Contents Section I. Diagnostic and Descriptive Terminology Macule. Patch. ErOSIon. Ulcer. Wheal. SCar. FISSUre.
2
SinuS
Papule. Plaque. Nodule. Tumor. Vesicle. Pustule, Bullil. Cyst
Section II. Oral Conditions Affecting Infants and Children
7
Section III.
Conditions Pecull.ar to the Up Actinic Cheilitis (Solar Elastosis). Monilial CheilitiS. Angular Cheilitis {PerJecheJ. ExfoliatIVe CheilitIS
34
P.r.aul Swellings
Congenital EpullS of the NevvtX:II'n. MelClnotlC
BOdl
32
4
Neuroectodermal Tumor of Infancy. Dental Lamina Cysts. Natal Teeth. GingIVal Eruption Cyst lEruption Hemat()ll"l
Nodules of the Up Mucocele {Mucous Retention Phenomenon, Mxous RetentJon Cyst). Accesscxy salivary Gland Tumor. Nasolabial CYSI {Nasoalveolar Cyst). ImplantatIOn Cyst (EpltheliallncJusl()(l Cystl. Me
8
,1
Abnormalities by Anatomic Location
Palatal Tori (Torus Palatinus), Incisive Canal Cyst INasopala!ine Duct Cyst), Periapical ,Abscess. Benign LymphOid Hyperplasia /Follicular lymphoid HyperplaSia)
36
Necroozlng SIaJometapiasla, Benign Accessory Salivary Gland Neoplasm, Malignant Accessory Salivai)' Gland Neoplasm, Primary lymphoma of the Palate
38
AJterations In Tooth Morphology Microdontla and Macrodontia. FUSion and Gemination.
Swellings of the Floor of the Mouth
Dens Invagmatus IDens In lleong's Tuberclel
Demloid CYSl Ranula /MucOCele of the Sublingual Gland). salivai)' Calcu~. Mucous Retention Phenomenon
Demel and Dens Evaglnarus t2
40
Alt.'iltlons In Numbers of Teeth Hypodontia. HyperdOntia. Cleidocranial Dysplasia. Gardner's Syndrome
14
Alt.rations In Tooth Structure Enamel Hypoplasia. Amefogenesis Imperfeeta. DentJnogene5'S Imperfeaa. Dentin DysplaSIa
16
Acquired Defects of Teeth Caries. Pulp Polyp. Attrition. Abrasion. Erosion
18
LocaUzed Glngtval Lesions Pyogefllc Granuloma. Peripheral GIiirlt Cell GranulOma. PerIpheral FlbrorTIa WIth CalCification (Peripheral Cemenl~fying Fibro~/. Gingival Carcino~. Parulis (Gumboil). Pericoronitis /OperculitiS). Periodontal Abscess. Epulis Fissuratum {Irri(aoon Hyperplasia)
20
22
Conditions Peculiar to the Tongue Normal Tongue Anatomy. Fissured Tongue {Plicated Tongue, SCrotal Tongue!, Ankyloglossia, lKlgual Yancosity rPhlebectasiaJ
42
SCalloped Tongue ICremated Tongue!. Macroglossia, H.my Tongue ILJngua Villosa. Coated Tongue). Hairy leukoplakia
44
GeographIC Tongue lBenign MigratOl}' GlossitJs, Erythema Migrans. Wandeong Rashl, Anerma. Xerrntorma
46
fv1edian Rhomboid GlossJliS (Central PapillaI}' IWophy of the Tonguel. Granular Cell Tumor (Granular Cell MyobIastomaj, Ungual Thyroid, Cym of B1andin-Num IUnguaI Mucous Retention Cyst)
48
Gener.nzlRd Gingival Enlargements
Section f\I.
Hereditary FibromatOSIS GingNae. Dr'ug-{nduced Gingival Hyperplasia. Mouthbreathing, Gingival Ede~ of Hypothyroidism
Intraoral Findings by Color Changes 24
Gingivitis GingMtis, Acute NecrooZJr"IQ UJcerauve GingIVitis. ActinomycotIC GingMtlS. Honnonal GingivitIS (Pregnancy GingivitIS), Diabetic Gingivitis
26
Spont.aneGus Gingival BI. .dlng Leukemic GingivitiS. AgranUlocytosis (Neutropenia/ and Cyclic Neutropenia, ThtQmbotytopenic and TlYombocytopathic Purpura
28
sw.mngs of the Up AnglC)edema /tVlgioneurotic Edema), Cheilitis Glandularis. Cheilitis Granulomatosa, Trauma. Cellulitis
30
51
White Lesions Fordyce's Granules. Linea,AJba Buccalis, LeuKoedema. Morsic:atio Buccarum IMucosal Cha.vingJ
52
White Sponge Nevus IFamll.ia1 \Mlite Folded DysplaSI3!. TraumatIC WhIte lesions V
54
TalNtco Assod.ted White Lesions Cigarette KeralOSls, Nicotine StomatilJS {Pipe Smokm Palate). Snuff Dipper'S Patch (Tobacco Che'vver's ~~ion. Snuff Keratosis), Vefrucous Carcinoma (of Ackerman/IOral Florid PapiliomatosiSl
56
XIII
Red Lesions Purpura Wetechiae, EcChymoses. Hematoma). Varicosity (Varix). Thrombus. Hemangioma
58
HeredJtary Hemorrhagic: Telangieaa5ia fRendu-OsIer-VleberJ. Sturge-Weber Syndrome (Encepl1alOtrigemlnal AnglOffiCltosis)
60
Red tlnd RedlWhite Lesions Erythroplakia. EryrhroIeukoplakia and Speckled Erythroplakia. Squamous Cell carcinoma
62
lichen Planus. ElecUogalvanic White lesfO(l
64
lupus Erythematosus. lKhenoid and lupus-like Drug Eruption
66
Acute Pseudomembranous Candidiasis (Thrush), Chronic Keratotic Candidiasis IHyperplasricl. Acute Atrophic candidiasis jAntlbiotic Sore Mouth). Angular Cheili£ls, Chronic Atrophic candidiasis /Demure StomatinS)
68
Varicella (Chickenpox), Herpes Zoster (Shingles). Hand-foot-and-Mouth Disease
86
Allergic Reactions
88
Erythema MultJforme. Stevens-Johnson Syndrome
90
Pemphigus \AJlgans, Benign Mucous Membrane (Cicatricial). Pemphigoid and Bullous PemptligOld
92
UlceratIve Lesions Traumatic Ulcer. Recurrent fl,phthous Stomatitis. IMinor Aphthae, Aphthous Ulcer). Pseudoaphthous Ulcer
94
Major Aphlhous lPenadenltis Mucosa NecfOtlCa Recurrens /PMNRj. Sunon's Disease, SCanfylng Stomatitis. Recurrent SCarring Aphthous UlCer). Herpetiform Ulceration. Behcet's Syndrome IOCulo-Oral-Genital Syndrome)
96
Granulomatous Ulcer. Squamous Cell carcinoma. Cherno£herapeutJC Ulcer
98
Pigmented Lesions Melanoplakia, Tattoo, Ephelis [Freckle). Smoker's Melanosis (TobacCo-Associated Pigmentation)
70
Oral Melanotic Macule. Nevus. Mallgnam Melanoma
72
Section VI. Sexually Related and Infectious Conditions
101
Sexually Related tlnd Infectious Conditions Peutz-Jeghers Syndrome /Hereditary Intestinal PoIyposisj. Add1SOfl'S DIsease !Adrenal Cortical JnsufficlO1C}1. Heavy Metal PIgmentatIOn
Section \f. Intraoral Findings by Surface Change
Traumatic Conditions. sexually Transmiaed Pharyngitis, InfectIoUS Mononucleosis. Syphilis
74 77
Irritation Fibroma and Peripheral OdontogenJC Fibroma, Upoma, Upofibroma. Traumatic Neuroma /Amputation Neuroma). Neurofibroma
104
Oral Viral Infections. Oral N'ialignancles
106
Appendices
Appendix I Rx Abbreviations
109
78
Appendix II Therapeutic Protocols
113
80
Appendix III Guide to Diagnosis and Management of Common Oral
Papulonodules Paprlloma ISquamous Paprlloma), Verruca \ll.Jlgans, CondylOma Acuminarum jVenereal Wart!,
lymphangioma
HIV Infection ilnd AIDS Oral Baaerlcll Infections. Oral Fungal Infections
I
NOdules Rettoeuspid Paprlla, lymphoepithelial C~ Torus, Exostosis and Osteomar
82
XIV
84
~s1ons
125
Appendix IV self-Assessment Quiz
141
Appendix V Glossary
147
VesiculobuJlous Lesions Primary Herpetic Gingivostomatitis, Recurrent Herpes Simplex.. Herpangina
102
I Index
161
DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY Macule IFig. 1-1) A macule is a circumscribed area of epidermis or mucosa dislinguished by color from its surroundings. The macule may appear as a slain or spot that is blue. brown. or black in color. This lesion is neither elevated nor depressed and may be of any size. MOSI frequently the tenn "macule" is reserved for lesions I em or smaller. The oral melanotic macule is an example of this condilion.
Wheal (Fig. 1-5) A wheal is an edematous papule or plaque that results from acute extravasation of serum into the upper dennis. Generally. wheals are pale red. pruritic. and of shorl duration: they often occur in allergic individuals. Wheals may be seen following insect bites. an allergic reaction to food. or mechanical irritation such as in patients who have dennatographia.
Patch IFig. 1·21 A patch is a circumscribed area that is larger than the macule and differentiated from the surrounding epidennis by color, or lexture, or both. Like the macule, the patch is neither elevated nor depressed. Lichen planus. mucous parch of secondary syphilis, and snuff dipper's patch represent patch.like lesions that may be seen immorally.
Scar (Fig. '-6) A scar is a permanent mark or cicatrix remaining after a wound heals. These lesions are visible signs that indicate a disruption in the integrity of the epidennis and dermis. Scars are infrequently found in the oral cavity, but may be of any shape or size. The color of an intraoral scar is usually lighter than the adjacent mucosa. Periapical surgery or intraoral trauma may induce scar fonnation.
Erosion (Fig. 1-31 Erosion is a clinical term that describes a soft tissue lesion in which the epithelium above !he basal cell layer is denuded. Erosions are moist. slightly depressed. and often result from a broken vesicle or Inuma. Healing rarely results in scaning. Pemphigus is a chsease that proctuces mucocutaneous erosions.
Ulcer (Fig. 1-41 An ulcer is an uncovered wound of cutaneous or mucosal tissue that exhibits gradual tissue disintegration and necrosis. Ulcers extend beyond the basal layer of the epithelium and into the dennis: thus scarring may follow healing. Ulcers may result from aphthous stomatitis. or infection by viruses such as herpes simplex. variola (smallpox), and varicella zoster (chickenpox and shingles). Ulcers are usually painful and often require topical drug therapy for effective management
2
Fissure (Fig. 1-71 A fissure is a normal or abnormal linear cleft in the epidermis that typically affects the lips and perioral tissues. When pathogenic organisms infect a fissure pain. ulceration. and innammation often result. Angular cheilitis and exfoliative cheilitis are examples of this condition.
Sinus fFig. 1·81 A sinus is an abnonnal tract or fistula that leads from a suppurative cavity, cyst, or abscess to the surface of the epidermis. An abscessed tooth ohen produces a sinus tract together with a clinically evident parulis. which is the terminal end of the sinus. Actinomycosis is a condition characterized by multiple sinus tracts that appear yellow in color.
DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY
...---------....,
Macule
t""tg. 1-1. Macule. A (l((umscnbed area of epIdeft11lS II'.e1!'d 11"I cokr from its surroundIngS
Erosion
Fig. 1·3. Erosion. AdenudatJOn of epithelium abOve
-ne basal celllayff.
Wheal/~~
Fig. 1-5. Wheal. A plnk·red. edematous. serufT'l.filJed
papule or plaque
Fissure
Fig. 1·7. Fissure. A linear crack In the eptdemlts
Patch
Fig. 1-2. Patch. A (Jrcumscnbed plgmenled or textured area larger Chan the macule.
Ulcer
Fig. 1-4. Ulcer. A los! of epttheIum that extends /:leIoIN' the basal cell layer
Scar /
_
Fig. 1-6. Scar. A permanent mark inchcatrve of prevIOUs INOUnd healing
Sinus
Fig. 1-8. Sinus. A tract leading from a suppuratNe Cavity. cyst or abscess..
3
DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY Papule fFig. 2-1 J A p;tpule is a superficial. elev3tl'd. solid lesion thai i~ smaller than I em in diameter. Papules may be of any color and may be attached by a stalk or firm
base. Examples of papules include the following conditions: condyloma acumm:uum. parulis. and squamous
papilloma.
Plaque {Fig. 2-21 A plaque is a flar. solid. raised area that is greater than I em in diameter. Though essentially superficial. plaques may extend deeper into the dermis Ihan papules. The edges may be sloped. and sometimes surface keratin proliferates. a condition known as lichenification. Lichen planus. leukoplakia or melanoma may initially
appear as a plaque.
Nodule (Fig. 2-3) A nodule is a solid mass of tissue that has the dimension of depth. like papules. these lesions are less than I em in diameter. but nodules extend dttper inlO the dermis. Palpalion provides deleclion of the nodule. The overlying epidermis is usually non·fixed and can be easily moved over the lesion. Benign mesenchymallUmors such as Ihe fibroma. lipoma. lipofibroma. and neuroma often appear as oral nodules.
Tumor /Fig. 2-41 "Tumor" is a term used to represent a !ootid mass of tissue larger than I em in diameter. The term is also used to represent a neoplasm - a new. independent growth of tissue with uncontrolled and progressive mulliplicution of cells that have no physiologic use. Tumors may be of any color and may be located in any intraoral soft tissue. Tumors often appear as raised rounded lesions Ihal have the dimension of depth. Persistent lumors may be umbilicated or ulceraled In the center. The term tumor is often used to describe a benign tissue mass such as a neurofibroma. granular cell tumor. and pregnancy lumor.
Vesicle 'Fig. 2·51 A \-esicle i~ a circumscribed. fluid filled elevalion in the epidermis thai is less than I em in diameter. The fluid of a vesicle generally consists of lymph or serum. but may conlain blood. 1be epithelial lining of wa vesicle is thin and will e\emually breakdown. thus giving rise 10 an ulcer and eschar. Vesicles are common in viral infeclions such as herpes simplex. herpes zoster. chickenpox. and smallpox.
Pustu'e IFig. 2--6) A pustule is a circumscribed elevation filled with purulent exudate resulting from an infection. Pustules are less than I cm in diameter and may be preceded by a vesicle or papule. They appear creamy white or yellowish in color and are often associated with an epidennal pore. Intraorally the pustule is represented by a pointing abscess. Herpes zoster is another condilion that produces pustules thai eventually ulcerate and cause intense pain.
Bulla 'Fig. 2·71 When a vesicle achieves a diameter greater than I em. il is termed a bulla. This condition develops from the accumulation of fluid in the epidermal· dermis junction or a split in the epidermis. Bullae are commonly seen in pemphigus. pemphigoid. bums. and epidermolysis bullosa.
Cyst IFig. 2-81 A cyst is an epitheliaJly lined. often fluidfilled mass in the dermis or subcutaneous tissue. CystS range in diameter from a few millimeters to several centimeters. Aspiration of a cyst mayor may not yield luminal fluid. depending on the nature of the cyst. CYStS that contain clear fluid clinically appear pink. to blue. whereas keratin-filled cyslS often appear yellow or creamy white. There are many types of oral cysls. A small list includes the demloid cyst. eruption cyst. implantation cyst. incisive canal cyst. Iymphoepithelial cySt. mucous retention cySt. nasoalveolar cyst. and radicular cysi.
• 4
.....--------...,
DIAGNOSTIC AND DESCRIPTIVE TERMINOLOGY Plaque
Papule
F.. .9 . 2-1. Papule. An elevated. solid lesion less than I "T' Io'l diameter.
Fig. 2-2. Plaque. A flat raised area greater than I em In diameter
oduIe
Fig. 2-3. Nodule. A raised, solid mass with the
dimenSIon of depth and IS less than 1 em In diameter.
Vesicle
Fig. 2-4. Thmot A solid. raIsed mass larger than J em in diameH'( with the dlmenslQ(l of depth
-----
Fig. 2-5. Vesicle. A CIrcumscribed. f1uid-fined skin Jess lhan I em In dlClmeter
eieval:fOI1
Pustule/
Fig.
2~.
_
Pustule. A vesICle filled With purulent
exudate.
