, especially ineffectual and painful straining at stool or in urination. [EU] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid
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hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thrush: A disease due to infection with species of fungi of the genus Candida. [NIH] Thymidine: A chemical compound found in DNA. Also used as treatment for mucositis. [NIH]
Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH]
Dictionary 341
Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tooth Loss: The failure to retain teeth as a result of disease or injury. [NIH] Tooth Movement: Orthodontic techniques used to correct the malposition of a single tooth. [NIH]
Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxaemia: 1. The condition resulting from the spread of bacterial products (toxins) by the bloodstream. 2. A condition resulting from metabolic disturbances, e.g. toxaemia of pregnancy. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group
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or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [NIH] Translating: Conversion from one language to another language. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Triad: Trivalent. [NIH] Trichomoniasis: An infection with the protozoan parasite Trichomonas vaginalis. [NIH] Triclosan: A diphenyl ether derivative used in cosmetics and toilet soaps as an antiseptic. It has some bacteriostatic and fungistatic action. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumorigenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH]
Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]
Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of
Dictionary 343
metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Ultraviolet radiation: Invisible rays that are part of the energy that comes from the sun. UV radiation can damage the skin and cause melanoma and other types of skin cancer. UV radiation that reaches the earth's surface is made up of two types of rays, called UVA and UVB rays. UVB rays are more likely than UVA rays to cause sunburn, but UVA rays pass deeper into the skin. Scientists have long thought that UVB radiation can cause melanoma and other types of skin cancer. They now think that UVA radiation also may add to skin damage that can lead to skin cancer and cause premature aging. For this reason, skin specialists recommend that people use sunscreens that reflect, absorb, or scatter both kinds of UV radiation. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Uranium: A radioactive element of the actinide series of metals. It has an atomic symbol U, atomic number 92, and atomic weight 238.03. U-235 is used as the fissionable fuel in nuclear weapons and as fuel in nuclear power reactors. [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Urease: An enzyme that catalyzes the conversion of urea and water to carbon dioxide and ammonia. EC 3.5.1.5. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73. [NIH]
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Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urokinase: A drug that dissolves blood clots or prevents them from forming. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [NIH] Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilators: Any nerve or agent which induces dilatation of the blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU]
Dictionary 345
Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Vinca Alkaloids: A class of alkaloids from the genus of apocyanaceous woody herbs including periwinkles. They are some of the most useful antineoplastic agents. [NIH] Vincristine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virilization: The induction or development of male secondary sec characters, especially the induction of such changes in the female, including enlargement of the clitoris, growth of facial and body hair, development of a hairline typical of the male forehead, stimulation of secretion and proliferation of the sebaceous glands (often with acne), and deepening of the voice. Called also masculinization) [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virulent: A virus or bacteriophage capable only of lytic growth, as opposed to temperate phages establishing the lysogenic response. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Visual Acuity: Acuteness or clearness of vision, especially of form vision, which is dependent mainly on the sharpness of the retinal focus. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] War: Hostile conflict between organized groups of people. [NIH] Wart: A raised growth on the surface of the skin or other organ. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH]
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Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xanthine: An urinary calculus. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] Xerostomia: Decreased salivary flow. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yolk Sac: An embryonic membrane formed from endoderm and mesoderm. In reptiles and birds it incorporates the yolk into the digestive tract for nourishing the embryo. In placental mammals its nutritional function is vestigial; however, it is the source of most of the intestinal mucosa and the site of formation of the germ cells. It is sometimes called the vitelline sac, which should not be confused with the vitelline membrane of the egg. [NIH] Zoledronate: A drug that belongs to the family of drugs called bisphosphonates. It is used to prevent bone fractures and reduce bone pain in people who have cancer that has spread to the bone. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
347
INDEX A Abdominal, 267, 268, 320, 323, 343 Abdominal Pain, 267, 343 Aberrant, 56, 76, 184, 267 Abortion, 267, 326 Abscess, 6, 42, 267, 322 Acceptor, 267, 320, 342 Accommodation, 267, 316 ACE, 171, 267 ACE Inhibitor, 171, 267 Acetylcholine, 267, 317, 318 Acetylgalactosamine, 267, 299 Acetylglucosamine, 76, 267, 299 Acid Phosphatase, 35, 168, 267 Acne, 173, 267, 286, 345 Acoustic, 169, 267 Actinomyces, 161, 162, 267 Acupuncture Therapy, 4, 267 Adaptability, 267, 280 Adaptation, 60, 268 Adipocytes, 268, 285, 309 Adipose Tissue, 9, 268 Adjunctive Therapy, 19, 268 Adjustment, 5, 10, 15, 216, 267, 268 Adrenergic, 142, 268, 292 Adverse Effect, 48, 268, 324, 335 Afferent, 268, 309 Affinity, 268, 336 Agar, 268, 324 Age Groups, 15, 122, 268 Age of Onset, 17, 268, 343 Aged, 80 and Over, 268 Agonists, 142, 173, 268 Albumin, 268, 320 Alendronate, 160, 269 Algorithms, 196, 269, 276 Alimentary, 269, 321 Alkaline, 269, 270, 278, 340 Allantois, 269, 294 Alleles, 48, 102, 126, 269 Allogeneic, 269, 299 Allograft, 29, 269 Alpha-1, 52, 269 Alpha-Defensins, 269, 287 Alpha-helix, 269, 308 Alternative medicine, 223, 269 Alveolar Bone Loss, 4, 19, 20, 28, 47, 64, 163, 269
Alveolar Process, 269, 331 Alveoli, 269, 288, 344 Amebiasis, 269, 314 Ameliorated, 54, 172, 269 Ameliorating, 177, 269 Amino Acid Sequence, 270, 271 Ammonia, 37, 270, 343 Amnion, 270, 294 Amniotic Fluid, 270, 298 Amoxicillin, 149, 270 Ampicillin, 270 Amplification, 9, 60, 186, 270 Amputation, 216, 270 Amyloid, 158, 175, 197, 270 Anaerobic, 8, 50, 56, 148, 178, 191, 213, 270, 300 Anaesthesia, 270, 305 Anal, 270, 292, 311 Analgesic, 270, 285, 303, 308 Analogous, 78, 270, 325, 341 Analysis of Variance, 29, 270 Analytes, 196, 270 Anaphylatoxins, 270, 284 Anatomical, 156, 270, 274, 281, 291, 304, 310, 333 Androgens, 173, 270 Anemia, 142, 271, 315, 320 Anesthesia, 115, 271, 285 Aneurism, 158, 167, 175, 197, 271 Angina, 271 Anginal, 12, 271 Angiogenesis, 167, 172, 184, 189, 194, 195, 271, 312 Anhydrous, 164, 271 Animal model, 30, 51, 57, 59, 61, 64, 65, 69, 158, 175, 197, 206, 271 Anorexia, 182, 189, 195, 271, 320 Antecedent, 29, 271 Antiandrogens, 271, 275 Antibacterial, 32, 66, 68, 164, 186, 217, 271, 336, 344 Antibiotic, 7, 15, 45, 47, 54, 67, 91, 149, 156, 157, 270, 271, 277, 322, 332, 336, 340 Antibodies, 35, 40, 52, 53, 73, 74, 81, 130, 161, 162, 189, 271, 272, 274, 304, 311, 324, 334 Anticoagulant, 271, 327 Anticonvulsant, 271, 323
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Antifungal, 210, 271 Antigen-Antibody Complex, 272, 283 Antigen-presenting cell, 51, 87, 272, 287 Anti-infective, 156, 157, 272, 281, 335 Anti-inflammatory, 28, 39, 46, 62, 64, 67, 69, 90, 133, 156, 174, 272, 273, 298, 303, 308, 333 Anti-Inflammatory Agents, 62, 90, 272, 273 Antioxidant, 36, 272, 273, 320 Antiplasmin, 178, 272 Antipyretic, 272, 308 Antiseptic, 48, 272, 342 Antiserum, 272, 274 Anus, 270, 272, 277, 283 Anxiety, 272, 285 Aorta, 272, 344 Aortic Aneurysm, 158, 197, 272 Aplastic anemia, 173, 272 Apoptosis, 33, 50, 54, 116, 272 Applicability, 42, 272 Aqueous, 273, 274, 287, 309, 310 Arachidonate 15-Lipoxygenase, 273, 310 Arachidonate Lipoxygenases, 273, 310 Arachidonic Acid, 65, 168, 273, 290, 309, 310, 327 Archaea, 273, 314 Arginine, 30, 177, 270, 273, 318, 319, 342, 343 Argon, 187, 273 Aromatic, 181, 273, 281, 323 Arterial, 273, 303, 328, 339 Arteries, 11, 12, 15, 25, 27, 272, 273, 276, 285, 286, 308, 314, 316, 340 Arterioles, 273, 276, 279, 316 Artery, 9, 15, 22, 92, 109, 120, 123, 273, 286, 308, 316, 329, 331 Articular, 180, 273, 319 Ascorbic Acid, 164, 228, 273, 303 Aspartate, 125, 273 Aspartic, 193, 273, 291 Aspartic Endopeptidases, 273, 291 Aspirin, 69, 273 Assay, 35, 40, 274, 304, 332, 343 Astigmatism, 274, 330 Astringent, 48, 274 Atrium, 274, 344 Atypical, 25, 274 Autoantibodies, 76, 274 Autoantigens, 274 Autoimmune disease, 274, 315 Autologous, 177, 274
Avian, 35, 274 Avidity, 40, 52, 274 B Backcross, 48, 274 Bacteremia, 77, 156, 274 Bacterial Infections, 11, 22, 26, 32, 74, 207, 250, 254, 274 Bacterial Physiology, 268, 274 Bacterial Proteins, 31, 78, 274 Bacterial toxin, 18, 274 Bactericidal, 31, 217, 274, 293 Bacteriophage, 274, 324, 341, 345 Bacteriostatic, 274, 342 Bacterium, 26, 31, 47, 54, 58, 66, 79, 81, 178, 274 Base, 59, 60, 183, 274, 275, 287, 296, 308, 339, 343 Base Sequence, 60, 275, 296 Basement Membrane, 43, 172, 174, 180, 184, 189, 195, 275, 294, 309 Basophils, 275, 300, 309 Benign, 275, 300, 317, 333 Benzene, 157, 158, 275 Beta 2-Microglobulin, 108, 275 Beta-Defensins, 32, 40, 45, 71, 275, 287 Beta-pleated, 270, 275 Bicalutamide, 173, 275 Bile, 275, 296, 302, 310, 337 Binding Sites, 60, 275 Bioassays, 33, 69, 275 Bioavailability, 190, 275 Biochemical, 11, 22, 26, 31, 33, 35, 62, 74, 90, 269, 275, 295, 299, 309, 319 Biodegradation, 67, 275 Biofilms, 18, 37, 38, 46, 54, 183, 275 Biological response modifier, 275, 276, 306 Biological therapy, 276, 300 Biomarkers, 48, 276 Biomass, 37, 276 Biometry, 38, 276 Biotechnology, 83, 85, 204, 223, 235, 276 Bladder, 276, 284, 315, 327, 343, 344 Blood Coagulation, 276, 278, 295, 332, 340 Blood Glucose, 22, 24, 57, 151, 255, 276, 301, 306 Blood pressure, 9, 10, 12, 267, 276, 279, 303, 315, 336 Blood vessel, 267, 269, 271, 276, 279, 280, 281, 291, 298, 308, 311, 324, 335, 336, 337, 340, 344 Blot, 82, 276 Body Composition, 91, 276
Index 349
Body Fluids, 276, 290, 336, 342 Body Mass Index, 32, 276 Bolus, 77, 276 Bolus infusion, 276 Bone Density, 112, 276 Bone Development, 34, 66, 276 Bone Marrow, 35, 58, 86, 168, 272, 275, 277, 304, 311, 315, 336, 337 Bone metastases, 277, 282, 293 Bone Morphogenetic Proteins, 166, 277 Bone Regeneration, 29, 277 Bone Remodeling, 34, 82, 183, 277 Bone Resorption, 35, 64, 76, 81, 83, 109, 159, 161, 167, 176, 183, 277, 282, 293, 322 Bony Callus, 277 Bowel, 19, 107, 157, 189, 270, 277, 289, 292, 305, 307, 323, 337, 343 Bowel Movement, 277, 289, 337 Bradykinin, 277, 318 Branch, 217, 263, 277, 297, 311, 321, 328, 336, 340 Breakdown, 57, 87, 161, 164, 166, 174, 177, 182, 193, 277, 289, 297, 319 Breeding, 41, 277 Broad-spectrum, 270, 277 Bronchi, 277, 292, 341 Bronchial, 277 Bronchitis, 4, 193, 277, 281 Bronchopulmonary, 73, 277 Bronchopulmonary Dysplasia, 73, 277 Buccal, 278, 337 Budgets, 38, 278 Bulimia, 182, 278 Burns, 158, 167, 175, 197, 278 Burns, Electric, 278 Butyric Acid, 157, 158, 175, 278 C Cachexia, 182, 189, 195, 278 Cadherins, 34, 278 Calcification, 278, 282, 293 Calcitonin, 35, 77, 168, 278 Calculi, 278, 299 Calculus I, 7, 278 Callus, 278, 308 Candidiasis, 50, 53, 74, 207, 210, 278 Candidosis, 279 Capillary, 277, 279, 345 Capsular, 40, 279 Capsules, 159, 279, 289, 297 Carbohydrate, 52, 76, 78, 279, 299, 325 Carbohydrate Sequence, 78, 279 Carbon Dioxide, 279, 331, 343
Carcinogen, 279, 314, 316 Carcinogenic, 275, 279, 306, 327, 337, 342 Carcinoma, 114, 279, 286 Cardiac, 15, 279, 285, 291, 292, 316, 337 Cardiac catheterization, 15, 279 Case report, 3, 7, 70, 92, 97, 120, 279, 282 Case series, 279, 282 Case-Control Studies, 8, 77, 279, 292 Catabolism, 37, 147, 280 Catheterization, 280, 316 Causal, 8, 280, 292, 307 Cause of Death, 65, 280 Cell Adhesion, 43, 278, 280, 306 Cell Death, 33, 54, 272, 280, 293, 298 Cell Differentiation, 280, 335 Cell Division, 274, 280, 293, 300, 314, 324, 334 Cell membrane, 280, 288, 291, 307, 308, 324 Cell proliferation, 44, 280, 335 Cell Size, 280, 295 Cell Survival, 280, 300 Central Nervous System, 172, 189, 195, 196, 267, 275, 280, 296, 300, 309, 315 Cerebral, 120, 158, 175, 197, 280, 285, 292 Cerebrovascular, 279, 280 Cerebrum, 280 Cervical, 97, 102, 123, 130, 280, 332 Cervix, 267, 280 Character, 280, 287 Chemokines, 35, 70, 91, 280 Chemotactic Factors, 281, 284 Chemotaxis, 40, 281 Chemotherapy, 72, 111, 281 Chin, 281, 313 Chiropractic, 137, 281 Chlorhexidine, 68, 96, 207, 228, 281 Chlorine, 190, 281, 303 Cholesterol, 12, 18, 25, 151, 206, 275, 281, 285, 303, 310, 313, 337 Chondrocytes, 180, 281, 295 Chorion, 281, 294 Chromatin, 272, 281, 292 Chromosomal, 47, 48, 270, 281, 324 Chromosome, 97, 281, 310, 334 Chronic Disease, 13, 14, 65, 191, 278, 281, 283 Chronic Obstructive Pulmonary Disease, 5, 97, 182, 281 Chronic renal, 20, 281 Chymotrypsin, 181, 193, 281 Cirrhosis, 172, 196, 281