Cyst
Fig. 2-7. Bulla. A flUid-filled skrn elevalJon greater than em Ir'I diameter
Fig. 2-8. Cyst. M epithelial lined. t1uid-frlled m.m In the dermIS
or sutx:utaneous tissue 5
ORAL CONDmONS AFFECTING INFANTS AND CHILDREN Congenital Epulis ot the Newborn (Fig. 3-1 J The congenital epulis of the newborn is a soft tissue polypoid growth arising from the gingiva of the edentulous alveolar ridge of newborn infants, It usually occurs in the anterior maxilla, and is len times more likely to occur in females than in males. The neoplasm is mOSI likely of pericyte origin and histologically resembles a granular cell tumor. Clinically the lesion is pink. soft, and compressible. It usually an3ches to the alveolar ridge by a pedunculated stalk and may reach several centimeters in diameter. Treatment is complete excision, and recurrence is unlikely.
Gingival Eruption Cyst (Eruption Hematoma) (Fig. 3-51 The eruption cyst is a soft tissue variant of the dentigerous Cysl Ihal fonns around a.'l erupting lOOlh crown. It is usually associated with primary teeth and manifests as a small. dome-shaped, bluish flucluant swelling. The cyst is lined by odontogenic epithelium and filled wilh blood or serum. No treatment is usually necessary, as the erupting loolh will eventually break the cystic membrane. Symptomatic relief can be obtained by incising the lesion and allowing the fluid to drain.
Melanotic Neuroectodermal Tumor of Infancy IFig. 3-21 The melanotic ncuroeclodermal tumor of infancy is a benign. rapidly growing neuroblastic neoplasm commonly located in the anterior maxilla of infants less than 6 months old. The tumor shows no sexual predileclion and begins as a small pink or red-purple nodule that resembles an eruption cyst. Localized and irregular destruction of underlying alveolar bone is the usual radiographic picture a... well as a primary tooth bud floating in a son tissue mass. Treatment is conservative excision. Histologic examination often reveals pigmentation. Recurrence and melaSlasis are rarely documenled complications.
Congenital Lymphangioma (Fig. 3-61 The congenital lymphangioma is a benign neoplasm of dilated Iymphalic channels Ihat occasionally occurs within the mouth of infants. The tongue, labial mucosa, and alveolar ridge are common locations. No sexual predileclion is evident. The lesion Iypically produces a swelling that is asymptomatic. compressible. and negative to diascopy. When superficial. the swelling is composed of single or multiple discrete papulonodules that may be pink to dark blue in color. Deep-seated tumors produce diffuse swellings with no alteration of the color of the overlying tissue. Large lymphangiomas of the neck are referred to as cystic hygromas. Surgical excision is the lreatment of choice for intraorllilymphangioma~.
Dental Lamina Cysts (Fig. 3-3) Remnants of the dental lamina that fail to develop into a tooth bud may degenerate 10 fonn dental lamina cysls. These cysls are classified, according to the clinical location in which they are found. as eilher Epslein's pearls or Bohn's nodules. Epstein's pearls are palatal keratin-filled cysts that develop from islands of epithelial cells that persist at Ihe site of fusion of opposing embryonic palatal shelves. The pearls are usually small, firm, and whitish, and are found in groups of about three. They are usually localed on the midline of the pahlle or at the junction of the hard and soft paJales. Bohn's nodules. or gingival cysts. appear similar to Epstein's pearls. but are restricted to the alveolar ridge of infanls. Dental lamina cysts vary in size from 1 mm to I em, and both types are self-limiting. Resolution of Bohn's nodules occurs upon tooth eruption, whereas palatal cysts may be incised if they fail to resolve spontaneously. Nata. Teeth fFig. 3-41 Natal teeth are supernumerary odontogenic structures that appear occasionally in infants; mOSI often as a familiaJ trait. These predeciduous teelh are commonly located in the anterior mandible and frequently consist only of cornified and calcific material. Root formation is dislinclly absent. and mobility is a common feature. Natal teeth are believed to arise from an accessory tooth bud. and simple eXlraction is the recommended treatment. Natal teeth should be distinguished from a prematurely erupting deciduous looth by taking the appropriate radiograph prior to dental treatment. 8
Thrush (Candidiasis, Moniliasis) jFig. 3-71 Thrush. or acute pseudomembranous candidiasis. is a fungal infection of mucosal membranes that is caused by Candida albicalls and is primarily seen in infants. Thrush is a surface infection that produces milky-white curds on the oral mucosa. These curds are easily wiped off. leaving a red. raw. painful surface. The buccal mucosa. palate. and tongue are common locations of infection. Newborns often acquire the infeclion from the mother's birth canal during partuition and show clinical signs of disease within the first few weeks of life. Fever and gaslrointestinal irritation may accompany the disorder. Treatment consists of antifungal agents applied topically. Parulis fGum Bolli fFlg. 3-8) The parulis is an inflammatory response to a chronic bacterial infeclion of a non-vital tooth draining through a sinus tract. The condition is most common in children following the spread of pulpal infection to the furcal area of a posterior tooth. It clinically appears as a small. raised. fluctuanl yellow-to-red boil that is located near the mucogingivat junction adjacent to the affected tooth. Pressure to the area and the resulting discharge of pus is pathognomonic. Spontaneous pain is not a feature. although palpation of the lesion, looth. or surrounding structures may elicit pain. Elimination of the odontogenic infection leads to resolution.
ORAL CONDITIONS AFFECTING INFANTS AND CHILDREN
Fig. 3-1. Conge"it... epulis of the newborn. -ourresy Dr Sheryl Hunter)
Fig. ]-). Dental lamina cysts on the maxillary alveolar ~ and epstein pear'IEPJ on median palatal raphe
Fig. 3-2. FIOOllng tooth In the mel..notic neuroectodermal tumor of Inl..ncy. ICourresy Or Chris NortJt?j
Fig. 3-4. Mandibular n ..tal teeth. (COUrtesy Dr Ron
.Jo(genson,
Fig. )-5. Dome-shaped ginglviI' eruption cyst. ,.. :1Urtesy Dr F Garcia-Godoyl
Fig. 3·6. Congenital alveolar lymphangioma.
f g. 3·7. Thrush caused by Cilndlda alblcam
Fig. 3-8. Parulis; nOrt-Vltal prUll<'lry first rnoI
Dr qon Jorgensonl
(Courtesy Dr Ron Jorgensonl
9
SECTION
III Abnormalities by Anatomic Location
II
ALTERATIONS IN TOOTH MORPHOLOGY Microdontia (Figs. 4-1and 4-21 and Macrodontia Microdonlia refers to permanent teeth thaI are considerably smaller than normal. II usually occurs bilaterally and is oftcn a familial tr"il. Microdontia may occur as an isolalcd finding. as a relative condition. or in a generali1-cd paltem. The most common form occurs as an isolated finding involving a single pemlanem tooth. usually the maxillary lateral incisor. The term "peg lateral" is often used to describe this variant. because the tooth is cone~ or pegshaped. Third molars are the second-most frequently affected teeth. When microdontia occurs in a generalized pallern il may be relative to the size of the jaws. True generalized microdontia is rare and occurs when the size of the jaws is nonnal and the actual tooth size is small. Generalized microdontia has been associated with pituitary dwarfism and cancer therapy during the formative stage of tooth development. True microdonts should be distinguished from small overretained primary teelh and examined for the presence of a frequently coexisting anomaly. the dens in dente (see Fig. 4-7). Macrodontia is Ihe opposite of microdontia and refers to an abnormal increase in tOOlh size. This condition may affect one. several or infrequently all teeth. It is usually a relative phenomenon. Macrodontia is often seen in incisors. in mandibular third molars. and in a developmental condition known as hemihypertrophy. in which the affected side is larger than the unaffected side. A single macrodont should be distinguished from fusion or gemination. a common fmd+ ing of incisors and cuspids. True generalized macrodontia is rare and may be a result of pituitary gigantism.
Fusion IFigs. 4-3 and 4-41 and Gemination IFigs. 4-5 and 4-6J Fusion and gemination are opposite conditions that involve alterations in tooth morphology resulting from a developmental disturbance during tooth formation. In fusion the union of twO 1000h buds at the level of the dentin forms a single tooth. This condition is often hereditary. and it affects the primary teeth more commonly than the permanent teeth. Incisor teeth are the most frequently involved. Clinically one sees an enlarged crown. often with an extra cusp. a notch at the incisal edge. and a vertical groove of variable length in the enamel. Radiographically a single large root or two roots with separate pulp canals may be observed. In rare instances. a normal tooth bud fuses wilh a developing supernumerary tooth. thus greatly resembling gemination. Geminmion is the condition in which one tooth allempts to split in two. It appears as an incompletely divided or bifid tooth. The teeth most often affected are the primary
12
mandibular incisors and permanent maxillary incisors. Heredity appears to be an important etiologic factor. The two developmental anomalies. fusion and gemination. appear similar clinically and radiographically. and may be difficult to distinguish. Geminated teeth appear wide in the mesio-distal dimension. and more commonly lack the vertical groove that delineates the two crowns. To confirm the diagnosis the teeth should be counted. If a clinically large tooth is seen and there is no increase or decrease in tooth number. the condition is gemination. If an enlarged tooth is seen and a neighboring tooth is missing. fusion has occurred. Treatment is usually cosmelic. in which case the pulp chambers should be located radiographically prior to crown preparation or endodontic treatment.
Dens Invaginatus 'Dens in Dente) (Fig. 4-7) and Dens Evaginatus fuong~ Tubercle, {Fig. 4·8} About I % of the population has dens invaginatus. a developmental anomaly in which enamel and dentin of the crown invaginate in an apical direction into the pulp chamber along the palatal or lingual aspect of the tooth. There are various degrees of invagination and the tenn "dens in dente." which literally means a tooth within a tooth. should be reserved for only the most severe fonn of this disorder. Dens invaginatus is usually bilateml. and the cingulum of maxillary lateral incisors is the most frequent point of invagination. followed by the maxillary central incisors. mesiodens. cuspids. and mandibular laleral incisors. Clinically. the condition may appear as either a deep crevice or an accentuated lingual pil. Food can easily impact in the invagination. resulting in caries. which can rapidly lead to pulpal necrosis and periapical innammation. Generally. prophylactic restorations are placed if the risk is high for carious involvement. Radiographically. one sees longitudinal and bulb-shaped layers of enamel. dentin. and pulp centmlly located within the crown of the tooth. The disturbance may extend apically to involve the entire root. Dens evaginatus is less common than dens invaginatus. II is represented by a small. dome-shaped accessory cusp emanating from either the central groove of the occlusal surface or the lingual incline of the buccal cusp of a pennanent posterior tooth. This condition occurs almost exclusively in mandibular premolars. and as such has been termed Leong's tubercle. Persons of Mongolian descent exhibit Leong's tubercle more frequently than others. The tubercle consists of enamel. dentin, and a prominent pulp chamber. Care should be taken to prevent pulp injury during tooth preparation. Pathologic exposure of the pulp may occur with atmtion.
ALTERATIONS IN TOOTH MORPHOLOGY
Fig. 4-1. Mlcrodontla; peg-lateral inCISor.
Fig. 4-2. Periapical radiograph of a microdont (peg lateri'll incisor).
Fig. 4-3. Bilateral fusion of primary mandibular IncIsors. (Courtesy Dr Rick Myers)
Fig. 4-4. Periapical radiograph of fusion; primary
Fig. 4-5. Gemination of mancllbular Iateral.f"'l(ISOI".
Fig. 4-6. PeriapICal radiograph of gemination.
Fig. 4-7 _PenaplcaJ radiograph of dens invaginatus
maxi/leuy incisors
Fig. 4-8. Dens evaglnatus of mandibular second ",,,,,,,,,,
13
ALTERATIONS IN NUMBERS OF TEETH Hypodontia (Figs. 5-1 and 5-21 Hypodomia is the congenital absence of one or a rev. teeth because of agene· sis. Similar in meaning is the lenn oligodontia. which is u~d (0 refer to "lImemus congenitally missing leeth. The term anodontia is reserved for the rare condition involving the failure of allteelh to develop. When missing teeth are discovered. careful patient questioning is required to determine the reason for hypodontia. If teeth are missing for reasons such as prior removal or lack of eruption. the use of the term hypodolliia is inappropriate. Hypodontia may involve either sex. any race. and the primary or pennancnI teeth: however. it 110 most common in the permanent dentition. About 5% of the population is affected. and a familial tendency is quite common. The most frequent congenitally missing teelh are the third molars. follo~ed by the mandibular second premolars. the maxillary second premolars. and the maxillary lateral incisors. Visible space or over~retained primary teeth are oftcn the clinicul signs of a missing tooth. Counting the teeth together with radiographs confirms the condition. Many syndromes are associated with congenitally missing teeth. They include Book's syndrome. chondroectodermal dysplasia. ectodermal dysplasia. incontinentia pigmenti, otodcntal dysplusia. and Rieger's syndrome. Both head and neck therapeutic radialion to infants or children and rubella (measles) during pregnancy have been implicated in the failure of tooth development. Excess space is a sequela of missing teeth that may result in drifling. tipping. 'and supraeruption of adjacent or opposing teeth. Alterations in occlusion may require orthodontic and proslhodontic therapy 10 restore function and aesthetics. Hyperdontla IFigs. 5-] and 5-4) Hyperdontia is a term describing an extra or supernumerary deciduous or permanent tooth. It occurs approximately eight times more frequently in the maxilla than in the mandible, and most often in the pennanent dentition. The most common supernumerary tooth is the mesiodens, which is located, either erupted or impacted. between the maxillary cenlral incisors. It may be of nonnal size and shape. but is usually a small tooth with a conically shaped crown and short root. The second most common supernumerary tooth is the maxillary fourth molar. which can be fully developed or microdontic in size. If the fourth molar is bocca.l or lingual to the erupted third molar. the term "paramolar" is used: if it is positioned behind the third molar, the term "distomolar" is used. Mandibular premolars are occasionally supernumerary. Supernumerary teeth are usually afunctional and may cause inflammation, food impaction. interference with tooth eruption. as well as positional. aesthetic. and masticatory problems. In addition, impacted supernumerary teeth may give rise to dentigerous cysls. Because hyperdonti:t occurs in association with cleidocranial dysplasia and
14
Gardner's syndrome. investigations should be performed to rule out these disordcrs.
Cleidocranial Dysplasia (Figs. 5-5 and 5-6) Cleidocranial dysplasia is an autosomal dominant hcreditary disturbance of unknown etiology. This syndrome affects women and men equally. and b usually discovered during childhood or early adolescence. Cleidocranial dysplasia is a dcvelopmental disorder characterized by defective ossification of the clavicles and Cfillli· urn together with oral and sometimes long bone disturbances. Prominent features include delayed closure of the frontal, pariet:!l. and occipital fontanelles of the skull. short stature. broad shoulders, prominent frontal eminences with bossing. small p:mmasal sinuses. an underdeveloped maxilla with a high narrow palate. and relative prognathism of the mandible. The clavicles may be absent or underdeveloped. permilling hypermobility of the shoulders whereby patient... can bring their shoulders togcther in front of the chest. The oral changes are dramatic. particularly on the panoramic radiograph. which can lead to early diagnosis of the condition. There is prolonged retention of the primary dentition. numerous unerupted supernumerary teeth, especially in the premolar and molar areas. and delayed eruption of the pemlanenl leeth. The pernlallem teeth are often short-rooted and lack cellular cementum. which may be the cause of the defective eruption pattern. Treaunent is compie-x. requiring surgical and orthodontic considerations. Gardner~ Syndrome (Figs. 5-7 and 5-8) Gardner's syndrome is an autosomal dominant condition with promi· nent orofacial features characterized by hyperdontia. impacted supernumerary teeth. and jaw osteomas. In addition to these features. patients have multiple epidermal cysts, multiple dermoid tumors. and multiple intestinal polyps. The osteomas occur most frequently in the craniofacial skeleton, especially in the mandible and paranasal sinuses: however, osteomas of the long bones are possible. Maxillofacial radiographs often demonstrate numcrous round osteomas and multiple diffuse enostoses that impart a collon-wool appearance to the jaws. When superficial in the skin. these slow-growing tumors are clinically detectable as rock-hard nodules. The skin cysts (epidermoid. dermoid. or sebaceous) are smooth-surfaced lumps that are commonly located on the ventral and dorsal thorax. Lipomas. fibromas. leiomyomas. and/or desmoid tumors may accompany this disorder. The most serious consideration of Gardner's syndrome are the multiple polyps that affect the colorectal mucosa. These intestinal polyps have an extremely high potential for malignant transformation. resulting in adenocarcinoma of the colon in nearly 100% of patients by the age of 40. Early recognition of the orofacial manifestations necessitates prompt referral to a gastroenterologist together with genetic counselling.
ALTERATIONS IN NUMBERS OF TEETH
F~.
5-1. Hypodontla; congeflllally rT!ISSI09 rnanc:l1Oular
~"'"
Fig. 5-3. Hype,dontla. 1'.J:tyerupr:ed ~
Fig. 5-5. Absent
clav,{~
In a patient with cleldoc:'itnial
d)'spliUi...
Fig. 5·7. Facial osteomas of Gardner's syndrome. /COUrtesy Dr GeZd Terezhalmvl
Fig. 5-2. Pendplcdl raa,ogl
Fig. 5-4. Hyperdontla eKl.'d~ldtef.'.ll1l'lC1SOf
Fig. 5-6. Mult,ple supernumerary and rmp<'Clf'd tet'lh?f c:leidoc,anlitl dyspliUI".