350
Periodontal Disease
CIS, 80, 82, 174, 281, 332 Citrus, 273, 282 Cleave, 60, 282 Cleft Lip, 238, 282 Clinical Medicine, 282, 326 Clinical study, 96, 282 Clinical trial, 16, 19, 26, 44, 63, 68, 70, 149, 151, 152, 235, 282, 285, 328, 329 Clodronate, 160, 282 Clodronic Acid, 160, 282 Clone, 74, 81, 83, 282 Cloning, 46, 75, 82, 166, 276, 282 Coagulation, 77, 276, 282, 309, 340 Coal, 275, 282 Codons, 282, 319 Coenzyme, 143, 169, 170, 273, 282 Cofactor, 5, 282, 328, 340 Cohort Studies, 282, 292 Colitis, 19, 283 Collagen disease, 283, 333 Collagenases, 172, 189, 194, 195, 283 Collapse, 174, 277, 283 Colon, 64, 283, 290, 305, 309, 343 Colostrum, 164, 283 Combination Therapy, 174, 283, 293 Commensal, 50, 55, 71, 83, 283 Community Health Centers, 238, 283 Complement, 33, 52, 76, 178, 201, 211, 270, 283, 284, 297, 306 Complement Activation, 52, 270, 284 Complementary and alternative medicine, 48, 137, 138, 145, 284 Complementary medicine, 137, 138, 284 Complementation, 47, 79, 284 Compliance, 80, 208, 284 Computational Biology, 235, 284 Conception, 267, 284, 285, 295, 326, 337 Concomitant, 53, 205, 284 Concretion, 278, 284, 287 Cone, 284, 308 Confounding, 32, 284 Congestion, 284, 293 Congestive heart failure, 189, 195, 284 Conjunctiva, 284, 305, 333 Connective Tissue Cells, 184, 284, 285 Conscious Sedation, 3, 285 Consciousness, 270, 285 Constitutional, 285, 316 Consultation, 80, 201, 285 Consumption, 4, 10, 285, 288, 318, 331 Contraception, 150, 285, 309 Contraindications, ii, 285
Contralateral, 19, 285 Control group, 12, 16, 18, 285 Conventional therapy, 285 Conventional treatment, 188, 285 Convulsions, 271, 285, 290, 326 Coordination, 285, 315 Cornea, 274, 285, 333 Corneal Ulcer, 158, 167, 172, 175, 179, 184, 189, 193, 196, 197, 285 Coronary Arteriosclerosis, 285, 316 Coronary Disease, 12, 285 Coronary heart disease, 5, 11, 13, 35, 50, 51, 113, 222, 279, 285 Coronary Thrombosis, 9, 175, 180, 286, 314, 316 Coronary Vessels, 285, 286 Cortex, 176, 286, 327 Corticosteroids, 286, 298, 333 Cost Savings, 42, 44, 286 Cranial, 286, 293, 300, 321, 323 Craniofacial Abnormalities, 237, 286 Criterion, 161, 173, 286 Cross-Sectional Studies, 8, 32, 286, 292 Crown Lengthening, 200, 286 Crowns, 286, 288 CSF, 275, 286 Cultured cells, 26, 286 Curative, 286, 340 Curettage, 5, 188, 217, 286, 332 Curette, 286 Cutaneous, 177, 278, 286, 307 Cyclic, 181, 286, 300, 318 Cyproterone, 286, 296 Cysteine Endopeptidases, 286, 291 Cytokine, 29, 53, 54, 58, 64, 70, 73, 77, 81, 182, 189, 287 Cytoplasm, 272, 275, 280, 287, 292, 300, 332 Cytoskeleton, 34, 56, 287, 306, 314 Cytostatic, 26, 287, 316 Cytotoxic, 26, 61, 174, 287, 304, 335 Cytotoxicity, 27, 287 Cytotoxins, 178, 287 D Data Collection, 186, 238, 287, 296 De novo, 82, 287 Deamination, 287, 343 Defense Mechanisms, 187, 249, 287, 306 Defensins, 40, 45, 71, 186, 269, 275, 287 Degenerative, 172, 177, 180, 189, 195, 196, 238, 287, 312, 319, 332 Deletion, 80, 82, 272, 287
Index 351
Delivery of Health Care, 22, 283, 287, 298 Demyelinating Diseases, 172, 189, 195, 196, 287 Dendrites, 287 Dendritic, 40, 54, 125, 287 Dendritic cell, 40, 54, 125, 287 Density, 32, 180, 181, 276, 287, 295, 310, 319 Dental Abutments, 287, 288 Dental Assistants, 210, 287 Dental Calculus, 131, 207, 287, 319 Dental Care for Children, 38, 288 Dental Caries, 35, 37, 41, 48, 110, 123, 150, 164, 165, 170, 205, 224, 237, 238, 288, 296 Dental Hygienists, 6, 16, 25, 108, 210, 248, 253, 288 Dental implant, 161, 164, 166, 180, 181, 200, 237, 288, 319 Dental Implantation, 161, 166, 180, 181, 288 Dental Plaque, 4, 10, 18, 20, 46, 48, 55, 83, 121, 150, 158, 164, 186, 201, 249, 288 Dentists, 9, 13, 22, 57, 179, 199, 210, 220, 236, 239, 247, 253, 288 Dentition, 22, 43, 89, 207, 211, 224, 236, 249, 288 Dentures, 253, 288, 339 Depolarization, 288, 335 Dermatitis, 49, 193, 288 Desmosomes, 34, 39, 56, 288, 301 Deuterium, 288, 302 Developed Countries, 74, 288 Dexterity, 158, 288 Diabetic Retinopathy, 57, 172, 189, 195, 196, 288, 324 Diagnostic procedure, 155, 223, 289 Dialyzer, 289, 301 Diastolic, 289, 303 Digestion, 52, 269, 275, 277, 289, 307, 310, 337 Digestive system, 153, 176, 289, 315 Digestive tract, 289, 335, 346 Dihydrotestosterone, 289, 330 Dilatation, 267, 271, 289, 327, 344 Dilation, 158, 197, 277, 289 Dimethyl, 191, 289 Diploid, 284, 289, 324 Direct, iii, 38, 40, 72, 76, 78, 81, 109, 167, 170, 179, 196, 227, 282, 289, 298, 311, 330, 339 Discrete, 47, 277, 289, 311, 339
Disease Progression, 13, 16, 19, 70, 84, 86, 87, 90, 99, 108, 110, 117, 121, 123, 124, 126, 169, 200, 208, 209, 211, 289 Disease Susceptibility, 38, 68, 71, 203, 289 Disparity, 68, 78, 289 Dispenser, 158, 159, 289 Distal, 75, 289, 328 Dosage Forms, 159, 289 Doxycycline, 139, 149, 150, 156, 157, 222, 228, 289 Drive, ii, vi, 10, 11, 12, 18, 24, 129, 200, 201, 206, 207, 208, 209, 211, 212, 289, 307, 310 Drug Interactions, 228, 290 Duct, 280, 290, 333, 337 Duodenum, 275, 281, 290, 321, 337 Dura mater, 290, 313, 320 Dyes, 270, 275, 290, 295, 338 Dysentery, 49, 269, 290 Dyspareunia, 290, 293 Dysplasia, 73, 290 Dystrophic, 290, 292 Dystrophy, 158, 175, 197, 290 E Echocardiography, 73, 290 Eclampsia, 290, 326 Ectopic, 290, 293 Edema, 288, 290, 316, 326 Effector, 267, 283, 290 Efficacy, 28, 38, 49, 68, 156, 157, 160, 161, 170, 188, 290, 342 Effusion, 290, 339 Eicosanoids, 65, 290 Ejaculation, 290, 334 Elasticity, 7, 285, 290, 335 Elastin, 283, 290, 294 Electrocoagulation, 282, 290 Electrolyte, 290, 336 Electroplating, 291, 338 Electroporation, 47, 291 Embryo, 267, 270, 276, 280, 291, 294, 298, 305, 313, 319, 325, 326, 336, 346 Embryo Transfer, 291, 326 Emphysema, 4, 193, 281, 291 Enamel, 14, 50, 97, 123, 169, 288, 291, 308 Endocarditis, 245, 279, 291 Endogenous, 27, 32, 63, 65, 158, 173, 175, 197, 274, 290, 291, 320, 341 Endometriosis, 291, 310, 318 Endopeptidases, 172, 177, 189, 195, 273, 286, 291, 313, 322, 327, 334 Endothelial cell, 18, 61, 184, 188, 291, 295, 301, 340
352
Periodontal Disease
Endothelium, 65, 188, 291, 318, 325 Endothelium, Lymphatic, 291 Endothelium, Vascular, 291 Endothelium-derived, 291, 318 Endotoxemia, 77, 291 Endotoxin, 18, 42, 77, 292, 342 End-stage renal, 281, 292 Energy balance, 292, 309 Enhancer, 292, 331 Enterocolitis, 73, 292 Enteropeptidase, 292, 342 Environmental Health, 234, 236, 292 Enzymatic, 37, 44, 55, 184, 190, 270, 278, 284, 288, 292, 313, 332, 333 Enzyme, 30, 37, 60, 70, 168, 171, 172, 180, 189, 193, 194, 225, 249, 267, 273, 282, 290, 292, 294, 300, 310, 313, 316, 325, 327, 328, 330, 332, 335, 338, 340, 341, 342, 343, 345, 346 Enzyme Inhibitors, 180, 292 Eosinophils, 292, 300, 309 Epidemiologic Studies, 18, 292, 298 Epidemiological, 8, 21, 27, 71, 79, 292, 331 Epidermal, 174, 292, 308 Epidermis, 292, 308, 327 Epidermolysis Bullosa, 171, 174, 292 Epinephrine, 268, 292, 317, 318, 343 Episcleritis, 292, 333 Epithelial Cells, 30, 31, 34, 43, 45, 50, 53, 56, 63, 70, 71, 74, 186, 191, 275, 292, 309 Epithelium, 22, 31, 34, 43, 56, 65, 186, 275, 286, 288, 291, 292, 321 Epitope, 53, 74, 78, 162, 293 Erythema, 50, 210, 293 Erythrocytes, 271, 277, 293 Esophageal, 160, 183, 293 Esophageal Ulcer, 160, 293 Esophagus, 160, 289, 293, 301, 323, 337 Estrogen, 13, 96, 109, 168, 173, 286, 293 Estrogen Replacement Therapy, 173, 293 Ethanol, 293, 294 Ether, 273, 293, 342 Ethmoid, 157, 293, 321 Ethnic Groups, 251, 293 Etidronate, 160, 293 Etidronic Acid, 160, 293 Etoposide, 174, 293 Eukaryotic Cells, 53, 293, 305 Excitation, 293, 295, 317 Exogenous, 36, 70, 291, 293, 343 Extensor, 294, 328
Extracellular Matrix, 30, 34, 43, 56, 57, 75, 171, 175, 184, 284, 294, 295, 301, 306, 312, 319 Extracellular Matrix Proteins, 171, 294, 301, 312 Extracellular Space, 294 Extraction, 8, 169, 177, 294 F Facial, 17, 161, 177, 286, 294, 335, 345 Facial Expression, 294, 335 Family Planning, 235, 294 Fat, 268, 273, 276, 277, 278, 283, 285, 294, 309, 310, 315, 326, 332, 336, 342 Fatigue, 294, 301 Fatty acids, 269, 290, 294, 299, 310, 327, 335 Femoral, 294, 302 Femoral Neck Fractures, 294, 302 Femur, 294, 302 Fermentation, 37, 294 Fertilization in Vitro, 294, 326 Fertilizers, 294, 338 Fetal Membranes, 172, 189, 196, 294 Fetal Weight, 63, 295 Fetus, 267, 276, 294, 295, 326, 336, 337, 344 Fibrin, 272, 276, 295, 325, 340, 341 Fibrinogen, 30, 35, 73, 178, 295, 325, 340 Fibroblast Growth Factor, 166, 295 Fibroblasts, 26, 33, 99, 177, 180, 184, 285, 295, 307 Fibronectins, 294, 295 Fibrosis, 193, 295, 333 Fibula, 295, 326 Fistula, 117, 295 Flatus, 295, 297 Flow Cytometry, 33, 295 Fluorescence, 50, 295 Fluorescent Dyes, 295 Fluoridation, 100, 238, 295 Fluorine, 295, 296 Flutamide, 173, 296 Foam Cells, 18, 296 Focus Groups, 80, 296 Fold, 53, 83, 162, 173, 296 Follicles, 296 Forearm, 276, 296 Fractionation, 48, 296 Frail Elderly, 212, 296 Frameshift, 296, 343 Frameshift Mutation, 296, 343 Free Radicals, 131, 272, 296, 316
Index 353
Fungi, 26, 157, 186, 271, 296, 300, 314, 340, 346 Fungistatic, 296, 342 Fungus, 278, 296 G Gallbladder, 267, 289, 296 Gallium, 96, 296 Ganglia, 267, 296, 317, 323 Gas, 187, 236, 270, 273, 279, 281, 295, 296, 297, 302, 316, 318, 344 Gasoline, 275, 297 Gastric, 174, 270, 289, 297, 301 Gastrin, 297, 302 Gastrointestinal, 157, 160, 183, 188, 277, 292, 293, 297, 309, 338, 342 Gastrointestinal tract, 157, 293, 297, 309, 342 Gelatin, 297, 299, 340 Gelatinase A, 103, 158, 197, 297 Gelatinases, 172, 189, 194, 195, 297 Gels, 190, 297 Gene Expression, 29, 32, 45, 55, 64, 67, 111, 148, 176, 185, 297 Gene Library, 297 General practitioner, 224, 297 Genetic Counseling, 7, 297 Genetic Engineering, 276, 282, 297 Genetic Screening, 51, 297 Genetics, 10, 47, 97, 112, 297, 315 Genomic Library, 30, 81, 297 Genotype, 78, 87, 89, 297, 323 Geographic Locations, 49, 298 Germ Cells, 298, 320, 339, 346 Germ Layers, 276, 298 Gestation, 10, 12, 14, 56, 298, 322, 336 Gestational, 21, 44, 63, 298 Gestational Age, 21, 44, 63, 298 Giant Cell Tumors, 168, 298 Giant Cells, 82, 168, 298 Giardiasis, 298, 314 Gingival Hyperplasia, 224, 298 Gingival Recession, 13, 194, 207, 298 Gland, 298, 311, 320, 321, 324, 327, 333, 337, 340 Glomerular, 172, 189, 196, 298, 331 Glomeruli, 298 Glomerulonephritis, 193, 298 Glomerulus, 298 Glucocorticoid, 161, 298 Glucose, 10, 11, 12, 37, 58, 73, 151, 273, 276, 288, 299, 301, 306, 333 Glucose Intolerance, 288, 299
Glucuronic Acid, 299, 301 Glycerol, 278, 299, 324 Glycerophospholipids, 299, 324 Glycine, 269, 299, 317, 334 Glycoprotein, 78, 272, 295, 298, 299, 309, 340, 342 Glycosaminoglycans, 104, 132, 294, 299, 328 Glycosidic, 299, 318 Glycosylation, 76, 299 Gonadal, 299, 337 Gonads, 299, 303 Gonorrhea, 70, 299 Gout, 182, 299 Governing Board, 299, 326 Grade, 4, 299 Graft, 100, 172, 189, 195, 196, 299, 302, 316 Graft Rejection, 172, 189, 195, 196, 299 Grafting, 204, 288, 300, 304 Gram-negative, 26, 29, 30, 41, 47, 79, 89, 95, 178, 186, 191, 292, 300 Gram-Negative Anaerobic Bacteria, 191, 300 Gram-Negative Bacteria, 89, 300 Gram-positive, 186, 267, 300, 337 Granulocytes, 300, 309, 335, 345 Granuloma, 209, 300 Grasses, 300, 301 Gravis, 158, 175, 197, 300 Growth factors, 59, 113, 161, 166, 182, 184, 300 Guanylate Cyclase, 300, 318 Guided Tissue Regeneration, 5, 300 H Habitat, 79, 300 Hair follicles, 180, 181, 300 Halitosis, 7, 157, 191, 196, 236, 300 Headache, 300, 305 Health Behavior, 17, 300 Health Education, 238, 252, 254, 301 Health Promotion, 6, 11, 25, 217, 301 Health Services, 38, 133, 287, 301 Health Status, 5, 71, 237, 300, 301 Heart attack, 5, 8, 9, 15, 25, 221, 279, 301 Heart failure, 158, 167, 175, 197, 301 Heartburn, 160, 301 Hemidesmosomes, 39, 43, 56, 301 Hemodialysis, 20, 121, 220, 289, 301 Hemoglobin, 42, 151, 271, 293, 301, 309 Hemorrhage, 73, 290, 300, 301, 316, 337, 345 Heparin, 67, 166, 301
354
Periodontal Disease
Heparin-binding, 166, 301 Herbicides, 196, 301 Heredity, 297, 301 Herpes, 207, 301, 302 Herpes Zoster, 302 Heterodimer, 277, 302 Heterogeneity, 61, 268, 302 Heterotrophic, 296, 302 Hip Fractures, 173, 294, 302 Hirsutism, 174, 286, 302, 303 Histology, 33, 87, 212, 302, 322 Homeostasis, 24, 34, 56, 59, 130, 176, 277, 302 Homologous, 30, 41, 269, 297, 302, 315, 334, 339 Hormonal, 5, 14, 105, 150, 179, 247, 249, 250, 293, 302 Hormone Replacement Therapy, 173, 302 Humoral, 34, 39, 42, 43, 81, 106, 107, 299, 302, 304 Humour, 302 Hybrid, 274, 282, 302 Hybridization, 35, 37, 50, 60, 302, 315 Hybridoma, 81, 302 Hydrogel, 29, 67, 302 Hydrogen, 191, 267, 274, 279, 288, 294, 302, 315, 318, 320, 323, 328 Hydrolysis, 37, 190, 273, 303, 307, 322, 324, 328, 342 Hydrophilic, 302, 303 Hydrophobic, 299, 303, 308, 310 Hydroxamic Acids, 172, 194, 195, 303 Hydroxylysine, 283, 303 Hydroxyproline, 269, 283, 303 Hypercalcemia, 159, 183, 282, 293, 303 Hypercholesterolemia, 11, 12, 117, 173, 303 Hyperglycemia, 57, 303 Hyperlipidemia, 9, 173, 303 Hyperopia, 303, 330 Hyperplasia, 209, 303 Hypersensitivity, 205, 303, 309, 332 Hypertension, 9, 10, 12, 88, 182, 279, 300, 303, 326, 340 Hypertrichosis, 302, 303 Hypertrophy, 57, 183, 303 Hyperuricemia, 299, 303 Hypochlorous Acid, 193, 303 Hypoglycemia, 24, 303 Hypogonadism, 173, 303 Hypoxic, 303, 314