Fig. 5-8. PanoramK rilCllOgr",O/1 of d patient syndrome.
With
Gardner's
15
ALTERATIONS IN TOOTH STRUCTURE Enamel Hypoplasia IFigs. 6-1 and 6-21 Enamel that is decreased in quantity is [cnned hypoplastic. This condition results from a disturbance in enamel deposition during amelogenesis. A variety of interfering influences, including genetic raclors (amelogenesis imperfocla). local [aclOrs (trauma). or
systemic factors (fluOJlY.)is. exanthemalic microbial infections. and nutrilional deficiencies). may be involved. Depending on lhe severilY of hypoplasia enamel discolorations. surface pil-
ling. or distinct horizontal grooves may appear. The pattern of enamel hypoplasia depends on the nature of the influencing factor. the phase of arneloblastic production at lhe lime of lhe
insult. and the duration of the insult. If the enlire phase of amelogenesis is affected, the enamel of the entire dentition will be thin and may appear "snow-capped:' yellowishbrown. rough. pined. or m()(tled. If the influence is systemic and lasts only a short lime. only enamel then being formed is affecled. producing a linear band of hypocalcificatiOll OIlleeth developing during Ihis period. If the injury is local. such as with trauma from an intruded primary tooth. damage to the labial enamel surface of the permanent successor is likely. Enamel hypoplasia of a single permanent looth thai results from periapical or peri furcal inflammation of a deciduous tOOlh is referred 10 as a "Turner's tooth." Am~logenesis
Imperfecta (Figs. 6-3 and 6-41 Amelogenesis imperfecla is a heredilary disorder that is characterized by a genemlized defect in enamel formation of the primary andlor permanent dentilion. The condition has been divided into four main types (hypoplaslic. hypo. malure. hypocalcified. and hypomaturalion·hypoplasia with taunxionlism) and II subtypes according to clinical. histologic. radiographic. and genelic features. TIle most common fonn. the hypoplastic type. is deficiem in normal enameL causing the crowns of Ihe leeth 10 appear blanched. "snow-capped." yellow-brown. pined. or grooved. Radiographically a full complement of teeth is usually seen; however. the crowns of the teelh demonstrate either very thin or absent enamel. The teeth resemble crown preparations wilh characlerislic excessive imerdental spacing. The hypomature type has quantitatively normal amounts of enamel, bUI Ihe enamel is soft and poorly mineralized; Iherefore a denial explorer under pressure will pit the enamel surface. In this Iype. Ihe crowns COniaCI inlerproximally but appear chalky. rough. grooved. and discolored. Fracturing of the enamel is common. The hypocalcified type. like the hypomature type, has soft enamel bUI loses il at a much faster rale. resulting in exposed dentin soon after eruption. PatienlS wilh hypocal· cified amelogenesis imperfecta usually have honey-colored teelh with roughened surface texlure. mulliple unerupted teelh. and an anterior open bite. The hypomaturalion-hypoplasia with taurodontism Iype exhibits yellowish teeth with opaque monling. cervical pit16
ting. attrition. and taurodontism. Trealmem for all forms of amelogenesis imperfecla is usually full veneer coverage for esthetic reasons.
Dentinogenesis Imperfecta {Figs. 6-5 and 6-6) Dentinogenesis imperfecla is a hereditary disorder that affecls the developmem of dentin. Three types have been classified according 10 systemic involvement. clinical fealUres. and hislologic findings. They are Shields Type L Shields Type" (heredilary opalescem demin). and Shields Type III (Brandywine type). Dentinogenesis impeJfecta Shields Type I is a manifestation of osteogenesis impeJfecta. a systemic condition involving bone fragility. blue sclerae. joint laxity, and hearing impairment. It is caused by a defect in collagen fonnation. Shields Type 1I demonstrates the same dentinal features as Type I. bul no osteogenic oornponem is presenl. Persons with Shields Type '" have leelh that are opalescent in color like Types I and U. but the leeth have a shell-like appearance. Dentinogenesis imperfecta affects the primary and per· manent teeth, the latter less severely. Clinically. the teeth look normal when they first erupt, bUI shortly thereafter become discolored gray-brown or opalescent: Ihe incisal and occlusal surfaces chip and flake away. resulting in fissuring and significant anrition. Radiographically one sees bulbous crowns. exaggeraled cervical constrictions. shon tapered roots. and progressive obliteration of the rool canal. Affected teeth are more susceptible to root fractures. Dentin Dysplasia fFigs. b-7 and 6-8) Dentin dysplasia is a hereditary disorder of dentin characterized by alterations in pulp configuration - the presence of pulp stones. and idiopathic radiolucencies of the root apices. The tenn "roolless leelh" has been used to describe Ihis condilion. The abnonnality has been classified into two types: Type I. radicular dentin dysplasia. and Type II. coronal demin dysplasia. Both types are autosomal dominant and may affect the primary and permanent dentition. The distinclion belween Types I and II is based on mdiographic and histopalhological findings. In Type Ilhe primary and permanem leeth look clinically normaL bUI radiographs reveal defeclive rool developmenl with almoSI complete absence of root formalion. as well as large pulp stones and complete pulpal obliteration of the primary teeth before tooth eruption. Loose teeth and multiple periapical radiolucencies of unknown etiology are characteristic. In Type II the pulp canals of !he primary leelh are often completely obliterated as Ihey are wilh deminogenesis imperfect3. The permanent leeth, in conlfast. clinically appear normal excepl for narrower. Ihistle-shaped pulp canals that are frequemly occupied by denticles. The roots may be shan. blunted. and tapered. and may have horizonlal radiolucent lines.
ALTERATIONS IN TOOTH STRUCTURE
G!; 6-1. Do~na grooves of ~namel hypoplasia.
'3'
t
6·3. Teeth of ame/ogene"!,, imperfecU. type lhat resembles crown preparaoons..
~Jtic
==
11 6-S. B ",e sclerilC of osteogenesis Imperfecta Type I. ICourresy Dr Jerald Katz)
Fig. 6-2. Turner\; teeth; maxlll
Fig. 6-4.
Hon~y-(oJored
teeth 01 amelogenesis
ImlMrfecta. hypocaltified type:.
Fig. 6-6. DIscOlored tee"ll of dentinogenesis imperfecta
~.
Shields Type I. (Courtesy Dr Charies ,'''oms)
~ag
Fig. 6·8. TMtle-rube pu:p chclmbe'rs and pulp calerflC
~
6-7. Op
17
ACQUIRED DEFECTS QF TEETH Caries (Figs. 7-1 and 7-21 Denial caries is one of the most common bacterial infections of man. characterized by demineralization and destruction of the organic matrix of leeth. Development of caries results from an intcmclion of b<Jcterial plaque. diet components. altered host responses. and lime. Electrochemical changes produced by acid generation and ion flow appear to be causative. The primary pathogen. S'repIO('o£'CIIS 111111011.\', together with AClil/om)'ces I'iSCO$IIS. Lac/oboeillll! species. and S,replOcoccUS .wnglli.~ arc closely involved in lOoth adherence and the production of lactic acid necessary for the dissolUlion of enamel.
There are two types of caries. which arc classified according to location: fissural and smooth surface. Fissural caries is the most common fonn. It occurs most often in deep fis.'>ures in the chewing surfaces of the posterior teeth. Smooth surface caries usually occurs at places that are protecled from plaque removal such as just below the interproximal contact. at the gingival _margin. and on the root surface. Caries begins as an enamel decalcification that appears as a Chlilky white spot or fissure. A dental explorer tip is used to delect the soft lesion. Maturation of the lesion permits progression through the enamel. then laterally along the dentin-enamel junclion. and evemually IOward the pulp. Sensitivity to hot. cold. and sweets are usual symptoms; however. color changes. loss of hard tissue. or infeclion of the pulp may occur before Ihe patiem becomes llware of the disease. When caries occurs at an extremely rapid pace. as in some children and young adulls. Ihe tenn "rampant caries" is used. "Radiation. or amputation caries." is another form of caries that occurs in radiotherapy patients who lack the protective aClion of saliva. "Nursing boltle caries" is the result of prolonged comact of teeth with sugar-comaining liquids in infants. "Root caries" are moSt frequently a result of xerostomia.
Pulp Polyp (Fig. 7-31 The pulp polyp is an inflammatory and hyperplastic response of a wide open pulp chamber to a chronic bacterial infection. Extensively carious deciduous molars lind 6-year molars of young children are most frequently affected. Clinically the soft. red. non painful. pedunculated mass is seen projecting up from the pulp chamber beyond the broken-down occlusal surface of the tooth. Although the tooth is initially vital. the condition will eventually erode and result in nonvitality. Treatment is extraclion or endodontic therapy. Attrition (Fig. 7-4J Attrition. considered a physiologic process. is the loss of occlusal or incisal tooth structure due to chronic tooth-Io-tooth frictional contact. Although the condition occurs most frequenl1y in the elderly population. the primary teelh of young children may be affected. Attrition is usually a generalized condition accelerated by
18
bruxism or abnormal use of selective teeth. Flattening of the interproximal region is a common sequela. whereas pulp exposure is a rare complication. since the deposition of secondary dentin and pulpal recession occur concurrently with the process. Close examination will reveal a smooth llnd highly polished tooth surface. Ihe outline of the dentin-enamel junction. and the receded pulp chamber. Restoration of worn teeth may be challenging becllUse of acquired changes in venical dimension. Abrasion {Figs. 7·5 and 7-61 Abrasion is the pathologic loss of tooth struclure due 10 abnormal mechanical wear. A variety 9f agents can cause abrasion. but the most common fonn is "toothbrush abrasion." which produces a V-shaped notch in the cervical portion of the facial aspect of the toolh. The abraded area is usually shiny and yellow because of exposed dentin. and often the deepest portion of the groove is sensitive to the tine of the explorer. In addition to dentinal sensitivity. complications of abrasion are eve11lual pulp exposure or tooth fraclure. Abrasive notching of the teeth can be created by clasps of partial dentures. pins or nails habitually held with the teeth. or a pipe stem persistently clamped between the teeth. Abrasion of the .incisal and occlusal surfaces often results from exposure to abrasive substances in the diet and occlusal wear from porcelain restorations placed in occlusion. The abrasive process is slow and chronic. requiring many years before giving rise to symptoms. Restoration of normal tooth contour may be unsuccessful if the patient is not made aware of the causative faclors. Erosion {Figs. 7·7 and 7·81 Erosion refers to the loss of tooth structure due to chemical action. Any chemical Ihat is placed in prolonged contact with the tooth and produces a drop in pH can produce erosion. The labial and buccal surfaces of Ihe teeth arc most commonly affected. The pattern of tooth erosion often indicates the causative agent or a particular habit. For example. lemon· sucking produces characteristic changes of the faciaJ surfaces of Ihe maxillary incisors. Horizontal ridges are initially apparent. followed by smooth, cupped-oul. yellowish depressions. A similar erosive pattern may be seen in dedicated swimmers who chronically expose their anterior teeth to chlorinated swimming pools. • Erosion of the lingual surfaces of the maxillary teeth. together with amalgams that show generalized raised margins. may indicate chronic regurgitation due to bulimia. anorexia. pregnancy. or hiatal hernia. Sensitivity of the exposed area is an early symptom. Excessive consumption of sweetened carbohydrate beverages may accelerate the condition. Fluoride treatments for early erosions and restorations that cover exposed dentin for more extensive lesions are the treatment of choice. Habit elimination or behavior modification is required for success.
• caUIRED DEFECTS OF TEETH
:::.,. 1-1. "lerprWlJrr;a1
Fig. ]-2. Radlogrilpl1lC evtdence of (aries of ~me p
Fig, 7-1
::"9 ]-3.1leOCl sn. exuberant pUlp polyp Pro.te
"""'''''
Fig. ]-4. Signs of attrition YI100ttl yeI\owlSh oenon e;o;posecl on mastlC<11ory surfaces
=''9 ]-5. Toothbrush abrasion aJong (efVlCa! margns of
Fig. ]-6. Abrasion d the rn
on ag<WlSl porce&a-'l
F"'9 7·7. Lemon-sucking erosion.
Fig. 7·8. ungual erosion of bulimia.
19
LOCAUZED GINGIVAL LESIONS Pyogenic Granuloma (Figs. B-1 and 8-21 The leon pyogenic granuloma is a misnomer. since it is neither pusfilled nor a granuloma: instead. it represcms a form of inflammatory hyperplasia rich in neocapillaries and immalure fibrous connective tissue. The exuberam growth is an exaggemlcd response to irritation and appears bright red. fleshy. and soft. The surface is glossy and the border is erythematous and ulcerated. The base may be polypoid or pedunculated. Allhough usually asymptomatic. minor manipulation will induce copious bleeding because of the thinn~d epithelium and highly vascular tissue. Maturation of Ihc lesion resulls in increased fibrosis. decreased vascu· larity. and decreased intensity of color. Pyogenic granulomas are prone 10 develop in palienu who have poor oral hygiene or a chronic or.ll irritant such as overhanging restorations and calculus. Females a~ more susceplible to !he condilioo because of honnonal influences. Pyogenic granulomas may correspond with honnonal imbalances thal occur during puberty. pregnancy. or menopause. and in such cases a~ called "hormonal or pregnancy tumors." About 1% of pregnant women develop this lesion. Pyogenic granulomas most frequently arise from the interdental papilla and enlarge from the labial and lingual aspects to several centimeters if left untreated. Other sites of devel· opment include the tongue. lips. buccal mucosa. and edentu· lous ridge. Treatment is surgical excision which. in the gravid female. should be delayed until afler panuition. Recurrence is possible. especially if excision and local debridement are incomplete or if plaque control is inadequate.
Peripheral Giant Cell Granuloma IFigs. 8·3 and 8-41 The peripheral giant cell granuloma is a reactive epulis-like growth on the gingiva that is generally associated with a history of trauma or irritation. It is thought to originate from the mucoperiosteum or periodontal ligament; therefore. the peripheral giant cell granuloma demonstrates a restricted area of development - the dentu· lous or edentulous ridge. The mandibular gingiva anterior to the molars is particularly affected. especially in females between the ages of JO and 40. Histologically multinucle· ated giant cells and fibroblasts are numerous throughout the sp;x:imen. The peripheral giant cell granuloma is characterized by a well-defined. finn swelling that seldom ulcerates. The base is sessile. the surface is smooth or slightly granular. and the color is pink to dark red-purple. The nodule is usually a few millimeters to Icm in diameter. although rapid enlargement may produce a large growth that encroaches on adjacent teeth. The lesion is generally asymptomatic. but because of its aggressive nature the underlying alveolar bone is often involved. prooudng a pathognomonic superficial "peripheral·cuff· radiolucency. Treatment is surgical excision including the base of the lesion and curettage of lhe underlying bone. Incomplete ~moval results in a
20
marked tendency for recurrence. Histologically, this lesion cannot be distinguished from the central giant cell granuloma and the brown tumor of hyperparathyroidism.
Peripheral Fibroma with Calcification {Peri· pheral Cemento-Ossitying FJbroma' (Figs. 8-5 and 8--6) The etiology of the peripheral fibroma with cal· cification is uncertain. but innammatory hyperplasia of superficial periodontal ligament origin has been suggested. It arises exclusively from the gingiva. usually the interden· tal papillae. When calcifications are present they may con· sist of bone. cementum, or dystrophic calcification. which are often difficult to distinguish microscopic.llly. The peripheral fibroma with calcification is a reactive growth that is especially prone to occur in the anterior region of the maxilla of young and middle-aged females. The salient clinical features of this solitary swelling are finnness. pink color. and sessile allachmenl. An imponant diagnostic clue is the condition's marked tendency to cause displacement of adjacent teeth. The chief complaint often involves an asymptomatic. slow·growing round or nodular swelling. Immature lesions are soft and bleed easily. whereas older lesions become firm and fibrotic. Radiographs m3Y reveal central radiopaque foci and mild resorption of the crest of the ridge at its base. Treatment is excision. Care should be taken to avoid damage to lhe adjacent teeth. The recurrence rate is low.
Gingival Carcinoma IFigs. 8-7 and 8-81 The gingiva accounts for approximately 5 to 10% of all cases of squamous cell carcinoma within the mouth. Generally. at the time of diagnosis the disease is advanced because of its. asymptomatic nature and posterior location, and because of delay of examination. Gingival carcinoma has a varied appearance. It usually appears as a reddish mass with focal white areas prolifer3ting from the gingiva. but may mimic benign inflammatory gingival conditions. erythroplakia. leukoplakia. or a simple ulceration. Carcinoma should be suspected when close examination reveals a pebbly surface. the presence of many small blood vessels in the overlying epithelium_ and surface ulceration. Etiologic factors include tobacco ,use. alcoholism. and poor oral hygiene. Elderly males are espe· cially susceptible. and the condition seems to have a slight predilection for the edentulous alveolar ridge of the poste· rior mandible. Completely dentulous persons rarely have this disease. Gingival carcinoma may extend onto the floor of the mouth or mucobuccal fold. or it may invade the underlying bone. Radiographs may reveal a "cupping out" of the alve· olar crest. Metastasis to regional lymph nodes occurs fre· quently. These nodes are finn. rubbery. matted. non·mov· able. and non-painful. Treatment consists of surgery and radiotherapy.