I Ibuprofen, 303, 308 Id, 133, 141, 245, 256, 262, 264, 303 Ileostomy, 303, 317 Immune function, 78, 303, 304 Immune system, 29, 39, 170, 272, 276, 304, 309, 311, 315, 323, 344, 345 Immunization, 304, 334 Immunoassay, 70, 304 Immunocompetence, 26, 304 Immunodeficiency, 6, 23, 25, 43, 201, 304 Immunodeficiency syndrome, 201, 304 Immunodominant Epitopes, 74, 304 Immunoelectrophoresis, 268, 272, 304 Immunogen, 61, 304 Immunogenic, 177, 304 Immunoglobulin, 30, 271, 304 Immunohistochemistry, 35, 45, 304 Immunologic, 73, 207, 281, 298, 304, 312 Immunosuppressive, 298, 304, 333 Immunosuppressive Agents, 304, 333 Impairment, 304, 313 Implantation, 178, 228, 284, 304 In situ, 35, 45, 82, 175, 304 In Situ Hybridization, 35, 45, 82, 176, 305 In vivo, 30, 35, 39, 50, 54, 61, 62, 64, 67, 69, 70, 77, 81, 82, 166, 180, 301, 305, 320, 340 Incision, 286, 305, 307 Incisor, 120, 305 Incubation, 52, 305 Indicative, 196, 201, 305, 321, 344 Induction, 28, 50, 54, 70, 75, 109, 138, 188, 271, 305, 345 Infant, Newborn, 268, 305 Infarction, 9, 305, 331 Infection Control, 102, 239, 305 Infertility, 41, 305 Infiltration, 76, 298, 305 Inflammation, 5, 7, 9, 10, 12, 14, 17, 19, 20, 22, 28, 40, 43, 44, 52, 54, 56, 62, 64, 65, 69, 72, 73, 81, 84, 100, 115, 116, 121, 131, 132, 158, 164, 165, 171, 172, 175, 178, 179, 184, 185, 188, 189, 192, 194, 195, 196, 197, 199, 202, 205, 206, 207, 208, 267, 269, 272, 273, 277, 283, 287, 288, 290, 292, 293, 295, 298, 302, 305, 307, 309, 313, 320, 322, 325, 329, 332, 333, 337, 339, 343, 344 Inflammatory bowel disease, 19, 41, 107, 172, 182, 189, 195, 196, 305 Influenza, 157, 305 Informed Consent, 44, 237, 305
Index 355
Infusion, 168, 306, 316 Ingestion, 300, 306, 325, 340 Initiation, 24, 29, 42, 55, 65, 72, 73, 170, 187, 188, 306, 327, 341 Initiator, 83, 306 Inner ear, 306, 344 Inorganic, 82, 306, 315, 338 Insecticides, 306, 323 Insight, 25, 35, 38, 51, 59, 82, 209, 306 Insulator, 306, 315 Insulin, 9, 10, 18, 24, 57, 58, 101, 108, 151, 166, 171, 173, 189, 195, 306, 343 Insulin-dependent diabetes mellitus, 306 Insulin-like, 57, 166, 173, 306 Integrins, 301, 306 Interferon, 40, 306 Interferon-alpha, 306 Interleukin-1, 41, 84, 85, 87, 95, 98, 108, 182, 306, 307 Interleukin-10, 95, 307 Interleukin-2, 306, 307 Interleukin-6, 41, 307 Intermediate Filaments, 39, 301, 307 Intermittent, 191, 307 Interstitial, 175, 180, 184, 294, 297, 307, 331 Interstitial Collagenase, 175, 180, 297, 307 Intervention Studies, 23, 307 Intestinal, 74, 157, 190, 269, 292, 307, 346 Intestinal Mucosa, 74, 292, 307, 346 Intestine, 277, 307, 309, 337 Intracellular, 31, 33, 35, 44, 62, 81, 301, 305, 306, 307, 313, 318, 335 Intramuscular, 307, 321 Intravenous, 162, 306, 307, 321 Intrinsic, 268, 275, 307 Introns, 297, 307 Invasive, 8, 67, 169, 184, 304, 307 Ion Transport, 76, 307 Ions, 274, 290, 302, 307, 308, 315, 328 Irritants, 210, 254, 290, 307 Ischemia, 308, 316, 331 Ischemic stroke, 13, 220, 308 Isoelectric, 165, 308 Isoelectric Point, 165, 308 Isoprenoid, 181, 308 J Joint, 7, 138, 156, 161, 166, 171, 172, 173, 180, 181, 189, 195, 196, 273, 308, 319, 338, 339 K Kb, 79, 83, 234, 308 Keratin, 39, 56, 308
Keratinocytes, 45, 75, 308 Keratoconus, 172, 189, 195, 196, 308 Keratolytic, 288, 308, 325 Keratosis, 112, 308 Keto, 193, 308 Ketoprofen, 132, 308 Kidney Disease, 121, 153, 234, 247, 267, 308 Kinetics, 26, 28, 308 L Labile, 283, 308 Lactation, 283, 309 Laminin, 34, 43, 56, 75, 178, 184, 275, 294, 309 Large Intestine, 289, 307, 309, 330, 335 Larynx, 309, 341 Laser Surgery, 21, 309 Latent, 139, 309, 326 Least-Squares Analysis, 309, 330 Lectin, 76, 309, 313 Lens, 279, 309 Leptin, 58, 309 Leptospirosis, 49, 309 Lethal, 274, 309, 316 Leucine, 30, 309 Leucocyte, 269, 309 Leukocytes, 27, 51, 158, 167, 175, 188, 193, 197, 275, 277, 280, 281, 292, 300, 306, 309, 342 Leukoplakia, 239, 309 Leukotrienes, 273, 290, 309, 310 Levonorgestrel, 150, 309, 318 Libido, 173, 271, 310 Library Services, 262, 310 Life cycle, 296, 310 Ligament, 184, 185, 187, 310, 322, 327 Ligation, 54, 310 Likelihood Functions, 310, 330 Linear Models, 310, 330 Linkage, 181, 310 Lip, 282, 310 Lipid, 18, 38, 62, 64, 65, 69, 73, 296, 299, 306, 308, 310, 315, 342 Lipopolysaccharide, 18, 27, 29, 116, 138, 300, 310 Lipoprotein, 300, 310 Liposomes, 162, 310 Lipoxygenase, 167, 168, 273, 309, 310 Lipoxygenase Inhibitors, 167, 168, 310 Liquor, 310, 329 Liver, 172, 189, 196, 267, 269, 273, 275, 281, 289, 296, 299, 301, 310, 315, 343
356
Periodontal Disease
Localization, 45, 47, 79, 176, 304, 310 Locomotion, 176, 311, 324 Logistic Models, 311, 330 Longitudinal Studies, 8, 286, 311 Longitudinal study, 32, 85, 112, 121, 126, 173, 311 Lucida, 309, 311 Lymph, 210, 280, 291, 302, 311 Lymph node, 210, 280, 311 Lymphatic, 291, 305, 311, 336 Lymphatic system, 311, 336 Lymphocyte, 64, 205, 206, 272, 311 Lymphoid, 271, 286, 304, 309, 311 Lymphokines, 311, 312 Lymphoma, 90, 239, 311 Lysine, 107, 161, 177, 303, 311, 325, 342 Lytic, 311, 334, 345 M Macrophage, 29, 41, 61, 99, 125, 132, 168, 306, 311, 312 Macrophage Activation, 29, 99, 312 Macula, 312 Macula Lutea, 312 Macular Degeneration, 172, 174, 189, 195, 312 Maintenance therapy, 8, 237, 312 Malaise, 182, 210, 312 Malignancy, 159, 168, 183, 190, 312, 321 Malignant, 159, 193, 312, 315, 317, 333 Malignant tumor, 193, 312, 315 Malnutrition, 210, 269, 278, 312 Mammary, 283, 312 Mandible, 269, 281, 312, 331 Manifest, 157, 312 Mastication, 176, 312 Masticatory, 36, 312 Matrilysin, 158, 167, 197, 312 Matrix metalloproteinase, 57, 60, 157, 158, 167, 170, 171, 172, 174, 175, 182, 184, 189, 194, 195, 197, 312, 317 Maxillary, 17, 97, 157, 282, 312, 321 Medial, 282, 293, 312 Mediate, 58, 75, 82, 115, 182, 205, 312 Medical Records, 12, 312, 332 Medicament, 165, 191, 312 MEDLINE, 235, 312 Melanin, 239, 312, 323, 343 Membrane Lipids, 313, 324 Membrane Proteins, 310, 313 Memory, 271, 313 Menarche, 313, 331 Meninges, 280, 290, 313
Meningitis, 83, 313 Menopause, 168, 173, 249, 250, 313, 322, 326, 331 Menstruation, 249, 250, 313, 331 Mental, iv, 26, 153, 234, 240, 281, 294, 313, 328, 343 Mental Disorders, 153, 313 Mental Health, iv, 26, 153, 234, 240, 313, 328 Menthol, 164, 313 Mentors, 79, 313 Mercury, 295, 313 Mesoderm, 282, 313, 346 Metabolic disorder, 299, 313 Metabolite, 289, 313 Metalloendopeptidases, 171, 291, 313 Metastasis, 60, 167, 171, 172, 174, 180, 184, 189, 194, 195, 312, 313, 314 Metastatic, 57, 114, 159, 161, 166, 180, 181, 183, 184, 190, 314, 333 Metastatic cancer, 57, 190, 314 Methionine, 191, 193, 289, 314, 338 Metronidazole, 91, 149, 150, 157, 314 MI, 9, 86, 132, 157, 167, 175, 190, 197, 221, 265, 314 Microbe, 62, 314, 341 Microbiological, 28, 43, 91, 96, 124, 125, 149, 150, 314 Microfilaments, 307, 314 Microorganism, 74, 178, 282, 314, 321, 345 Micro-organism, 187, 288, 314 Microscopy, 37, 50, 275, 314 Microtubules, 307, 314 Migration, 34, 39, 43, 56, 75, 187, 188, 282, 312, 314, 322 Milliliter, 276, 314 Mineralization, 160, 314, 319 Mitosis, 272, 314 Mitotic, 293, 314 Mobility, 13, 16, 82, 156, 211, 216, 314 Mode of Transmission, 70, 314 Modification, 25, 75, 158, 175, 197, 270, 297, 314, 329 Molecular Probes, 291, 315 Molecular Structure, 315, 342 Monitor, 8, 77, 236, 315, 318 Monocyte, 31, 115, 116, 132, 168, 315 Mononuclear, 76, 168, 300, 315, 342 Morphological, 26, 291, 296, 315 Morphology, 75, 273, 301, 312, 315 Moths, 43, 315 Motility, 35, 43, 315
Index 357
Mucins, 288, 315, 333 Mucociliary, 315, 335 Mucosa, 19, 31, 54, 65, 71, 177, 210, 315, 317, 337 Mucositis, 71, 315, 340 Mucus, 290, 315, 343 Multiple Myeloma, 159, 315 Multiple Organ Failure, 193, 315 Multiple sclerosis, 137, 157, 158, 167, 172, 175, 197, 315 Multivalent, 274, 315 Muscle relaxant, 315, 323 Muscle Spindles, 316, 324 Muscular Dystrophies, 290, 316 Mustard Gas, 308, 316 Myalgia, 182, 305, 316 Myasthenia, 158, 175, 197, 316 Mydriatic, 289, 316 Myelin, 287, 315, 316 Myeloma, 302, 316 Myocardial infarction, 8, 9, 12, 15, 118, 286, 314, 316 Myocardial Ischemia, 193, 285, 316 Myocardial Reperfusion, 316, 331 Myocardial Reperfusion Injury, 316, 331 Myocardium, 314, 316 Myopia, 172, 189, 195, 196, 316, 317, 330 N Nasal Cavity, 156, 157, 317, 321 Nasal Mucosa, 305, 317 Nasal Septum, 317 Nausea, 289, 317, 343 NCI, 1, 152, 233, 282, 317 Nearsightedness, 316, 317 Necrotizing Enterocolitis, 73, 317 Neonatal, 44, 317 Neoplasia, 317 Neoplasm, 317, 333, 342 Neoplastic, 192, 311, 317 Nephropathy, 57, 308, 317 Nerve, 268, 271, 281, 287, 315, 317, 319, 320, 326, 332, 333, 337, 340, 344 Nervous System, 172, 180, 189, 195, 196, 268, 280, 317, 323, 344 Networks, 56, 317 Neural, 268, 270, 302, 317 Neurologic, 137, 317 Neuropathy, 17, 317 Neurotransmitter, 267, 270, 277, 299, 317, 318, 335, 338 Neutrophil, 32, 40, 50, 52, 62, 65, 78, 115, 121, 138, 139, 158, 167, 186, 193, 197, 317
Neutrophil Collagenase, 138, 139, 158, 167, 197, 317 Nitric Oxide, 101, 182, 318 Nitrogen, 173, 271, 273, 294, 318, 342 Norepinephrine, 268, 317, 318 Norgestrel, 309, 318 Nuclear, 29, 60, 65, 173, 293, 318, 343 Nucleic acid, 275, 302, 305, 318, 327, 329 Nucleic Acid Hybridization, 302, 318 Nucleus, 272, 275, 281, 286, 287, 288, 292, 293, 307, 315, 318, 328, 337 Nutritional Status, 4, 318 O Ocular, 172, 189, 195, 196, 318 Odds Ratio, 4, 63, 162, 318, 331 Odour, 273, 318 Ointments, 289, 318, 335 Oligosaccharides, 78, 318 Opacity, 287, 319 Open Reading Frames, 83, 319 Operon, 27, 79, 319, 327, 331 Optic Disk, 288, 312, 319 Oral Hygiene Index, 205, 319 Oral Manifestations, 16, 200, 207, 211, 212, 319 Organ Transplantation, 193, 319 Organoleptic, 8, 236, 319 Ornithine, 162, 319 Orofacial, 191, 209, 237, 319 Osseointegration, 276, 319 Osteoarthritis, 35, 77, 171, 172, 174, 179, 182, 184, 189, 195, 308, 319 Osteoblasts, 34, 45, 81, 161, 166, 182, 319 Osteoclasts, 34, 77, 82, 161, 166, 168, 182, 183, 278, 319 Osteogenesis, 276, 319 Osteolysis, 159, 183, 319 Osteolytic, 58, 161, 166, 180, 181, 319 Osteomalacia, 160, 319 Osteopetrosis, 77, 320 Otitis, 83, 320 Ovalbumin, 40, 320 Ovary, 26, 299, 320, 325, 337 Ovum, 298, 310, 320, 327, 346 Oxidants, 131, 320 Oxidation, 64, 178, 267, 272, 273, 320 Oxidation-Reduction, 320 P Pachymeningitis, 313, 320 Palate, 238, 320, 337 Palliative, 286, 320, 340 Pamidronate, 160, 320
358
Periodontal Disease
Pancreas, 267, 276, 281, 289, 306, 320, 321, 342 Pancreatic, 64, 173, 281, 320, 321 Pancreatic cancer, 173, 320 Pancreatic Juice, 281, 320 Pancreatic Neoplasms, 64, 321 Papilla, 156, 321 Papillomavirus, 239, 321 Paranasal Sinuses, 321, 335 Parasite, 51, 61, 81, 202, 321, 342 Parasitic, 290, 321 Parathyroid, 168, 321, 339 Parathyroid Glands, 321 Parathyroid hormone, 168, 321 Parenteral, 160, 168, 321 Patch, 309, 321 Pathogen, 26, 29, 30, 31, 37, 46, 54, 61, 64, 71, 74, 75, 81, 83, 305, 321 Pathologic, 28, 41, 57, 272, 279, 285, 303, 321, 328, 331, 338 Pathologic Processes, 57, 272, 321 Pathologies, 17, 35, 321 Pathophysiology, 18, 35, 77, 200, 321 Patient Compliance, 200, 321 Patient Education, 6, 24, 200, 247, 248, 252, 253, 255, 260, 262, 265, 321 Pediatric Dentistry, 80, 207, 321 Pelvic, 291, 322, 327 Pelvis, 322, 344 Penicillin, 83, 270, 322 Penicillin Resistance, 83, 322 Peptide Fragments, 30, 322 Peptide Hydrolases, 291, 322 Peptide Library, 60, 322 Pericoronitis, 209, 245, 322 Perimenopausal, 173, 322 Perinatal, 237, 322 Periodontal Abscess, 22, 209, 322 Periodontal Attachment Loss, 5, 7, 322 Periodontal Index, 12, 205, 322 Periodontal Ligament, 26, 43, 177, 185, 187, 192, 211, 248, 300, 322 Periodontal Pocket, 13, 19, 42, 50, 67, 149, 164, 179, 188, 192, 194, 199, 248, 322 Periodontics, 33, 36, 46, 48, 60, 77, 81, 105, 130, 131, 161, 206, 208, 215, 217, 237, 322 Periodontist, 10, 248, 249, 322 Perioperative, 6, 323 Perioral, 215, 323 Peripheral blood, 51, 81, 90, 96, 306, 323 Peripheral Nervous System, 287, 317, 323, 338
Peritoneal, 138, 323 Peritoneum, 323 Periventricular Leukomalacia, 73, 323 Peroxide, 164, 323 Pesticides, 196, 275, 301, 306, 323 PH, 276, 323 Phagocyte, 320, 323 Phagocytosis, 41, 323 Pharmaceutical Solutions, 289, 323 Pharmacologic, 23, 271, 323, 341 Pharynx, 83, 305, 317, 323 Phenotype, 35, 47, 78, 79, 284, 323 Phenyl, 188, 323 Phenylalanine, 323, 343 Phenytoin, 207, 323 Phospholipases, 324, 335 Phospholipids, 162, 294, 310, 313, 324 Phosphorus, 278, 321, 324 Phosphorylated, 282, 324 Phosphorylation, 58, 65, 324 Photocoagulation, 282, 324 Physical Examination, 298, 324 Physical Fitness, 88, 324 Physiologic, 18, 313, 324, 330, 331 Physiology, 28, 35, 37, 41, 49, 75, 131, 201, 254, 322, 324, 344 Pigmentation, 239, 324 Pilot study, 40, 57, 64, 91, 119, 151, 324 Pituitary Gland, 295, 324 Plants, 277, 279, 282, 287, 299, 301, 309, 315, 318, 324, 325, 326, 333, 341, 344 Plasma cells, 76, 271, 315, 316, 324 Plasmid, 29, 30, 47, 324, 344 Plasmin, 272, 324, 325, 341, 343 Plasminogen, 192, 272, 324, 325, 341, 343 Plasminogen Activator Inhibitor 2, 192, 325 Plasminogen Activators, 324, 325 Platelet Activation, 325, 335 Platelet Aggregation, 9, 18, 270, 318, 325, 340 Platelets, 318, 325, 340 Platinum, 174, 325 Pleated, 308, 325 Pneumonia, 51, 157, 206, 253, 285, 325 Podophyllotoxin, 293, 325 Poisoning, 313, 317, 325, 334 Pollen, 157, 325 Polylysine, 29, 325 Polymers, 275, 325, 328 Polymorphism, 87, 95, 121, 325 Polysaccharide, 40, 272, 325, 328