_lXAlIZED GINGIVAL LESIONS
Fig. S-2. Pregnillncy turnor; thR'e day!;
_
post-pattultJOn.
&-3 JTIOCXtKUrfacea perfpheril' giant-cell grany. 'rom marginal 91l191'l/a jCourresy Dr Ed Heslop)
Fig. 8-4. A rapKlly enlarging perfpheril' giantoCitll granuloma. 'Courtesy Drs.James Cottone & SIeve Bnckefl
&.5. Peripheral fibroma with c..lc:iflUltJon ansng O"{~ paprlae ICourtesy Or .James COttonet
Fig. 8-6. F.'m. pw1k peripheral fibroma with c.alclfic"tion. [COUrtesy Dr Pele Semon)
8-7. Glnglv
U1rdnoma of the gi"gll;'4I. (Courtesy Dr Tom ,A,ufClemone)
leY' """'d
Fig. 3-8. ReddISh, granular surface of sq"ilmous nil
2.
LOCALIZED GINGIVAL LESIONS Parulis fGumboil) lFigs. 9-1 and 9-21 The parulis. or "gumboil"" - a
s)'nonymou~
tenn rCS/,"l"\cd for children-
is a locnlized area of inflammalOry hyperplasia that occurs at the endpoint of a draining dental sinus tract. It appears a.'> a soI'l. solitary reddish papule. located apical and facial
to a chronically abscessed 1001h. usually on or near Ihe labial mucogingival junction. Occasionally the parulis is slightly yellow in the center and emits a purulent yclJo~ish exudate upon palpation. Acute swelling and pain may accompany the condition if the sinus lract is obstructed. To locate Ihc non-vital looth from which the parulis arises. a sterile gutta-peTeha poinl may be inserted into the fistuhL Periapical radiographs are then taken to demonstrate the proximity of the gUlla-percha point 10 the apex of the offending tooth. Afler diagnosing the non-vital tooth. the treatment of choice is root canal therapy. Regression of the parulis usually ensue:. shonly mercafter. If the problematic tooth is left untreated. the parulis may persist for years. A persistent lesion may mature into a pink-colored fibroma.
Pericoronitis 'OperculltlsJ {Figs. 9-] and 9-41 Pericoronitis is inllammation of the soft tissue surrounding the crown of a partially erupted or impacled tooth. Pericoronitis may develop at any age. but mosl frequently occurs in children and young adults whose teeth are erupting. Generally. it is associated with an erupting mandibular Ihird molar that is in good alignment but is limited in its eruption by insufficient spacc. Radiographs of the region reveal a flame· shaped radiolucency surrounding the tooth. with the cortical outline on the dislal a<;pect of the lucency either absent or di:.tinctly thickened because of the deposition of reactive bone. Pericoronitis de\elops from bacterial contamination beneath the operculum. resulting in gingival swelling. redness. and halitosis. The presence of pain is variable and may be extreme. but the discomfort usu:llly resembles that of gingivitis. a periodontal abscess, or tonsillitis. Regional lymphadenopathy. malaise. and low-grade fever are common. If edema or cellulitis extends 10 involve the masseter muscle. trismus often accompanies the condition. Pericoronitis is frequently complicated by pain induced by tmuma from the opposing toolh during closure. Pericoronitis is best managed by entering the follicular space. llushing the purulent material from the gingival sulcus with saline solution. and eliminating "ny occlusal trauIn". Definitive treatment is usually extraction of the involved tooth. Antibiotic coverage is ~ommended when conslitutional symptoms are present and the spread of infection is likely. Recurrences and chronicilY are likely if the condition is managed only with antibiolics.
22
Periodontal Abscess {Figs. 9-5 and 9·61 A periodontal abscess is a fluctuant !'>welling of the gingiva resulting from pathogenic bacteria that are occluded in the gingival crevice. The condition is evidcnced clinically by a smooth fluctuant nodule. increased mobility of the periodontal1y involved tooth. purulence. and tissue necrosis. Chamcleristically the attached gingiva is mised. red·purple. and without stippling or a free marginal groove. Patients often complain of well-localized. dull. and c;minuous pain. especially if the purulent exudate has no avenue for escape. Intensification of pain occurs when vertical or horizomal pressure is applied. or whcn the overlying soft lissuc is palpated. Diagnostic evaluation utilizing a periodontal probe may initially produce discomfort. but is often therapeutic for a short time because it may drain the ab!'>cess. An unpleasant tasle oflen accompanies the condition. The pulp of a tooth associated with a periodontal abscess usually tests vital. unless the inflammatory process has extended into the pulp via the apex or accessory canals. Fever. mal"ise. and lymphadenopathy may coexist, and radiographic evidence of localized bone loss may be seen. Treatment should be directed toward necrotic material removal. adequate dminage. localized pcriodonraltherapy. and improved plaque control measures. Failure to fully treat the problem can result in recurrence or spread of infection along fascial planes. Epulis Fissuratum ,Irritation Hyperplasia, {Figs. 9-7 and 9·81 TIle epulis lissuratum is a reaclive inflanuna~ tory fibrous hyperplasia caused by :I chronic irritant. usually the flange area of 1m old. poorly fining complete or partial denture. Initially the overextended denture margin produces an ulcer that heals incompletely because of repeated tmuma. Hyperplastic healing results and a pink·red. fleshy exuberance of mature granulation tissue is produced. 1lle hyperplastic lesion. located where the denture flange rests. is found most commonly in females. It is nonpainfuL grows slowly on either side of the denture. and causes the pCopit examination of me excised tissue. and correction or reconstruction of the denture.
_OCALIZED GINGIVAL LESIONS
Fig. 9-2. PInk parulis at moc:ogll19....dI }JllCtlOfl adjaCent to it fl()(l-VIt
~-.3
9·7.
Pericoronitis surrounarng a partially erupled
Fig. 9-4. Flafne..wpe
N
underlYIng
Wnl swelling caused by a periodontal
Fig. 9-6. Dlamlng of puruleflt m
~stl( fc>lm
at M epulis fissu,,,tum (<,used
a (lert!u-e Range
Fig. 9-8. Epulis ffssuratum where the p,:!rtial denture
flange ''''''
23
GENERALIZED GINGIVAL ENLARGEMENTS Hereditary Fibromatosis Gingivae (Figs. '0-1 and 10-21 Hereditary fibromatosis gingivae is a rare progressive fibrous enlargement of the gingiva that is inherited as an autosomal dominant nail. The condition has an early childhood onset and becomes more prominent with age. The enlargement is usually generalized and noninflammatory. affecting the buccal and lingual surfaces of bOlh jaws equally. The free. interproximal. and marginal gingiva are enlarged, ullifonnl)' pink in color, finn. non· hemorrhagic. and often nodular. There are two varieties of hereditary fibromatosis gingi. vae: generalized and localized The generalized type is nodular and diffuse. exhibiting multiple coalesced areas of globular gingival overgrowths that encroach on and eventually cover the crowns of the leeth, The localized variely is occasionally seen in which solitary overgrowths are limited to the palatal vaull of the maxillary tuberosity or the lingual gingiva of the mandibular arch. These gingival overgro"1hs appear smooth. finn. and symmetrically round. The localized involvement may be unilateral or bilater.t1. and the term "focal gingival fibromatosis" has been suggested for this variant. Hereditary fibromatosis gingivae may interfere with tooth eruption. mastication. and oral hygiene. In severe cases. noneruption of the primary or pennanent teeth may be the chief complaint of the patient. Regression is not a fealUre of this disease. even with effective oral hygiene measures. Gingivectomy, with either a blade or a carbon dioxide laser. is the treatment of choice. Continued growth may require multiple operations. The condition may be accompanied by acromegalic facial features. hypertrichosis. or mental deficits. Drug-Induced Gingival Hyperplasia (Figs. 10-3 and '0-4} In approximately 25 to 50% of patients taking the therapeutic prescription drugs phenytoin (Dilantin). nifedipine (Procardia). and cyclosporin-A. bulbous enlargement of the gingiva is a common side effect. The condition is usually seen in young patients after pUberty, and can occur in either sex. Though the enlargement results from a hyperplastic response. an inflammatory component induced by dental bacterial plaque often coexists and tends to exacerbate the condition. The gingival enlargement is usually generalized and often appears most exaggerated on the labial aspects of the anterior teeth. The overgrowth begins at the interdental papillae and enlarges to fonn soft red lumpy nodules that bleed easily. Progressive growth results in fibrotic changes: the interdental tissue becomes enlarged. pink. finn. and resiliem to palpation. With time the condition can completely engulf the crowns of the teeth. which aggravates home care. limits mastication. and compromises aesthetics. Treatment may involve changing drug therapy and/or minimizing the overgrowth with meticulous plaque control measures. The gingival swelling usually does not completely regress even
24
with reduced drug doses: thus. once present. the excess tissue often requires surgical removal. Mouthbreathing {Figs. 10-5 and T0-61 Chronic mouthbreathing is characterized by nasal obstruction. a high narrow palatal vault. snoring. xerostomia. a sore throat upon wakening. and a chamcleristiC' form of gingivitis. Classically the gingival changes are limited to the ante· rior labial gingiva of the maxilla and, sometimes. the mandibular gingiva. These changes may be an incidental finding. or may be noticed in conjunction with caries limited to the incisors. Therefore. multiple anterior restorations often sen'e as a diagnostic clue. Early changes involve diffuse redness of the labial. marginal and interdental gingiva. Shortly thereafter. the interproximal papillae become red. bulbous. and hemor· rhagic. Progression of the condition results in inflamma~ tory changes of the entire attached gingiva and bleeding upon probing. Improved oral hygiene will reduce the features. but will not resolve the condition. The diagnosis of mouthbreathing is made by objective and subjective information. Confirmation is achieved when healing occurs after a protective dressing is placed on the affected gingiva al night. together with the return of gingivitis upon discontinuance of the dressings. Treatment should address the re-establishment of a patent nasal airway: thus. the aid of an otorhinolaryngologist is often required to effectively manage this condition. Gingival Edema of Hypothyroidism IFigs. 10-7 and 10-81 Hypothyroidism is a relatively common disorder in which clinical manifestations are dependent on the age of onset. duration. and severity of the thyroid insufficiency. When the patient is deficient in hormone at an early age. cretinism results. This disease is characterized by soon stature. menial retardation, disproponionate head-tobody size. delayed tooth eruption. mandibular micrognathism. and swollen lips and tongue. Regardless of the age of onset, hypothyroid patients exhibit coarse. dry. yellowish skin. intolerance to cold. and lethargy. Swelling is the classic feature and is most prominent in the face. particularly around the eyes. Intraorally macroglossia and macrocheilia are common and may cause an altered speech pattern. The gingiva appears unifonnly enlarged, pale pink in color. and compressible. Swelling occurs in all directions on both the facial and lingual sides of the dental arches. When secondary inflammation is present. the tissues become red and boggy and have a tendency to bleed easily. Treatment for the gingival condition depends on the degree of thyroid deficiency. Patients marginally deficient require only strict oral hygiene measures. whereas frank cases require supplemental thyroid therapy to achieve resolution of the systemic and oral condition.
::il:
ERALIZED GINGIVAL ENLARGEMENTS
!)oJ, :::ieneralllM glngrval enlargement of heredlt..ry "";"__ ~m gIngivae. I(ourtesy Dr Kenneth AbramoVltchj
~3.
Oilantin-induced gingival hyperpliula.
:r -"'!I"""IeS (otlOf1ej
~s Early ginglvi'l' inflammation as\.Ooated . ' ; '••"'~.uthing.
With
Fig. T0-2. Fibromatosis gingivae, localized type, limited to the tuDermrly ICourtesy Dr Ron Jorgenson)
Fig. T0-4. Fibrotic ginglv..' hyperplasl.. inolcalNe of prolonged dllantln therapy
Fig. 10-6. Progressive glngllo'o1' changes
and caries seen
In a chronic mouthbreather. lCoortesy Dr Charles Morris)
Fig. '0-8. GeneraliZed gingival edemi1 of l1ypothyroldlsm; same patient as In Fig 10-7
25
GINGIVITIS Gingivitis (Figs. II·) and 11-2) Inflammation of the gingiva. or gingivitis. is the result of bacterial infection. Initially, gram-positive streptococcal organisms predominate. Over a 3-week period. however. gram-positive rods species. specifically Actinomyces. gram-negative organisms such as Fusobacterium, Veil/of/ella. and spirochetal organisms including Treponema colonize the gingival sulcus. Persistence of supragingival microbial plaque results in characteristic gingival changes and the eventual establishment of subgingival microbial populations that may lead 10 periodontitis. Gingivitis can occur at any age, bUI most frequently arises during adolescence. It has no sexual or racial predilection. Gingivitis can be classified according to distribution. duration, etiology, pathogenesis. and severity. The distribution may be general, local, marginal, or papillary; the duration acute or chronic. An abbreviated list of the different types of gingivitis based on etiology includes: actinomycotic, diabetic, hormonal, leukemic, plasma celL psoriasifonn. scorbutic, and human immunodeficiency virus (H1V). Gingivitis is most often chronic and nonpainfuL but acute, painful episodes may superimpose over the chronic state. The severity is often judged by the alterations in color, contour. and consistency, and by the presence of bleeding. Chronic gingivitis features red swollen marginal gingiva with bulbous interdental papillae that have a redpurple tinge. Stippling is lost as the marginal tissues enlarge. The condition may be difficult for the patient 10 control because hemorrhage and pain are induced by the slightest provocation; therefore patients will reduce brushing frequency and effectiveness. Treatment for acute and chronic forms of gingivitis consists of removal of dental plaque followed by daily oral hygiene measures. Acute Necrotizing Ulcerative Gingivitis (Fig. 11-31 A type of acute gingivitis that is linked to specific bacterial species and stress is termed "acute necrotil-ing ulcerative gingivitis"' (ANUG). also known as Vinl:ent's infection. or "trench mouth."' This multifactorial disease has a bacterial population high in fusiform bacillae and spirochetes that can be demonstrated in smears using darkfield microscopy. ANUG is charactcril-ed by fever. lymphadenopathy. malaise. fiery red gingiva. extreme oral pain. hypersaliva· tion. and an unmistakable fetor oris. The interdental papillae are punched out. ulcerated and covered with a grayish pseudomembrane. ANUG is common in persons between the ages of 15 and 25. particularly students and military recruits enduring times of increased stress and reduced host resistance. and in patients with HIV infection. In rare instances the condition can extend onto other oral mucosal surfaces. or recur if mismanaged. Treatment of ANUG requires irrigation. gentle debridement. antibiotics (if constitutional symptoms are present). and stress reduction.
26
Partial loss of the interdental papillae can be expected despite nonnal healing. Actinomycotic Gingivitis {Fig. 11-41 Actinomycotic gingivitis is a rare intraoral finding that may appear as a fonn of marginal gingivitis. Redness, intense burning pain. and lack of a response to nonnal therapeutic regimens are common features. A tissue biopsy reveals the Mn-acid fast. filamentous fungal organism. Gingivectomy or long-tenn antibiotic therapy provides effective treatment. Hormonal Gingivitis (Pregnancy Glngivitisl (Figs. 11-5 and 11-6) Honnonal gingivitis is an inflammatory hyperplastic reaction to microbial plaque that generally affects females during puberty. pregnancy, or menopause. Although alteration in estrogen/progesterone levels as a result of hormonal shifts and the use of birth control pills have been implicated. the exact causative mechanism remains unknown. The condition begins at the marginal and interdental gingiva and becomes most prominent interproximally. The marginal gingiva appears fiery red. swollen, and tender, while the papillae become compressible. swollen. and lumpy. Close inspection reveals hyperemic engorgement of the inflamed tissue. Severity is related to microbial accumulation; thus poor oral hygiene can exacerbate the condition, which is often the case with the gravid female, since tooth brushing may precipitate nausea. Honnonal gingivitis is usually transitory and responds to meticulous horne care and frequent oral prophylaxis. Diabetic Gingivitis (Figs. 11-7 and 11-8) Diabetes mellitus is a common disease affecting approximately I to 3% of the population in the United States. It is a progressive metabolic disorder characterized by hyperglycemia. glucosuria. polyuria. polydipsia. pruritis. and weight loss. Poor control of blood glul:ose levels is related to lack of production or utilization of insulin. Complications of diabetes include a variety of vascular-related problems such as atherosclerosis, retinopathy. peripheral forms of neuropathy. and renal failure. In addition. altered neutrophil chemotaxis increases the diabetic's risk of infection. A dry mouth. burning tongue. persistent gingivitis. or candida I infection may be the first intraoral signs of the disease. The severity of diabetic gingivitis depends on the stage of the disease and the patient's oral hygiene. In the unC()lltrolled diabetic peculiar proliferations of exuberant tissue arise from the marginal and attached gingiva. The welldemarcated swellings are soft. red. irregular. and hemorrhagic. The surface of the hyperplastic tissue is usually bulbous and. in some cases. papulonodular. This type of gingivitis is difficult to manage when blood glucose level .. remain elevated. Successful treatment requires meticuloU', home care and control of the blood glucose concentration with diet. hypoglycemic agents. or insulin.