Index 359
Polyunsaturated fat, 64, 326, 340 Popliteal, 27, 326 Posterior, 270, 320, 326, 333 Postmenopausal, 32, 173, 269, 293, 320, 326 Postoperative, 252, 315, 326 Postsynaptic, 326, 335 Potentiates, 306, 326 Potentiation, 326, 335 Practicability, 326, 342 Practice Guidelines, 240, 256, 326 Preclinical, 70, 326 Precursor, 35, 84, 189, 273, 277, 290, 292, 318, 323, 325, 326, 328, 342, 343 Predictive factor, 112, 326 Predisposition, 97, 326 Preeclampsia, 113, 220, 246, 326 Pregnancy Complications, 63, 326 Pregnancy Outcome, 6, 10, 56, 252, 326 Pregnancy Tests, 298, 326 Prenatal, 12, 44, 57, 73, 291, 295, 297, 326 Prenatal Care, 12, 326 Prickle, 308, 327 Prion, 158, 175, 197, 327 Probe, 30, 43, 68, 169, 194, 322, 327 Proenzyme, 180, 185, 327 Progesterone, 309, 318, 327, 337 Progressive, 32, 44, 54, 59, 147, 177, 183, 184, 199, 280, 281, 285, 293, 300, 315, 316, 319, 325, 327, 331, 342 Projection, 287, 318, 327 Proline, 283, 303, 327 Promoter, 55, 80, 82, 95, 121, 173, 186, 327 Promotor, 327, 331 Prophylaxis, 188, 212, 245, 288, 327 Proportional, 36, 178, 327 Prospective study, 28, 56, 311, 327 Prostaglandins, 130, 273, 290, 327 Prostate, 172, 173, 276, 327, 342 Protease, 30, 83, 193, 283, 327, 341 Protease Inhibitors, 193, 327 Protein C, 30, 37, 61, 177, 178, 184, 269, 270, 274, 297, 308, 310, 327, 343 Protein Kinases, 44, 328 Protein S, 60, 75, 82, 171, 204, 276, 328, 332, 340 Proteinuria, 172, 179, 189, 195, 196, 315, 326, 328 Proteoglycan, 90, 328 Proteolytic, 43, 61, 139, 178, 180, 193, 269, 277, 283, 292, 295, 325, 328, 341, 343 Prothrombin, 328, 340
Protocol, 20, 138, 328 Protons, 302, 328, 329 Protozoa, 290, 314, 328 Proximal, 75, 158, 289, 317, 328 Psoriasis, 193, 316, 328 Psychic, 310, 313, 328, 334 Puberty, 173, 207, 249, 250, 251, 252, 328 Public Health, 28, 38, 44, 47, 49, 57, 64, 68, 71, 73, 97, 125, 178, 203, 205, 237, 240, 328 Public Policy, 235, 328 Pulmonary, 41, 200, 276, 277, 281, 285, 309, 328, 329, 344 Pulmonary Artery, 276, 328, 344 Pulmonary Edema, 281, 329 Pulse, 169, 315, 329 Pupil, 285, 289, 316, 329 Purines, 275, 329, 334 Purulent, 267, 322, 329, 344 Pyogenic, 209, 329 Pyrimidines, 275, 329, 334 Q Quality of Life, 176, 206, 329 R Race, 4, 5, 12, 57, 78, 205, 309, 314, 318, 329 Racemic, 309, 318, 329 Radiation, 295, 296, 314, 329, 343, 346 Radiation therapy, 296, 329 Radioactive, 302, 304, 315, 318, 329, 339, 342, 343 Radiography, 20, 298, 329 Radiological, 117, 329 Radiology, 86, 97, 113, 329 Randomized, 12, 41, 44, 63, 290, 329 Randomized clinical trial, 44, 329 Reactive Oxygen Species, 62, 131, 330 Reagent, 281, 330 Receptor, 27, 35, 53, 58, 61, 62, 70, 76, 89, 126, 131, 172, 173, 268, 272, 284, 330, 335 Recombinant, 26, 41, 45, 62, 81, 132, 166, 330, 344 Rectum, 272, 277, 283, 289, 295, 297, 305, 309, 327, 330 Recur, 25, 330 Reductase, 135, 181, 330 Reentry, 59, 330 Refer, 1, 18, 278, 283, 296, 301, 311, 312, 330, 341 Refraction, 169, 316, 330, 336 Refractive Power, 316, 330 Refractory, 161, 290, 330
360
Periodontal Disease
Regeneration, 22, 25, 33, 54, 104, 161, 176, 177, 194, 200, 295, 330 Regimen, 8, 290, 321, 330 Regression Analysis, 73, 330 Regurgitation, 301, 330 Reinfection, 188, 330 Relapse, 25, 330 Relative risk, 56, 330 Remission, 312, 331 Renal failure, 275, 331 Reperfusion, 193, 316, 331 Reperfusion Injury, 193, 331 Replicon, 47, 331 Repressor, 319, 331 Reproduction Techniques, 326, 331 Reproductive History, 32, 331 Respiration, 279, 294, 315, 331 Respiratory distress syndrome, 67, 193, 278, 331 Response Elements, 173, 331 Restoration, 286, 316, 331, 346 Retina, 274, 288, 309, 312, 316, 332 Retinal, 284, 289, 319, 332, 345 Retinopathy, 172, 189, 195, 196, 288, 332 Retrospective, 4, 28, 56, 86, 113, 119, 332 Retrospective study, 4, 28, 332 Reversion, 332, 343 Rheology, 11, 332 Rheumatism, 303, 332 Rheumatoid, 57, 76, 109, 111, 157, 171, 172, 174, 179, 182, 184, 189, 196, 283, 308, 320, 332 Rheumatoid arthritis, 57, 76, 109, 157, 171, 172, 174, 179, 182, 184, 189, 196, 283, 308, 332 Ribonuclease, 45, 332 Ribosome, 332, 342 Ristocetin, 332, 344 Rod, 31, 178, 267, 274, 292, 332 Rodenticides, 323, 332 Root Caries, 17, 99, 332 Root Planing, 11, 15, 19, 20, 149, 161, 164, 200, 225, 248, 254, 255, 332 Rural Population, 112, 332 S Saliva, 37, 41, 46, 59, 78, 100, 101, 104, 108, 121, 150, 163, 164, 225, 249, 251, 333 Salivary, 17, 46, 59, 78, 84, 132, 225, 288, 289, 320, 333, 346 Salivary glands, 59, 225, 288, 289, 333 Salivary Proteins, 46, 78, 333 Saponins, 333, 337
Sarcoma, 239, 333 Sclera, 284, 292, 333 Scleritis, 171, 174, 333 Scleroproteins, 308, 333 Sclerosis, 158, 175, 197, 283, 315, 333 Screening, 30, 51, 60, 70, 81, 82, 89, 138, 181, 238, 254, 282, 297, 333 Scurvy, 117, 192, 333 Sebaceous, 308, 333, 345 Sebaceous gland, 308, 333, 345 Secondary tumor, 313, 333 Secretion, 18, 45, 57, 173, 184, 302, 306, 309, 315, 333, 334, 345 Secretory, 163, 269, 333 Segmental, 161, 333 Segmentation, 333 Segregation, 34, 334 Seizures, 323, 334 Self Mutilation, 207, 334 Semen, 70, 290, 327, 334 Semisynthetic, 270, 293, 334 Senile, 320, 334 Sepsis, 172, 174, 334 Septic, 41, 172, 174, 179, 182, 188, 189, 193, 195, 196, 334 Septicemia, 41, 83, 86, 334 Sequence Homology, 186, 334 Sequencing, 30, 46, 49, 54, 60, 83, 334 Sequestrum, 210, 334 Serine, 30, 44, 193, 281, 291, 334, 341, 342 Serine Endopeptidases, 291, 334 Seroconversion, 70, 74, 334 Serologic, 304, 334 Serous, 283, 291, 334 Sex Characteristics, 271, 328, 334, 339 Shedding, 50, 334 Shock, 41, 74, 104, 132, 174, 182, 188, 189, 193, 195, 292, 334, 342 Side effect, 68, 150, 157, 160, 227, 268, 276, 303, 335, 341 Signal Transduction, 29, 35, 53, 61, 64, 65, 75, 77, 335 Signs and Symptoms, 5, 9, 14, 17, 21, 23, 70, 255, 330, 331, 335 Sinusitis, 157, 335 Skeletal, 32, 35, 139, 161, 180, 183, 271, 315, 316, 335 Skeleton, 114, 277, 294, 308, 335 Skin Aging, 172, 189, 196, 335 Skull, 183, 335, 339 Small intestine, 186, 290, 298, 302, 307, 335, 342
Index 361