'~"(j IVI TI S
1-1
UJe-lnduced marginal gingivitis.
Fig. 1 1-2. Chronic gingivitis exten<Jlng onto me attached gingiva (Courtesy Dr Tom McD
...
'-3 ({'ff't1 papin",..: acute necrotizing . . . ._ _ e gingivitis iANUGI ICoorte~y Dr Bril BClker)
1-5. Hormonal gingivitis In a pubertal female
1-7 _Gingivitis In a 19-year-{)lcl woman With diabetes mellitus.
Fig. T1-4. Red, ,nfBmed IT'i1ndlbular gingiva (!U~ed by AclJOOmyce.s Inff;.'(liofl of gingiva
Fig. 11-6. Severe glr'lgNill ch<1nges associated With pregnallC)': hormona' ginigivitis.
Fig. I 1-8. Inflamed, papulonodu!ar hyperplasia of the
gingiva In a diabetic patient.ICouttesy Dr Iv1
27
SPONTANEOUS GINGIVAL BLEEDING Leukemic Gingivitis fFigs. 12-' and 12-21 Leukemia. a malignant condition characterized by while blood cell overproduction. is classified according to cell morphology (monocytic. myelogenous. or lymphoblastic) and
the clinical course of the disease (acute or chronic). Oral manifestations are more frequently encountered in acute leukemia of the monocytic and myelogenous subtypes. Oral features occur early in the course of the disease because of neoplastic proliferation of one blood cell type. which reduces the normal production of the other hematopoietic cells.
Consislenl signs of acute leukemia afe cervical lymphadenopathy, malaise, anemic pallor. leukopenia-induced ulcerations. and gingival changes. Leukemic gingival tissues are usually red. tender. and spongy. and tend to peel away from the teeth. With progression of the disease the swollen gingiva becomes purple and shiny. Stippling of the tissue is lost and spontaneous bleeding from the gingival sulcus eventually occurs. The edematous tissue is most prominent interdentally and results from leukemic infiltration of white blood cells. In certain patients the neoplastic cells may invade pulpal and osseous tissue, inducing vague symptoms of pain without corresponding radiographic evi· dence of pathosis. Purpuric features such as petechial lesions and ecchymoses on pale mucosal membranes. togelher with gingival hemorrhage. occur frequently. Systemic control of leukemia often involves intensive radiOlherapy, chemotherapy. blood transfusions, and bone marrow transplantation. Difficulty may be encountered in maintaining optimal oral health because of the chemotherapeutic-induced oral ulcerations. Meticulous oral hygiene combined with antimicrobial rinses is recommended 10 reduce the innammatory and ulcerative sequelae of chemotherapy.
Agranulocytosis (Neutropenia) and Cyclic Neutropenia IFlgs. 12-3 and 12-41 Neutropenia refers to a disease characterized by a decrease in the num· ber of circulating polymorphonuclear neutrophils (PMNs). In most instances. the condition is recognized by its clinical symptoms. which consist of chronic infections and an almost complete absence of neutrophils in laboratory blood tests. Anti-metabolic. antibiotic. and cytotoxic drugs are the etiologic agents involved in over half of all cases. In rare instances the condition may be congenital. An uncontrollable infection in the neutropenic patient can resuil in bacterial pneumonia, sepsis, or death. A distinct fonn of agranulocytosis is cyclic neutropenia. which is characterized by a periodic dimunition of circulating PMNs that occurs about every 3 weeks and lasts for about 5 days. The condition is idiopathic and usually begins in childhood. II is sometimes accompanied by arthritis. pharyngitis. fever. headache, and Iymphadenopa-
28
thy. A history of repeated infections of the ear and upper respiralory tract is common. Intraorally patients demonstrate inflammalory gingival changes and mucosal ulceralions. The ulcerations are usually large. oval. and persistent. They vary in size and location; sometimes found on ttfe aU8ched gingiva and other times on the tongue and buccal mucosa. The gingivitis is periodic and ulcerative. At stages corresponding to elevated levels of PMNs. minimal inflammation is evident. In contrast, when the level of PMNs drops precipitously. general· ized inflammatory hyperplasia and erythema occurs. If left untreated Ihe condition is exacerbated by the presence of local factors such as plaque and calculus. resulting in alveolar bone loss. tooth mobility. and early exfoliation of leeth. The periodic appearance and spontaneous regression of signs and symptoms should cause the clinician to suspect cyclic neutropenia. Daily repetition of the white blood cC'1I count is required to diagnose this condition. Curative treatment is unavailable: therefore management is palliative, with antibiotic and antimicrobial therapy together with repeated oral prophylaxis.
Thrombocytopenic and Thrombocytopathlc Purpura IFlgs. 12-5 through 12-81 Platelets play an integral role in maintaining hemostasis by providing the primary hemostatic plug and by activating the intrinsic system of coagulation. A decrease in the number of circulating platelets (thrombocytopenia) may be idiopathic. or it may be due 10 decreased platelet production in the bone marrow. increased peripheral destruction. or increased splenic sequestration. Decreased function of circulating plate leiS (thrombocytopathia) is often related to hereditary syndromes or acquired states such as drug·induced bone marrow suppression, liver disease. or dysproteinemic states like uremia. Vascular-related clinical manifestations of platelet disorders include petechiae. ecchymoses, epistaxis, hematuria. hypennenorrhea. and gastrointestinal bleeding resulting in melena. Spontaneous gingival bleeding is a frequent. early. and dramatic occurrence. The blood oozes from the gingival sulcus profusely. eilher spontaneously or following minor trauma such as toothbrushing. Later the fluid turns into purplish-black globs of cloned blood that adhere to the oral slTUctures. Occasionally, clotted blood may be swallowed. which results in nausea. Mild traumas. panicularly at the occlusal line of the buccal mucosa and tongue. are siles of extensive hemorrhage. Multifocal red petechial spots on the so£! palate is another frequent clinical sign of bleeding disorders. The platelet count, clot retraction time. tourniquet test, and template bleeding time should be ordered to diagnose a platelet disorder. Platelet transfusions may be necessary if local measures prove ineffective in controlling oral bleeding.
;oQNTANEOUS GINGIVAL BLEEDING
on shiny. l)leedWI9
_
~e"OUJ 'eukemi~.
glngJV~ of
a patient WIth
(Courtesy Dr Mornque
l-J Cyclic neutropenia assoclJlec! gingival 'C eo:heoal erosion
• 2-5 - ~ ","1m cirrhosis d ttle liver and a dotting- - . oef'kfc:ncy. lCOUrtesy Dr Rogef Raol
2-7 Thtombocytopenlil; 91119.....<11 bleedmg ana tl'Il! 'J{ Courtesy Dr l.ao'y Skoczylas)
Fig. 12-2. Acute lymphOcytic men:;nj
leukem~; gtngwal eriarge--
sp::lnIaI'leOUs b/e«.ltr9 (COUrtesy Dr o'.1onque MKhau<:lJ
Fig. 12-4. RiKllogl(1ph revealing loss Of penod()l'l[
F'9 12-3
Fig. 12.(). Spont.lneolots gingiva' bleeding of same paoent WI{h tirrhosls III FIQ 12-5 !Courtesy Dr Roger Raol
Fig. '2-8. RadIOgraphic: evidence of ctvonc Irrlt
lnF'912-7
29
SWELLINGS OF THE LIP Angioedema fAngioneurotic Edema, (Figs. 13-1 and T3·21 Angioedema is a hypersensitivity reaction characterized by the accumulation of fluid within the facial lissues. resulling in soft. swollen areas under the skin. It occurs in hereditary and acquired fonns. and may be generalized or localized. When the nonpainful swelling affects the lips it is usually unifonn and diffuse. but may be asymmetrical, involving pans of the lip in varying degrees. Angioedema develops within minutes or gradually over a few hours. and is of Iransient duration. The vermilion border appears
stretched, evened, pliable. and less distinct than usual, whereas the surface epithelium remains normal in color, or is slightly red. Swellings of the tongue. floor of the mouth. eyelids. face. and extremities may accompany the condition, and complaints of burning or itching are common. Although Ihe cause of angioedema is poorly understood, foods, wine, drugs, and stressful situations may be causative factors for the acquired type. In this fonn of the disease. antigenic stimuli appear to trigger an immunoglobulin-linked. histamine-mediated increase in capillary penneability. The hereditary type. on the other hand. appears 10 be linked 10 an enzyme deficiency. Angioneurotic edema is usually recurrent and self-limiting. Generally it poses little threat to the patient. Wilhdrawal of the allergen together with the administration of antihistamines is the trealment of choice. In cases involving swelling of the pharyngeal tissues. airway compromise is of prime concern.
Cheilitis GJandularls IFig. 13-31 Cheilitis glandularis is of unknown etiology and is most frequently encountered in adult males. II is a chronic inflammatory disorder of the accessory labial salivary glands. panicularIy those of the lower lip, that is characterized by diffuse enlargement and eversion of the lip. Although poorly understood. this condition may be associated with smoking. JXXlr oral hygiene. or chronic exposure to the sun and wind; it may also be auributable to bacterial infection or congenital disposition. Cheilitis glandularis clinically produces a symmeuically enlarged, evened. and finn lower lip. As time passes. the inflammed labial accessory salivary glands become dilated and appear as multiple small red spots. From these ductal openings a viscous. yellowish. mucopurulent exudate is secreted that can cover the entire lip. making it sticky. Progression of the condition causes the lip to appear atrophic, dr)'. fissured, and scaly. Distinction of the vennilion border is eventually losl. and secondary infection of a deep labial fissure often results in fistulation and scarring. Emollienls and sunscreens afford protection. but severe cases require vennilionectomy. which produces an excellent esthetic result. Patients with cheilitis glandularis are at an increased risk of malignant transformation.
30
Cheilitis Granulomatosa (Figs. 13-4 through' 3-(6) Cheilitis granulomatosa is a noncascaling gntnulomatou.~ condilion resulting in nonpainful symmetric enlargement of the lips. Its etiology is unknown. and it has no sexual predilection. The swelling, which involves the entire lip. is large and develops slowly at"il young age. BOIh lips may be finn and swollen. but symmetric enlargement of the lower lip is more common. The diffuse enlargement is asymptomatic and does not affect the color of the lip. but discrete nodules can often be palpated. Granulomatous swellings of the tongue. buccal mucosa. gingiva, palatal mucosa. and face have also been associated with this condition. When unilateral facial paralysis and a fissured pebbly tongue are exhibited. the Melkersson-Rosenthal syndrome should be suspeCted. Steroids and surgery have been used with limited succcess. while in selected patients elimination of an odon· togenic infection has proved curdtive. Spontaneous regres· sian is possible.
Trauma (Fig. 13-71 Trauma to the lips often resullS in edema thai is fluctuanl. irregular. and exquisitely painful. The trauma may originate from an external source or it may be self-induced. EXlemallrauma may damage the soft tissue of the lip. resulting in laceration or hemorrhage. Tooth fmcture may accompany the condition. Traumatic enlargement of the lip is orten a problem of children and menially handicapped patients who inadver· tently chew their lip while under local anesthesia. The best management for this type of lip injury is to limilthe traumat· ic influence, apply ice compresses. and treat any lacemtions or hemorrhage as soon as possible.
Cellulitis IFig. 13-81 Cellulitis, in the strictest sense. means "inflammation of the cellular tissue:' This degeneralive process is caused by a bacterial infection in which localization of purulent material has yet to occur. When of dental origin. it typically produces grossly edematous facial tissue lhat is warm and painful to touch and i extremely hard to palpation. A firm. diffusely swollen lip may be the first sign of cellulitis of odontogenic origin. A nonvitaltOQth is usually the root of the problem. and is where the bacterial invasion begins. Failure of host defense mechanisms to control the infection usually results in inOammatory edema. pus for· mation. and a clinically evident swelling of the vestibule. cheek. and/or lip. Delay in initiating treatment can result in cervical lymphadenopathy. malaise. trismus. encroachment of the swelling on the lower eyelid. elevated temperature. and increased pulse. Treatment involves extirpation of necrotic pulpal tissue. drainage. cuhurt, antibiotic sensiti ...• ity testing, and antibiotic therapy. Injection of local anesIhetic into the inflammatory region should be avoided to minimize spread of the infection.
"EWNGS OF THE LIP
en lO\Ne( Ifp of angioedema. Otis)
Fig. 13-2. Reddish, edematous upper lip and philtrum indicative of angioedema.
~
>3:-:
ged, everted 10000er lip with discrete red dWilitis glandularis.
).-5
'T'If'trlC enlargement of the upper lip, SdfTlf'
Melkerson-Rosenthal syndrome as
.J.- - Traumatic swelling of the upper lip.
III
Fig. 13-4. Melkerson·Rosenthal syndrome. cheilitis granulomatosa, and facial paralysis
Fig. 13-6. Fissured tongue; same pcltlent with Melkerson-Rosenthal syndrome as in Fig 13-4
Fig. 13-8. Odontogenic infection resulting In cellulitis and a swollen upper lip {Courtesy Dr Geza Terezhalmy!
31
NODULES OF THE LIP Mucocele fMucous Retention Phenomenon, Mucous Retention Cyst, (Figs. 14·' and T4-2)
salivary gland neoplasia consists of surgical excision. If the excision is incomplete, recurrences are possible,
The retention of mucous secretions in subepithelial tissue is called a mucous retention phenomenon. which has been subdivided into two types. The first type. the mucous retention phenomenon-retention type. or mucous retention cyst, is lined by ductal epithelium and results from the pooling of mucous in an obslrucled and dilated c:
Nasolabi<11 Cyst ,Nasoalveolar Cyst) 'Figs. 1 ~5 and 14-61 The nasolabial c),st. or nasoalveolar cyst. is a fissural cyst of soft tissue located intraorally in the cuspidlateral incisor PQrtion of the upper lip. The etiology is uncertain, and two theories have been suggested. The most accepted theory is that epithelial remnants become entrapped during the embryologic fusion of the lateral nasal, globular, and maxillary processes. A more recent theory suggests that the tissue originates from the nasolacrimal ducl. Proliferation and cystic degeneration of the entrapped tissue usually do not become clinically evident until after age 30, even though the tissue has been entrapped since biM. The condition has a slight female predilection. The nasolabial cyst is a palpable soft tissue mass under the upper lip that may cause elevation of the ala of the nose, as well as dilation of the nostril and alteration of the nasolabial fold. The cyst may be tense or fluctuant. depending on size, Aspiration will yield a yellowish or straw-colored fluid. It is most often unilateraJ and is gener· ally not in contact with the adjacent bone; thus the maxillary teeth remain vital. Infrequently, if the nasolabial cyst applies pressure to the adjacent bone. local resorption of osseous structures can result. Treatment is simple excision.
Accessory Salivary Gland Tumor (Figs. 14·3 and 14-4) Nodular swellings of the upper lip are infrequent and are usually caused by benign neoplasia of the minor salivary glands, i.e., the canalicular or monomorphic adenoma, and the pleomorphic adenoma. Benign accessory salivary gland tumors constitute approximately 10% of all salivary gland tumors and are characterized by encapsulation, slow growth, and long duration (several months). Persons over the age of 30 are usually affected. Clinically the pleomorphic adenoma is a pink to purple dome-shaped or multinodular lesion that commonly protrudes from the inner aspect of the lip or vestibule. It is usually semi-solid, freely movable, painless, and especially firm on palpation. The border is well-circumscribed, and although it has unlimited potential for growth. the tumor generally remains less than 2 em in diameter. Auctuance and surface ulceration are nOl usual clinical features. Malignant salivary gland tumors are rare in the upper lip and may be distinguished from benign neoplasia by their rapid and aggressive growth, short duration, and tendency to ulcerate and cause neurologic symptoms. Treatment for
32
Implantation Cyst ,Epithelial Inclusion Cyst, {Fig. 14-7} An implantation cyst is an unusual cyst arising from a foreign-body reaction to surface epithelium that is implanted within epidermal structures after traumatic laceration. The cyst can occur intraoraJly or extraoraJly, al any age. and in any race or sex. Within the mouth the lesion appears as a firm, dome-shaped. freely movable nodule located at the site of impetus, which is often the lip. Implantation cysts are usually small, solitary, and asymp· tomatic. Growth appears to remain constant, and the overlying mucosa appears smooth and pink. A previous history of trauma should lead the clinician to suspect this lesion. Surgical excision and histopathologic examination is Tt:commended.
Mesenchymal1\lmors (Fig. 1 ~8) A variety of mesenchymal tumors can cau~ nodular swellings of the lip. One example is the neurofibroma, Neurofibromas may be solitary or found in conjunction with von Recklinghausen's disease. When solitary. the neurofibroma is usually an asymptomatic, sessile. smooth-surfaced nodule of the buccal mucosa. gingiva, palate, or lips. Histologically the tumor consists of connective tissue and nerve fibrils. The discovery of a solitary neurofibroma requires close examination for multiple neurofibromatosis, since the latter condition is associated with a marked tendencj toward malignant transfonnation.
:JULES OF THE LIP
1m mucocele of the mandibular
....] Pleomorphic adenoma; a firm bluish
Fig. 14-2. Large dome-shaped mucocele that appeared fOllOWing trauma.
Fig. 14·4. PurpliSh canalicular adenoma of the f'TlaXlllary labial
.... 5 ""uolo1blal cyst; a fluctuant nodule on
mucosa
Fig. 14-6. Lateral skull radIOgraph of a nasolabial cyst injeCted WIth contrast medium (COUrtesy Dr ChriS NortJe)
nc..;ced Implantation cyst.
Fig. 14-8. SmaR neurofibroma of the IO'Ner lip
ICOUftesy Dr John fv1cDowE."lIJ
..
CONDITIONS PECULIAR TO THE LIP Actinic Cheilitis (Solar Elastosis) {Figs. 15-1 and 15-2) Actinic cheilitis is a clinical lesion of the lower lip due to excessive solar radiation damage. Elderly fair-skinned men with outdoor occupations are typically affected. [n early stages, the lower lip is mildly keratotic with a subtle blending of the vennilion border with the adjacent skin. With increased exposure to the sun. focal white zones that have distinct or diffuse borders become apparent. Slowly the lip becomes finn, scaly. slightly swollen, and evened. Ulceration with encrustation is typical of the chronic condition. Development of ulcerations may be due to loss of elasticity, or they may be an early sign of carcinomatous transfonnation. Histologic features include atrophic thinning of the epithelium, subepithelial basophilic degeneration of collagen, and increased elastin fibers. Biopsy is recommended to rule out other sun-related diseases that should be distinguished from actinic cheilitis, including epithelial dysplasia, carcinoma in situ, basal cell carcinoma, squamous cell carcinoma, malignant melanoma, keralOacanthoma. cheilitis glandularis, and herpes labial is. Actinic cheilitis is considered a precancerous condition and should be treated accordingly, Clinicians should warn the patient of the likelihlXXl of disease progression without the use of sunscreen protectives. Dysplastic changes should be treated surgically or by topical application of 5-tluorouracil. Monilial Cheilitis (Figs, 15~3 and 15-4) Monilial cheilitis is an inflammatory condition of the lips associated with Candida albicans and a lip-licking habit. It is believed that the candidal organisms obtain access to the surface layers of the labial epithelium following mucosal breakdown. which is caused by repeated wetting and drying of the labial tissues. Desquamation of the surface epithelium results, and a fine whitish MOale consisting of dried salivary mucous may be seen. In children the affected peri labial skin appears red, atrophic, and fissured. Chapped. dry. itchy, burning lips and the inability 10 eat hot spicy flXXls are frequent complaints. Chronic situations are characterized by painful venical fissures that ulcerate and are slow to heal. A hypersensitivity reaction to ingredients contained within lip balms or lip sticks may mimic the condition. In monilial cheilitis the lip-licking habit perpetuates the condition. Although nystatin ointment is helpfuL ultimate resolution requires habit elimination, AngUlar Cheilitis 'Perleche) {Figs. 15-5 and 15-6} Angular cheilitis is a painful condition consisting of radiating erythemalOus fissures at the comers of the mouth. The
.4
condition is most commonly seen after the age of 50 and is usually encountered in females and denture wearers. The etiology is believed 10 be associated with a mixed infection of Candida albicans and Sraphylococcus aureal/.I. The linear abrasions of angular cheilitis result from repeated pooling of saliva. Initially the mucocutaneous tissue at the comers of the mouth become soft. red. and ulcerated, With time the erythematous fissures become deep and extend several centimeters from the commissure onto the peri labial skin, or they ulcerate and involve the labial and buccal mucosa. The ulcers frequently develop crusts that split and reulcerate during normal oral function. Small yellow-brown granulomatous nodules may eventually appear. Bleeding is infrequent. Angular cheilitis is chronic, usually bilateraL and often associated with denture stomatitis or glossitis. Predisposing conditions include anemia. poor oral hygiene, frequent use of broad-spectrum antibiotics, decreased vertical dimension. flaccid perioral folds. and vitamin B-group nutritional deficiency. Treatment should include preventive measures (such as elimination of traumatic factors, meticulous oral hygiene, and reestablishment of the correct venical dimension) combined with topical antifungal and antibiotic therapy. Vitamin supplementation may also prove beneficial.
Exfoliative Cheilitis fFigs. 1 5~7 and 15-81 Exfoliative cheilitis is a persistent condition affecting the lips that is characterized by fissuring, desquamation, and the formation of hemorrhagic crusts. Candida albicans. oral sepsis, stress, and habitual lip biting are etiologic agents, This condition usually begins as a single fissure near the midline of the lower lip and spreads to produce multipk fissures. The fissures may ultimately develop a yel1owwhite scale or ulcerate and fonn hemorrhagic crusts over the entire lip. The condition is often bothersome and unsightly, with the lower lip being more adversely affected than the upper lip. When the condition is symptomatic. burning is the usual chief complaint. Exfoliative cheilitis has a predisposition for teenage girls and young women. and stress has been reponed to cause acute exacerbations. Because the condition appears to be multifactorial, exfoliative cheilitis is difficult to manage and may persist for many years, Treatment is best rendered through the elimination of predisposing factors together with topical application of antifungal ointments.
·::DiNIDITIONS PECULIAR TO THE LIP
-;"'1 Actinic cheilitis; loss of the vermiJion -e' p. due to chronic sun exposure.
associated WIth actinic cheilitis.
;"3 Monilial cheilitis with ch<'!racterisfic '''Xl red Inflammatory borders jCourtesy
caused by Candida Infection; monilial cheilitis
~...,
'XJj perioral folds and angular cheilitis.
Fig. 15-2. KerCllotlC foci and thickened lower rip
Fig. 15-4. DesquamaliOn and fissunng of the lips
Fig. 15-6. Erythematous areas extending from the cor~ of mouth IndiCatIVe of angular cheilitis.
Fig. 15-8. Hemorrhagic crusts of a severe case of exfoliative cheilitis.
35
PAlATAL SWELLINGS Palatal Tori fTorus PalatinusJ fFigs. 16-1 and 16·21 A palatal IOrus is a form of bony exoslosis thai affects approximately 20% of Ihe adult population. It is frequently inherited: thus multiple family members are affected. The incidence of palalal IOri is higher in femates Ihan it is in males. Tori vary greally in clinical size and shape. and they lend 10 increase slowly in all dimensions after pubeny. The IOCalion is always in Ihe midline of Ihe hard palale adjacent 10 either the bicuspid or molar leelh. The torus palatinus is usually a single. smooth. dome-shaped. bony-hard swelling; however, bosselated versions are occasionally seen with a midline groove and several locular outgrowths. The covering mucosa is pale pink. thin, and delicate: the boundary of the lesion is delineated from the palatal vault by a raised oval contour. The palatal torus is frequently asymptomatic unless traumatized, and patients may insist that they were unaware of the torus's presence until the traumatic episode occurs. The resultant ulcer should always be observed until resolution; if healing does not occur chronic irritants should be identified and eliminated. Palatal tori should be removed if they interfere with phonetics. mastication. or the construction of prosthetic appliances.
Incisive Canal Cyst (Nasopalatine Duct Cyst) (Figs. 16-3 and 16-4) 1lle incisive canal cyst is a developmental cyst that fonns from entrapped squamous or respiratory epithelial remnams. It may occur at any age and anywhere along the course of the incisive canal. but generally the cyst is confined 10 the palatal bone between the maxillary central incisors althe height of the incisive canal. The incisive canal cysl is usually asymptomatic and is discovered as an incidental finding during routine examination. Symptomatic cysts are usually bacterially infected. Infrequently the cyst arises entirely in the soft tissue of the incisive papilla. where it appears as a small. superficial, fluctuant swelling. A well-developed incisive canal cyst may swell the entire anterior third of the hard palate. The radiographic features of the incisive canaJ cyst are characteristic. The cyst appears as a well-delinealed, mid· line. symmetrically oval or hean-shaped radiolucency located between the roots of vital maxillary central incisors. The cystic border is contiguous with the incisive canal and may vary greatly in size. Root divergence and root resorption of the central incisors are occasional findings associated with large cystic lesions. A similar cyst thai is located more posteriorly in the palate has been referred
36
to as the median palatal cyst. Current beliefs are that 1M incisive canal cyst and the median palmal cyst represenl the same anomaly found in slightly differenl location. Treatment for both is surgical enuclealion.
Periapical Abscess {Figs. '6-5 and 16-61 A periapl· cal abscess is a flucluant sofl-lissue swelling consisling purulent malerial that results from bacterial infection of the pulp. It appears adjacent to a diseased tooth. which is often tender 10 percussion, mobile. and slightly "high" in occlusion. Regional lymphadenopathy, fever. malaise. and trism~ are common accompanying features. Careful examination ol the teeth and their supporling tissues along with diagnostic testing reveals the offending nonvital tooth. Radiographicall) an oval periapical radiolucency is usually seen. Any abscessed maxillary toolh may produce a swelling of the palate. Generally the swelling is red-purple. SOfL tender. and laleral 10 the midline if a maxillary posterior tooth is involved. In comraSI. an abscessed maxillary incisor may cause a midline swelling in Ihe amerior third of the palale. Aspiration or incision produces a creamy )ellow or yellow-green purulenl discharge. Immediate drainage. endodomic Iherapy. or extraction is indicated 10 prevenl spread of !he infection. Antibiotics. analgesics. and amipyretics may also be needed.
Benign Lymphoid Hyperplasia (Folllcula, Lymphoid Hyperplasia) fFigs, 16-1 and 16-8) Benign lymphoid hyperplasia is a rare. benign. reacti\e process thai involves proliferation of the lymphoid tissr.ae of the palale. Persons over the age of 50 are mosl common· ly affected. The etiology is unknown. Authorities dispule whelher the proliferation is a reaction to regional or generalized stimuli. Clinically the exuberant lesion arises at the poslerior extent of the hard palate and grows slowly. either uniiaterally or bilalerally. The enlargemenl may reach 3 cm ID diameter, yet palients rarely complain of pain. The surface of the mature lesion is pink to purple. nonulcerated. and dome-shaped or lumpy. The mass is usually soft. on occasion may be finn 10 palpation. Surgical excision the lreatmem of choice. followed by radiation therap) the lesion recurs. The condition may clinically resemb pal alai lymphoma. benign Iymphoepilhelial lesion. Sj(jgren's syndrome. whereas histological fealures oft mimic nodular lymphoma. Fortunately. benign Iympho· hyperplasia fails 10 disseminale like lymphoma.
...........TAL SWELLINGS
.. ' Torus palatinuJ, slightly lobulated
Fig. 16-2. LObular torus palatinus with a denture SI(Wted around the torus
>3.
Fig. 16-4. Heart-shapecl radiolucency characterIStIC of an incisive tanaf cyst. (Courtesy Dr Olaf l.i.mgland)
-\..C..... nt "f"'ll'
incisive canal cyst Invoiving the
PiJlate ICourtesy Dr Geza TerE'zhalmyl
..50 "Ie!"l..plc..,' abscess arISing from the non-vital
Fig. 16-6. Radiolucency typical of a periapical abscess.
"'=
1 Benign lymphoid hyperpl,i'I$ia ariSing at the .=;nj soft palate, ICourtesy Dr Dale Mllesl
Fig. 16-8. Inappropriate management of benign lymphoid hyperplasia. denture accomor::l<1tes nodule.seen In Fig, 16-7, ICourtesy Dr Dale Milesl
37
PALATAL SWEWNGS Necrotizing Sialometaplas'. IFigs. 17-' and 17-21 Necrotizing sialomelaplasia is a benign reaclive lesion. chieOy of accessory palatal salivary glands. that has histologic features suggestive of malignancy. The inflammatory lesion begins after trauma as a rapidly growing nodular swelling on the lateral aspect of the hard palate. particularly of adult males. Tissue infarction as a result of vasoconstriction and ischemia has been implicated in the pathogenesis of this condition. Rarely Ihe sofl palate or buccal mucosa is involved. and bilateral cases have been reported. Initially. necrotizing sialomclaplasia is a small painless nodule that eventually enlarges and ulcerates. causing pain. The Si7..e of the SOfllissue swelling is variable. and growth up (0 2 em is possible. A deep cenlTal ulcer with a grayish pseudomembrane is characteristic. The surface of the depressed ulcer is irregular and pebbly. and the border is oflen rolled. Healing occurs spontaneously over 4 to 8 weeks. Biopsy is recommended to rule out similar-appearing lesions such as salivary gland tumors and malignant lymphoma. Necrotizing sialometaplasia demonstrates squamous metaplasia of ductal epithelium. which may be misdiagnosed for mucoepidennoid carcinoma or adenocarcinoma of the palate. Ben'gn Accessory Salivary Gland Neoplasm IFigs. 17-3 and' 7-4) The pleomorphic adenoma. or benign mixed IUmor. is the mOSI common benign neoplasm of accessory salivary glands. II occurs in major or minor salivary glands. and the palate is the most common location when accessory salivary glands are affected. Occurrences are most frequent in females between the ages of 30 and 60. They lend to occur Ialeralto the midline and distal to the anterior third of the hard palate. 1lle classic clinical presentation of the pleomorphic adenoma is a finn painless. nonulceraled. irregularly domeshaped swelling. Palpation may reveal isolaled softer areas and a smooth or lobulated surface. Slow persistent enlargement over a period of years is typical. and lesions may achieve sizes greater than 1.5 cm in diameter. Histologically this tumor has epithelial cells in a nestlike arrangement. with pools of myxoid. chondroid. and mucoid material. A distinct fibrous connective tissue capsule comaining tumor cells surrounds and usually limits the extension of the tumor. Thorough excisional biopsy is the recommended treatment. since recurrences are frequent following simple enucleation or incomplete excision. Tumorous involvement of the capsule may playa role in recurrence. The monomorphic adenoma is a benign salivary gland tumor that can occur in the palate. 11 consiSIS of a regular glandular pattern. usually one cell type, and lacks a mesenchymal component like that of the pleomorphic adenoma. Treaunent is surgical excision. Malignant Accessory Saltvary Gland Neoplasm fFlgs. 1 ]-S and t 7-61 Adenoid cystic carcinoma (cylindroma) and mucoepidermoid carcinoma are the two most
J8
common immoral malignant accessory salivary gland ne0plasms. Persons between the ages of 20 and 50 are most fre· quently affected by the mucoepidennoid tumor. whereas the adenoid cystic carcinoma usually occurs aller the age of 50. In addition to Slllivary glands. adenoid cystic carcinoma occurs in respiratory, gastrointestinal. and reproductive tissues. wherea!o 111ucoepidennoid tumor may occur in the skin. respir.lt~ tract. or centrally within bone. particularly the mandible. Malignant accessory salivary gland neoplasms occur frequently in the posterior palate. Classically they are asympIOmatic. finn. dome·shaped swellings that occur lateral to the midline. The overlying tissue appears normal in tlK early stages. but later lhe mucosa becomes erythematou with multiple smalltelangieactactic surface vessels. Growth is more rapid and more painful than with benign salivary gland tumors. Induration and eventual sponlaneous ulceration are common. indicating rapid malignant growth. A bluish appear.l.nce and/or a mucous exudate emanating from the ulcerated surface of the swelling are distinctive for mucoepidennoid carcinoma. Treatment is usually radical excision. The prognosi varies depending upon the degree of histologic differentiation. the extent of the lesion. and the presence of metasta· sis. Adenoid cystic carcinoma rarely metastasizes bul is an infLItrating malignancy with a propensity for distam spread by perineural invasion: therefore lifetime followup is necessary. In comrast. the mucoepidennoid tumor infrequently metastasizes and is more easily cured by surgical means.