Smiling, 247, 335 Smooth muscle, 65, 270, 285, 296, 335, 338 Sneezing, 334, 335 Soaps, 335, 342 Social Environment, 24, 329, 335 Sodium, 164, 299, 335, 336 Sodium Bicarbonate, 164, 336 Soft tissue, 5, 10, 17, 61, 74, 156, 185, 188, 190, 191, 200, 216, 277, 282, 298, 335, 336 Solid tumor, 172, 189, 195, 271, 336 Solvent, 275, 293, 299, 323, 336 Somatic, 302, 314, 323, 336 Soybean Oil, 326, 336 Specialist, 257, 289, 322, 336 Species, 7, 17, 26, 36, 37, 46, 49, 50, 59, 73, 89, 95, 162, 201, 267, 269, 274, 289, 292, 296, 302, 314, 319, 321, 329, 330, 334, 336, 337, 338, 340, 342, 345, 346 Specificity, 51, 60, 73, 75, 79, 211, 268, 273, 278, 291, 304, 336, 341 Spectrum, 24, 26, 45, 49, 157, 336 Sperm, 271, 281, 325, 336 Spermatogenesis, 173, 336 Spinal cord, 158, 175, 197, 280, 281, 286, 290, 313, 317, 320, 323, 336 Spinous, 292, 308, 336 Spirochete, 49, 61, 105, 336, 339 Spleen, 302, 311, 336 Splenomegaly, 320, 336 Spontaneous Abortion, 326, 336 Spotting, 150, 336 Stabilization, 323, 336 Stasis, 177, 337 Statistically significant, 5, 12, 15, 337 Steady state, 35, 337 Stenosis, 15, 337 Sterile, 157, 321, 337 Sterility, 305, 337 Steroid, 76, 333, 337 Stillbirth, 326, 337 Stimulants, 32, 337 Stimulus, 290, 293, 337, 340 Stomach, 157, 267, 289, 293, 297, 302, 317, 323, 335, 336, 337 Stomatitis, 23, 210, 337 Stool, 283, 309, 337, 339 Strand, 159, 337 Streptococcal, 161, 162, 337 Streptococci, 46, 83, 162, 337 Streptococcus, 46, 54, 55, 83, 121, 162, 337 Stress, 5, 19, 24, 33, 53, 65, 74, 92, 107, 120, 148, 210, 250, 252, 317, 326, 332, 337
Stricture, 337 Stromal, 168, 291, 337 Stromal Cells, 168, 337 Structure-Activity Relationship, 69, 337 Students, Dental, 80, 338 Subacute, 305, 335, 338 Subclinical, 50, 72, 84, 107, 305, 334, 338 Subcutaneous, 58, 166, 268, 290, 321, 338 Subspecies, 336, 338 Substance P, 313, 332, 333, 338 Substrate, 34, 60, 163, 168, 178, 292, 301, 310, 338 Substrate Specificity, 178, 338 Subtrochanteric, 302, 338 Sulfur, 7, 126, 191, 294, 314, 338 Sulfur Compounds, 7, 126, 191, 338 Sulfuric acid, 187, 338 Superoxide, 66, 338 Supplementation, 96, 338 Suppression, 57, 86, 167, 338 Suppuration, 237, 338 Survival Rate, 74, 338 Symphysis, 281, 327, 338 Symptomatic, 23, 338 Synapse, 268, 338, 339 Synaptic, 317, 335, 339 Syncytium, 298, 339 Synergistic, 27, 48, 164, 339 Synovial, 298, 339 Synovial Membrane, 339 Synovitis, 182, 339 Syphilis, 49, 339 Systemic, 6, 7, 11, 12, 13, 14, 18, 23, 24, 25, 26, 27, 32, 42, 43, 44, 45, 46, 48, 50, 53, 56, 59, 61, 73, 74, 78, 84, 92, 96, 106, 111, 122, 133, 141, 151, 157, 168, 176, 191, 200, 206, 208, 210, 212, 224, 228, 237, 238, 247, 250, 252, 254, 256, 272, 276, 279, 283, 292, 305, 329, 333, 334, 336, 337, 339 Systolic, 303, 339 T Tachycardia, 274, 339 Tachypnea, 274, 339 Tartar, 247, 248, 339 Tear Gases, 308, 339 Technetium, 131, 339 Temporal, 32, 35, 37, 77, 82, 312, 339 Tendon, 298, 339 Tenesmus, 290, 339 Testicular, 173, 339 Testis, 299, 339
362
Periodontal Disease
Testosterone, 330, 339 Tetany, 321, 339 Tetracycline, 47, 67, 94, 130, 156, 157, 161, 228, 289, 340 Therapeutics, 39, 65, 217, 229, 340 Threonine, 44, 334, 340 Threshold, 303, 340 Thrombin, 193, 295, 325, 327, 328, 340 Thrombolytic, 325, 340 Thrombomodulin, 327, 340 Thrombosis, 9, 120, 306, 328, 337, 340 Thromboxanes, 273, 290, 340 Thrombus, 286, 305, 308, 316, 325, 340 Thrush, 207, 278, 340 Thymidine, 45, 340 Thyroid, 278, 321, 340, 343 Thyroid Gland, 321, 340 Tin, 325, 340 Tinnitus, 320, 340 Tissue Distribution, 278, 341 Tissue Plasminogen Activator, 36, 192, 341 Tomography, 276, 341 Tone, 319, 341 Tooth Loss, 6, 17, 20, 32, 35, 42, 51, 56, 64, 66, 112, 119, 120, 126, 139, 156, 160, 161, 164, 177, 192, 208, 216, 220, 224, 237, 238, 247, 250, 254, 255, 341 Tooth Movement, 286, 341 Tooth Preparation, 268, 341 Topical, 94, 123, 130, 168, 191, 238, 274, 281, 293, 335, 336, 341 Toxaemia, 326, 341 Toxic, iv, 66, 68, 274, 275, 287, 290, 300, 304, 317, 325, 341, 344 Toxicity, 290, 313, 332, 341 Toxicology, 236, 341 Toxin, 26, 93, 292, 341 Trachea, 186, 277, 309, 323, 340, 341 Transcription Factors, 82, 331, 341 Transduction, 53, 75, 335, 341 Transfection, 29, 39, 53, 82, 276, 291, 341 Transferases, 299, 341 Translating, 6, 342 Translation, 38, 79, 269, 342 Translocation, 33, 342 Transplantation, 281, 291, 304, 342 Trauma, 4, 158, 175, 177, 197, 209, 300, 340, 342 Treatment Outcome, 50, 342 Triad, 123, 141, 193, 342 Trichomoniasis, 314, 342
Triclosan, 122, 342 Tricyclic, 145, 197, 342 Triglyceride, 151, 342 Trypsin, 30, 178, 193, 281, 292, 327, 342 Tryptophan, 283, 342 Tumor marker, 276, 342 Tumor Necrosis Factor, 9, 18, 41, 53, 174, 182, 194, 342 Tumorigenic, 64, 342 Tumour, 132, 342 Tunica, 315, 342 Type 2 diabetes, 9, 11, 23, 103, 151, 342 Typhimurium, 74, 343 Tyrosine, 77, 343 U Ulcer, 207, 220, 293, 343 Ulceration, 171, 174, 192, 194, 343 Ulcerative colitis, 19, 172, 182, 305, 343 Ultrasonography, 295, 298, 343 Ultraviolet radiation, 335, 343 Unconscious, 287, 303, 343 Uranium, 339, 343 Urea, 37, 319, 343 Urease, 37, 343 Uremia, 20, 331, 343 Urethra, 327, 343, 344 Uric, 299, 303, 329, 343 Urinary, 278, 341, 343, 344, 346 Urinary Plasminogen Activator, 341, 343 Urine, 57, 275, 276, 328, 343, 344 Urogenital, 299, 344 Urokinase, 325, 344 Uterine Contraction, 23, 267, 344 Uterus, 172, 267, 280, 313, 327, 344 V Vaccine, 42, 81, 328, 344 Vagina, 279, 280, 313, 336, 344 Vaginal, 63, 344 Vaginitis, 279, 344 Vancomycin, 83, 344 Vascular, 12, 15, 18, 73, 77, 120, 126, 168, 188, 291, 305, 318, 325, 340, 344 Vasculitis, 23, 344 Vasodilators, 145, 318, 344 Vasomotor, 173, 293, 344 Vector, 47, 341, 344 Vegetative, 276, 344 Vein, 188, 307, 318, 344 Venereal, 339, 344 Venoms, 287, 344 Venous, 177, 328, 344 Ventilation, 278, 344
Index 363
Ventricle, 88, 329, 339, 344 Ventricular, 158, 197, 220, 316, 344 Venules, 276, 279, 291, 345 Vertebrae, 336, 345 Vertigo, 320, 345 Veterinary Medicine, 130, 131, 235, 345 Vinca Alkaloids, 345 Vincristine, 174, 345 Viral, 35, 50, 71, 285, 295, 298, 305, 341, 342, 345 Virilization, 174, 345 Virulence, 26, 30, 31, 37, 46, 53, 55, 58, 61, 74, 75, 81, 83, 89, 99, 178, 341, 345 Virulent, 31, 37, 83, 178, 345 Virus, 6, 23, 25, 43, 207, 274, 292, 297, 298, 306, 307, 324, 341, 345 Viscosity, 332, 345 Visual Acuity, 333, 345 Vitreous, 288, 309, 332, 345 Vitreous Hemorrhage, 289, 345 Vitro, 29, 30, 34, 35, 37, 39, 49, 50, 51, 54, 55, 57, 62, 65, 67, 70, 81, 82, 147, 166, 168, 291, 301, 305, 332, 345
Vivo, 31, 35, 39, 64, 70, 345 W War, 10, 316, 345 Wart, 308, 345 Weight Gain, 12, 345 White blood cell, 15, 271, 283, 309, 311, 315, 316, 317, 324, 345 Windpipe, 323, 340, 345 Womb, 344, 346 X Xanthine, 188, 346 Xenograft, 271, 346 Xerostomia, 224, 237, 238, 249, 346 X-ray, 57, 179, 276, 295, 318, 329, 346 Y Yeasts, 279, 296, 323, 346 Yolk Sac, 294, 346 Z Zoledronate, 160, 346 Zymogen, 281, 327, 346
364
Periodontal Disease