Primary Lymphoma of the Palate /Figs. 1]·] and 17-81 Malignant lymphomas are solid neoplastic growths of lymphocytes or histiocytes that are classified imo Hodgkin's or non-Hodgkin's lymphoma and subdivided between nodal and eXlranodal disease. Primary nooHodgkin's lymphoma may develop at any site at whle lymphoid tissue is present, including the cervical lympll nodes, mandible. and pal ale. When the primary lewoa affecls the palate the condition is sometimes referred to lymphoproliferatlve disease of the palate. Rarely lym phoma may affectlhe gingiva. Primary lymphomas ofthe palate occur most commonl. in patients over the age of 60. but may be seen in young patients. especially those with AIDS. Primary Iymphom may be solitary or associated with widespread disease though they usually precede disseminated disease Clinically the lesion arises at the junclion of {he hard a soft palates. The slow-growing palatal swelling is asym 10matie. soft. spongy. and nonulcerated. and rarely affe the underlying palatal bone. The surface is often lump and pink to blue-purple in color. Early recognition a biopsy is extremely important. as the disease may be c fined entirely to the palate in the early stages. Palatally phomas are usually irradiated. whereas disseminated di ease necessitates the use of chemotherapy.
"",,~:rAL
SWELLINGS
Fig. '7-2. CIne \-\!€E'k later: necrotblng sialoml!tapli1sia Clppeared as. a Iilrge depress!"d ulce< (Courtesy Dr J L .Jerlsenj
~f5!I
• S
;ng ff"'l nod.ie. pleomorphic Dr J<>mes COl!Of'lt'!
"'",COlIS l"~UOlf'lg 'rom ~
_ _ _ _.....m oid carcinoma. (CO..Jrtesy 0-- .kxk SherfTk'r;
T
lymphoma of the pal.Ue. f(ou"lesy
Fig. 17-4. ~omal'C monomorphic adenoma year-olO fema:e fCoum"sy Dr S Bre"1l Dove;
II"'
a 25-
Fig. 17-6. RilPK1,y 9rowm9 /lOdUit' 'M111 \urfilCe UICefil,'Dn
adenoid cystic carcinomit.
Fig. '7-8. Primary lymphom01l of the palate appeanng as il DHeller-al purplish swelling
39
SWEWNGS OF THE FLOOR OF THE MOUTH Dermoid Cyst {Figs. 18-' and 18-2) The dermoid cyst is a soft tissue swelling derived from the cystic degeneration of epithelium entrapped during embryonic development. The cyst may occur anywhere on the skin, bot has a propensity for the noor of the mouth. Allhaugh a small percentage appear very early in life, these cysts are more frequently seen in young adults under the age of 35. There is no sex predilection. Tbe dennoid cysl classically appears as a painless mid· line, dome-shaped mass arising in the noor of the mouth. The overlying mucosa is a natural pink, the tongue is slightly elevated, and palpation yields a dough-like consistency. Palients may complain of difficulties in ealing and speaking. Growth of the cyst is slow, but diameters in excess of 5 em may be seen. Dermoid cysts may appear below the floor of mouth if the original site of development is inferior to the mylohyoid muscle. In this inslance a submental swelling is nOled. Histologically the lesion is distinguished from an epideonoid cyst by the presence of adnexal structures in the fibrous wall such as sebaceous glands. sweat glands. and hair follicles. Dennoid cystS typical1y are lined with stratified squamous epithelium, but respiratory epithelium may also be present. The lumen contains semisolid keratin and sebum. which accounts for the doughy consistency and makes aspiration difficult. Surgical enucleation is the preferred treatment. Ranula (Mucocele of the Sublingual Gland) IFigs. 18-3 and 18-41 The ranula is a large mucin-eontaining cyst in the floor of the mouth. It is identical to the mucous retention phenomenon except that the ranula is of greater size. The ranula forms as a result of inhibition of normal salivary flow through a dilated or severed major excretory duct of the sublingual gland (Ranholin's duct) or submandibular gland (Whanon's ducc). No sex predile<:tion is apparent, and persons under the age of 40 are most commonlyaffected. There are two types of ranulae - the more common superficial ranula that appears as a soft compressible swelling rising up from the floor of the mouth. and the dissecting or plunging ranula that penetrates below the mylohyoid muscle to produce a submental swelling. The superficial ranula characteristically is tmnslucent or has a bluish cast. It is unilateral, dome+shaped, and fluctuant. As the asymptomatic lesion enlarges. the mucosa becomes stretched, thinned. and tense. Digital pressure will not cause the lesion to pit. but rupture will cause the escape of mucous fluid. The entire floor of the mouth may be fi1Jed by the swel1ing, which elevates the tongue and hinders movement. This impairs mastication, deglutition, and speech.
40
A ranula can be differentiated from other floor-of-themouth swellings such as a dermoid cyst and mucoepidermoid carcinoma of the submandibular gland by sialography. Treatment is excision or marsupialization (Pansch operation). which consists of excising the regional mucosa and suturing the remaining cystic lining to the floor of the mouth. Incision and drainage is not the treatment of choice. since it will lead to reaccumulation of fluid as healing occurs. Recurrences are common in cases involving a plunging ranula or superficial ranula that is ill-managed. Removal of the affected major salivary gland is the indicated treatment for recurrent and plunging ranulae. Salivary Calculi 'Figs. 18·5 and 18·61 Sialoliths. also known a salivary calculi or stones. are concretions of calcium complexes within a salivary gland or duct that may obstruct salivary flow and cause floor-of-the-mouth swellings. Fonnation of stones occurs most frequently after the age of 25. twice as often in males as in females. and usually in the submandibular gland. The ascending course of the excretory duct. along with high mucous content and alkaline pH of the saliva, are significant factors in stone foonation. Calculi are usually oval and smooth or irregularly surfaced. Obstruction of salivary flow by a calculus results in a f1oor-of-the-mouth swelling that is firm. tender. nnd painful. Acute symptoms often recur at meal lime. Swelling may extend along the course of the excretory duct and last for hours or days. depending on the blockage. TIle overlying mucosa usually remains pink. Secondary infe<:tion results in pus emanating from the ductal opening or in redness of the swollen floor of the mouth. Treatment involves appropriate occlusal radiographs. sialography (if no infection is present). and surgical removal of the sialolith. Localized cellulitis and fever require the use of antibiotics prior to invasive procedures. Mueous Retention Phenomenon {Figs. 18-7 and 18-8) The mucous retention phenomenon is a soft. fluctuant lesion involving the retention of mucous fluid itt subepithelial tissue. usually as a result of trauma. Thesr clear or bluish swellings may occur on the lip. floor of the mouth. ventral tongue, or buccal mucosa. They are usually asymptomatic and less than I cm in diameter. The base of the mucous retention phenomenon is commonl_ sessile. although pedunculated bases are possible Children and young adults are most frequently affected. Treatment is excisional biopsy along with histopathologic examination. If the condition is managed properly. recurrences are rare.
WNGS OF THE FLOOR OF THE MOUTH
.
5-1 Dermoid cyst pl'OO\Jdll""'9 below the
""'""'
3 --
• 3-5. Siillolith produCing a firm and tender ~·the-mouth sweJllng.
8-7. Small POlYPOId mucocele on sublingual
Fig. 18-2. Dermoid cyst appeanng as a soft £Issue swelhng In me floor of the mouth
Fig. 18-4. large ranula eleVating the tongue (Courlesy Dr Charles Morns)
fig. 18-6. Radlopilque (onere-nons of slaloliths which obstructed salivary flow.
Fig. 18-8. Mucocele In the floor of the mouth (",used by tri'luma dunng crown preparation
41
CONDmONS PECULIAR TO THE TONGUE Normal Tongue Anatomy (Figs. 19-1 through 19-41 The tongue is a compact muscular organ covered by a pfO(eclive layer of stratified squamous epithelium. II fullCtions primarily in deglutition. taste. and speech. The dorsum of the longue has numerous mucosal projections forming papillae. There are four types: filiform. fungifonn. circumvallate. and foliate papillae. Filifonn papillae are the smallest. bUI are also the most numerous. They are slender. hairlike, cornified stalks that may appear red. pink. or white. depending on the degree of daily irritation experienced. In contrast to filifonn papillae. the fungiform papillae are fewer in number, brighter red in color, and broader in diameter; they also contain taste buds. Fungiform papillae are noncornified. round or mushroom-shaped. and slightly elevated. They are most numerous on the lateral border and anterior tip of the tongue. Occasionally fungifonn papillae contain brown pigmentation, especially in melanoderms. The largest papillae are the circumvallate papillae, which appear as 2- to 4-mm pink papules. They are surrounded by a narrow trench and also contain taste buds. These papillae are 8 to 12 in number and are arranged in a V·shaped row along the sulcus tenninalis at the posterior aspect of the dorsum of the tongue. They anatomically divide the tongue into two unequal sections. the anterior two thirds and the posterior third. If one looks carefully at the lateral border of the posterior region of the tongue the foliate papilla can be identified. These papillae are leaflike projections oriented as venical folds. Occasionally. corrugated hypenrophic lymphoid tissue (lingual tonsil) extending into this area from the posterior dorsal TOOl of the tongue may be mistakenly called foliate papillae. The plica fimbriata are linear projections on the ventral surface of the tongue. Sometimes the plica fimbriata have a brown pigmentation. Fissured Tongue fPlicated Tongue. Scrotal Tongue) {Figs. 19·5 and '9·61 Fissured tongue is a variation of nonnal tongue anatomy that consists of a single midline fissure. double fissures, or multiple fissures of the dorsal surface of the anterior two thirds of the tongue. Various fissural patterns, lengths, and depths have been observed. The cause is unknown, but fissured tongue is probably developmental and increases with age. Fissured tongue affects about I to 5% of the population.
42
The frequency of occurrence is equal between both sexe _ Fissured tongue occurs commonly with Down's syndrome and in combination with geographic tongue. It is a component of the Melkerson-Rosenthal syndrome (fissured tongue. cheilitis granulomatosa. and unilateral facial nene paralysis). The fissures may become secondaril~ inflammed and cause halitosis as a resull of food impaction: therefore brushing the tongue to keep the fissures clean is recommended. The condition is benign.
Ankyloglossia 'Fig. 19·71 The lingual frenum is normally auached to the ventral tongue and genial tubercles of the mandible. If the frenum fails to attach properly to tlK tongue and genial tubercles, but instead fuses to the floor of the mouth or lingual gingiva and the ventral tip of th~ tongue, the condition is called ankyloglossia. or "tonguetie." This congenital condition is characterized by both an abnormally short and mal positioned lingual frenum and a tongue that cannot be extended or retracted. The fusion rna) be partial or complete. Panial fusion is more common. If the condition is severe. speech may be disturbed. SurgicaJ correction and speech therapy are necessary if speech is defective. or if a mandibular denture or removable panial denture is planned. Ankyloglossia occurs with an estimated frequency of one case per 1000 binhs. Lingual Varicosity fPhlebectasia) 'Fig. 19-8) Lingual varicosities. or venous dilations. are a common finding in elderly adults. The etiology of these vascular dililalions is either a blockage of the vein by an intemal foreign body, such as a plaque. or the loss of elasticity of the vascular wall as a result of aging. Intraoral varicosities most commonly appear superficially on the ventra! surface of the anterior two thirds of the tongue and ma~ extend onto the lateral border. Males and females are affecled equally. Varicosities appear as red-blue to purple. fluctuant nodular growths. Individual varices may be prominent and tortuous. or small and punctale. Palpation elicits nu pain. but can disperse the blood from the vessel, flattening the surface appearance. When many lingual veins are prominent the condilion is called "phlebectasia linguae" or "caviar longue." The lip and labial commissure are other frequent sites of phlebectasia. No treatment is required of this condition.
_u"OITlONS PECULIAR TO THE TONGUE
..,
ge pln~ circumvallate papillae "'I<3ped
row
(Courtesy Dr Jilmes Cottonel
...3 Ungual tonsil apparent poslenor to the ~o
~-7
Ankyloglossia.
Fig. 19·4. Plica limbriata which IS pigmented in thiS IndlVlClual
.at"
....5 Fissured tongue, a mild
Fig. 19-2. Foliate papilla on the lateral bOrder of the tongue
case
fig. '9-6. Fissured tongue and subtle manifestations of geographic tongue
Fig. 19-8. 1V1ultlpie purple lingual varicosities; ventral tongue /Courtesy Dr linda OtJsj
4.
CONDmONS PECULIAR TO THE TONGUE Scalloped Tongue 'Crenated Tongue' ,Figs. 201 and 20·21 A scalloped longue is a common entity characterized by indentations on the Imeral margins of the longue. The condition is usually bilateral, but may be uni· laleral or isolated to a region where lhe longue is held in close contact with the leeth. Abnormal pressure of the teeth on the longue imprints the characteristic pattern. which appears as depressed ovals thaI are circumscribed by a raised white scalloped border. Causes of scalloped tongue include situations thai cause abnonnal longue pressure such as frictional movement of the tongue against teeth and diastemata. longue thrusting, tongue sucking. clenching. or an enlarged longue. A crenated longue may be seen in association with temporomandibular join! disorders, systemic conditions such as acromegaly and amyloidosis. and genetic disorders such as Down's syndrome. as well as in normal patients. The condition is harmless and asymptomatic. Treatment is often aimed at habit elimination,
Macroglossia (Figs. 20-3 and 2().4J Macroglossia is the term used to indicate an abnormally enlarged tongue. To assess tongue size. the tongue should be completely relaxed. The normal height of the dorsum of the tongue should be even with the occlusal plane of the mandibular teeth: lhe lateral borders of the tongue should be in contact with. but nOI overlapping. Ihe lingual cusps of the mandibular teeth. A tongue that extends beyond these dimensions is said to be enlarged_ Macroglossia is either congenital or acquired. Congenital macroglossia can be caused by idiopathic muscular hyperlrophy. muscular hemihypenrophy. benign lumors. hamartomas, or cysts. Idiopathic muscular hypenrophy is oflen associated with a mental deficiency. or may be a component of a syndrome such as Beckwith-Wiedemann's syndrome. Acquired macroglossia may be the result of passive enlargement of the tongue when mandibular teeth are lost. In this case the enlargement may be localized or diffuse, depending on the size of the edentulous area. Systemic disease such as acromegaly, cretinism, and amyloidosis. or malignant neoplasms. which can occlude lymphatic drainage and produce a swollen tongue, can cause macroglossia. Indicators of an enlarged longue are speech difficulties. displaced leeth. mal· occlusion. or a scalloped tongue. Often Ihe affected region of the tongue demonstrates enlarged fungiform papillae. If lhe enlarged longue is hindering function, eliminalion of the primary cause and/or surgical correction is recommended. Hairy Tongue (Ungua Vlllosa. Coated Tongue) (Figs. 20-5 and 20·6) Hairy longue is an abnormal elongation of the fLIiform papillae that gives the dorsum of the tongue a hairlike appearance. The cause of Ihe hyper-
44
trophic response of the filiform papillae is poorl~ underslOod but seems to be related to either increased keralin deposition or delayed shedding of the cornified layer_ Patienls who fail to cleanse their longues are most commonly affected. Cancer Iherapy, infection with Candida albicafls. inadiation. poor oral hygiene, change in oral pH. smoking. and the use of antibiotics have also been associated with this condition. Hairy tongue may be while. yellow. brown, or blacL.; hence the names while coaled longue and yellow. brO\l;Q. or black hairy longue. The color of the lesion is a result of inlrinsic faclors (chromogenic organisms) combined with eXlrinsic factors (food and tobacco stains). Hairy tongu~ occurs more frequently in males. primarily in persons O\ef the age of 30. and the prevalence seems to increase witb age. The lesion bcgios near the foramen cecum on the dorsal surface of the tongue and spreads laterally and anteriorly, The affected filiform papillae discolor, progressivel~ elongate, and may reach a lenglh of several millimelef'i Usually the lOngue remains asymplomatic, but severe ca~ may become uncomfortable because of pruritis. Generall~. hairy tongue is only of cosmetic concern. Vigorous brushing wilh abrasive pasles and topical antifungal agenls lead! 10 resolulion. In cases Ihal are rerraclory an underlyin~ endocrinopathy such as diabeles mellilus should be sought.
Hairy Leukoplakia 'Figs. 20·7 and 20-81 Han} leukoplakia is a significant leukoplakic-Iike finding th. indicates human immune deficiency virus (HIV: HTLV-III infection and immunosuppression. This lesion is primant;. localed on the lateral borders of the tongue. bul may exteoO to cover the dorsal and ventral surfaces. A viral origin I likely since Epstein-Barr virus has been idenlified wilh the affected epithelial cells. Hairy leukoplakia is so named because hair-like peeling of Ihe parakeratotic surface la)ef is evident histologically. Candida albicans is frequend. associated with this lesion. Hairy leukoplakia produces white vertical raised fol on the lateral border of the tongue. Initially the lesion tu., alternating faint white folds and adjacent nonnal pi troughs thai produce a characteristic vertical while-banded washboard appearance. The bands evenlually coalesc~ form discrele while plaques or extensive thick white COmlgated parches. Large lesions are usually asyrnptomallc have poorly demarcated borders. and do not rub off_ bilateral occurrence is common. but unilateral lesions m possibility. Hairy leukoplakic lesions have been docurnesaed on the palate and buccal mucosa. Antiviral agenls reduce the size of the lesion. 001 do liltle to alter Ihe Cout1&. of HIV infection.
r::.:::~-omONS
PECULIAR TO THE TONGUE
scalloped tongue caused by abnormal .....-e against the teeth.
_
3: Hemihypertrophic tongue.
Fig. 20-2. Localized scalloping due to tongue sucking.
Fig. 20-4. Macroglossia due to a hemangioma. (Courtesy Dr Kenneth I\bramovitChl
ns White hairy tongue.
f. -.e"WIIe white corrugations of hairy leuko;:z~t with !\IDS.
ICourtesy Or Sol SHvermanj
Fig. 20-6. Brown hairy tongue in an individual that smokes.
Fig. 20-a. Hairy leukopli'lkla in an Individual who just received dental treatment. ICourtesy Dr Micheal Huberj
45
CONDITIONS PECULIAR TO THE TONGUE Geographic Tongue 'Benign Migratory Glossitis, Erythema Migra"s. Wandering Rash} IFigs. 21·) through 21-6) Geographic tongue is a benign intlammatory condition caused by desquamation of superficial kcmtin and the filifonn papillae. The etiology is unknown. but emotional stress, nutritional deficiencies. and heredity have been suggested. The condition is usually restricted to the dorsal and laleral borders of the anterior two thirds of the tongue. affecting only the filiform papillae and leaving the fungifonn papillae intact. Geographic tongue is chamClcrized by single or multiple pink to red denuded patches of desquamated filiform papillae that mayor may nOI be bordered by a raised white serpiginous rim. An adjacent red band of inflammation al the leading edge of the lesion may be concurrent. When innammution is present. pain is often a feature. The lesion continuously changes patterns and migrates from site to sile; hence the synonymous name "benign migratory glossilis:' "erythema migrans," and "wandering rash." Geographic tongue is common, affecting approximately I to 2% of the population. Females and young to middleaged adults are most frequently affected. The condition may appear suddenly and persist for months or years. Spontaneous remissions and recurrences have been observed. Geographic tongue is occasionally seen in association with a mucosal counlerpan. areata erythema migrans (migratory mucositis, geographic stomatilis. ectopic geographic tongue), and fissured tongue. Erythema migrans. when asymptomatic, is harmless and requires no treatment. More often than not, erythema migrans produces red annular patches that bum. Topical aneslhelics or lopical Sleroids may be given to the symptomatic patient. Histologically Ihis lesion resembles psoriasis: however, it is generally accepted that these conditions are distinct entilies, Ihough Ihey may sometimes co-exist.
Anemia fFig. 21-7) Anemia is a condition of impaired oxygen delivery to bodily tissues that results from a deficiency in red blood cells, hemoglobin, or total blood volume. Underlying causes of anemia include increased destruction of red blood cells due to hemolysis, increased blood loss due to hemorrhage. or a decreased production of red blood cells due to a nutritional deficiency state or bone marrow suppression. Anemia is not a final diagnosis. but a sign of an underlying disease; thus the cause of anemia must always be sought. Iron deficiency is the most common type of anemia, frequemly affecting middle-aged women and young teenagers. Deficiencies in vitamin B Il and folic acid will also cause anemia and produce oral signs of the condition. Anemia produces characteristic changes in the appearance of the oral mucous membranes. These manifestations. although suggestive of anemia, are not helpful in distiguishing the lype of anemia causing lhe features seen. Analysis
46
of red blood cell morphology is recommended for a mo~ accurate diagnosis. Imraoral manifeslations of anemia are most promiocm on the tongue. The dorsum of the lOngue initially appears pale. with fl3ttening of the filifom' papillae. Continued alrophy of the papillae re..<;uhs in a surface devoid of papillae thaI appean smooth. dry. and glazed. This condition is commonly referred to as "bald tongue." In Ihe final stage. a beefy or fiery red tongue is seen. possibly wim concurrent oral aphthae. Anemic patients may complain of a sore. painful lOngue (glossodynia) or burning longue (glossopyrosis). The lips may be thinned and taut. while the width of the mouth ma~ develop a narrowed appearance. Other clinical signs associaled with anemia include angular cheilitis. 3phthous ulceration. dysphagia. mucosal erythema and erosions. pallor. shonness of breath. fatigue. dizziness. and a bounding pulse. Palienls with a vilamin B'l deficiency may complam of weight loss, weakness. neurological diSlurbances such :b numbness and lingling of Ihe extremilies. and difficully in walking. Therapy should be directed loward correcling t~ underlying cause. Improvement after therapy is reneCled in changes in the oral appearance. Xerostomia IFlg_ 21--81 Saliva functions to keep the oral cavily moisl and aids in mastication, deglutition. digestion. speech. and immunologic neutralization. When impaired sa.1Jvary function causes a dry mourn Ihe condition, is called xerostomia. Manifestations of decreased salivary flow can be subtle with no patient complaints, or severe with a myriad of complaints. Xerostomi3 may result from advancing age. anemia. avitaminosis. dehydration, diabetes. emotional stress. mechanical blockage. surgery, collagen vascular disease. et"todermal dysplasia. mumps, Mikulicz's disease, multiple sclerosis. Sjogren's syndrome. acquired immunodeficiency syndrome. and head and neck irradiation. Many therapeulK drugs. principally antidepressants, antihistamines. antihypertensive and cardi3C agents, decongestants, ganglionic bloc ing agents, and tmnquilizers will also produce xerostomia. Mild cases of xerostomia are relatively free of symptoms, and the mucosa appears normal. In moderate case\ the tongue is dry. pale. red. and atrophic, with its dorsal surface wrinkled or smooth. In severe situations the tongue may be devoid of papillae. fissured. and inflamed. The mucosa appears dry. shiny. and sticky, while the lips awecracked and fissured. Stagnant. rope-like accumulations of saliva on the tongue along with burning longue (glossop)rosis) and alterations in taste are usually presenL Progression of xerostomia can result in halitosis. multiple carious lesions evident at the gingival tooth margin. and difficulty with speech. maSlicalion. and retention prosthodontic appliances_ Chronic xerostomia requires lODE term multiphasic support. including such items as emollients, artificial saliva. pilocarpine. fluoride treatment. ora hygiene instruclions. and nutritional counseling.
:::0
~
OIT/ONS PECULIAR TO THE TONGUE
.'
'1He
geographic tongue.
O::Ofl"lo3tIC geographic tongue n:'larnmatOl)' borders
1. -5 Erythema migrans of the L3bIal mucosa
___
~
7
:h bald. burning tongue, iron
"'Yanemia.
Fig. 21-2. ExtenSIVe CoClse of geographic tongue with while orOndte borders jCourtesy Dr BJII &!O
Fig. 21-4. SymptomaliC geographic tongue W1[h a promncnt red-wtule ln~mma[oty bof(ler
Fig. 21-6. Annular pc1t1ern of syrnptornaoc erythema mlgrans of the hard and soft palate
Fig. 21-8. Xerostomla-iIlduced dry. fi.ssured atrophK tongue (COurtesy Dr Pete Bemon/
47
CONDITIONS PECUUAR TO THE TONGUE Median Rhomboid Glossitis lCentral Papillary Atrophy 01 the TongueJ {Figs. 22·1 through 22-
41 Median rhomboid glossitis was once thought to be a developmental defect of incomplete desccm of the tuberculum impar. Recently this theory has fallen into disfavor: it is now believed Ihat median rhomboid glossitis is a permanenl end result of a Candida a/bicans infection in conjunction with other factors (possibly smoking or a change in oral pH). Median rhomboid glossitis frequently affects middleaged adult males and rarely affects children. Blacks and whites are affected equally. Diabetics, immune-suppressed patients. and patients who recemly completed a course of broad spectrum antibiotics have a higher prevalence of this condition. Median rhomboid glossitis is a smooth. denuded. beefy red patch devoid of filifonn papillae. With time lIle lesion becomes granular. lobular. and induraled. The most common location is Ihe midline of Ihe dorsum of the lOngue. jusl anlerior 10 the circulTl\'allale papillae. The size and shape of Ihe lesion varies. bUI il frequently appears as a well-demarcated I 10 2.5 cm oval or rhomboid with irregular bUI rounded borders. The condition is generally asymptomalic. Occasionally an erythematous palatal candida I lesion is observed directly over the lesion of the tongue. Median rhomboid glossitis is easily recognized by its clinical appearance. characterislic location, and asymptomatic nature. Early recognition and treatmenl wilh anlimonilial agents may lead to resolution. End-slage median rhomboid glossitis is usually asymptomalic but refractory 10 antifungal treatment. The rare possibility of anaplastk transfonnation exists. Granular Cell Tumor (Granular Cell Myoblastoma) fFigs. 22-5 and 22-6) The granular cell lumor is a rare benign soft-tissue tumor composed of oval cells lhat have an extremely granular cytoplasm. This tumor may occur in a variety of cutaneous. mucosal. and visceral sites, but its favorite oral site of occurrence is the dorsal-lateral surface of the tongue. Theories of histogenesis have been controversial. Most investigalors believe Ihat the tumor is actually a benign proliferalion of neurogenic cells. The granular cell tumor can occur al any age and in any race. but it has a slight predilection for females. Usually the lesion consists of a symptomless. solitary. dome-shaped submucosal nodule covered clinically by nonnal. yellow. or white tissue. The surface may be ulcerated when it has been traumatized. The granular celliumor is often sessile. well-circumscribed. and finn to compression. Growlh is very slow and painless. with some tumors achieving sever-
48
al cenlimeters in size. Larger lesions may demonstrate I slightly depressed central area. Rarely these lesions art found on lIle ventral surface of the tongue. Approximatel~ 10% of affected patients experience multiple lesions. The granular cell tumor is characterized by pseudoepitheliomatous hyperplasia and granular cells thai may histologically resemble epidennoid carcinoma and the con· genital epulis of the newborn. respectively. Conservati\e local excision is the preferred treatment. and these lesions do not tend 10 recur.
Lingual ThyrOid {Fig. 22-7J Lingual thyroid is an uncommon nodule of thyroid lissue found jusl poslerior 10 the foramen cecum on Ihe posterior Ihird of Ihe tongue. 11 occurs when embryonic tissue from the thyroid gland fail to migrate to the anterolateral surface of Ihe trachea. Persistent thyroid tissue occurs much more frequently in women Ihan in men (the ratio is 4: I) and may appear at any age. If lIle remnant tissue becomes cystic the conditioo becomes a Ihyroglossal duct cyst. The lingual thyroid is a raised asymptomatic mass thaI usually measures about 2 em in diameter. Increased surface vascularity is a prominent feature. Hemorrhage. dysphagia. dysp~ nia, symptoms of hypothyroidism. and (rarely) pain can be associated with the condition. The lesion may be differentiated from similar lesions by confinning its distinctive location p0sterior to Ihe circumvallate papillae and by ulilizing radionuelide studies. Biopsy should be deferred until it is ascertLnc:d that the remainder of the thyroid gland is present and function. ing. In over 50% of patients with ectopic thyroid !he lingual thyroid is the only active thyroid tissue present. Cyst of Blandl~uhn (Ungual Mucous Retention Cyst) (Fig. 22-81 The glands of Blandin-Nuhn art the accessory salivary glands on the venlral surface of Iht tongue composed of mixed serous and mucous elements. When trauma of the ventral tongue induces eXlravasatioo of saliva into the surrounding tissues, a relatively smaU painless swelling develops. which is termed the cysl Blandin-Nuhn. This infrequent accessory salivary gland cyst is located near the lip of Ihe ventral surface of t~ tongue. The borders are raised and well-demarcated, lhe mucosal surface appears pink-red. and Ihe lesion is so and fluctuant. When superficial. Ihe cyst has balloon-I" features and a pedunculated base. Deeper lesions have seY sile bases. Although usually lfaumatically induced. Ihe C) of Blandin-Nuhn may be congenital. These cysts rarel. exceed I cm in diameter. Trealment is excisional bioJ>$) and recurrence is rare.
OITIONS PECULIAR TO THE TONGUE
~.
21-1. o-typertrophic median rhomboid PUs.
Fig. 22-2. Smooth denuded patch with irregular borders; median rhomboid glossitis. (Courtesy Dr lInda OtIS/
n-3. Cenual area of tongue dE'VOld of filiform
Fig. 224. Red palatal lesion of atrophic: candidiasis dlrea:ly ~ medliV1 rhombclId g\o5s«Is seen Ifl Fig 22-3
22-5 Granular cell tumor appearing as a pink
Fig. 22-6. Granular cell tumor; lateral VI~ of same patient as In Fig 22-5. (Courtesy Dr Jerry Cioffi)
<'(,emIl( of median rhomboid gloni'is.
.JO.J1e (COUrtesy Dr Jerry Cioffi)
22-7
'Kular lingual thyroid; post('flor to the .., - s ICOUrtesy Dr Tom AufdemotteJ
Fig. 22-8. Cyst of Blandin-Nuhn. (Courtesy Dr James Cottone)
.9
SECTION
IV Intraoral Findings by Color Changes
51
WHITE LESIONS Fordyce's Granules fFigs. 23-1 and 23-2) Fordyce's granules are ectopic sebaceous glands found within the mouth thai are considered a variation of normal oral mucosal anatomy. These granules consist of individual sebaceous glands that arc 1 to 2 mm in diameter. Characteristically they appellr on the buccal mucosa as white. creamy white. or yellow slightly raised papules. They usually occur in multiples. fonning clusters, plaques. or patches. Clusters Ihal are enlarged may feel rough to palpation. Occasionally they are an isolated finding. Less common locations include the lip. labial mucosa. retromolar pad. allached gingiva. longue. and frenum. Fordyce's granules arise from sebaceous glands embryologically entrapped during fusion of the maxillary and mandibular processes. They become more apparent after sexual maturity as the sebaceous system develops. Rarely an intraoral hair may be seen in association with the condition. Fordyce'S granules occur in approximately 80% of adults. and no predilection in race or sex has been reponed. Histologically. rounded neSlS of clear cells. 10 to 30 per nes!. with darkly slaining. small. centrally located nuclei are found encapsulaled in the lamina propria and submucosa. The clinical appearance is adequate for diagnosis of Fordyce's granules: biopsy is not usually required.
Linea Alba Buccalis IFigs. 23-3 and 23-4) The linea alba buccalis is a common intraoral finding that appears as a raised while wavy line of variable length located at the level of the occlusion on the buccal mucosa. Generally this asymplOmalic cornified emily is I to 2 mm in width and extends from the second molar 10 the canine region of Ihe buccal mucosa. The lesion is usually found bilaterally and cannot be rubbed off. The thickened epithelial changes consisl of hyperkeratotic lissue that is a response to frictional aClivilY of the teelh. The condition is often associated with crenated tongue and may be a sign of bruxism. clenching. or negative oral pressure. The clinical appearance is diagnostic and requires no treatment.
Leukoedema (Figs. 23-5 and 23-61 Leukoedema is a common mucosal variant associated with dark-pigmemed individuals. but may be seen infrequently in Iighler-pig-
52
mented persons. The incidence of leukoedema tends increase with age. and 50% of black children and 92ttadult blacks are affected. Leukoedema usually appe bilalerally on the buccal mucosa as an opalescenl. white. gray thin surface film. The labial mucosa and soft palauare less common locations of occurrence. Leukoedema is often faint and may be difficult to sec Prominence of the lesion is related to the degree of under· lying melanin pigmenlalion. level of oral hygiene. amounl of smoking. Close examination of leukoede reveals fine white lines. wrinkles. or overlapping folds lissue. The borders of the lesion are irregular and diffll5t:: Ihey fade into adjacent lissue making it difficult to determine where Ihe lesion begins and ends. Diagnosis oblained by strelching the mucosa, causing the whitt appearance 10 significantly diminish or disappear in some cases. Wiping the lesion fails to remove it. The edolog) leukoedema is unknown. No serious complications art associated with this lesion, nor is treatment required.
Morsicatlo Buccarum ,Mucosal Chewing' {Figs.. 23-7 and 23-8) Morsicalio buccarum. or cheek biting. a common habit Ihat produces a progression of mucosa. changes. Initially, slightly raised white plaques and fo1 appear in a diffuse pattern covering areas of Irauma. Increased injury produces a hyperplastic response tha' increases the size of the plaque. A linear or strialed patte... is sometimes observed. with thick and thin areas seen sideby-side. Persislent injury leads to interadjacenl Iraumata. erythema and ulceralion. Mucosal chewing is usually seen on the buccal mucosa. less frequently on the labial mucosa. The lesions rna) be unilaleral or bilateral and can occur al any age. No sell: race predileclion has been reponed. Diagnosis requires vi al or verbal confirmation of the nervous habit. AlIhou_ morsicatio buccarum has no malignant polential. patienb should be advised of the mucosal altemtions. Because of Ibc similar clinical appearance. speckled leukoplakia and caDdidiasis should be ruled OUI. Microscopically Ihere is a nor· mal maturing epithelial surface wilh a corrugated parakentOlic surface and minor subepilhelial inflammation.
LESIONS
:J.
.~: ~e
--.iC0Scl
Z.J..3
creamy .......nlte fordyce granules (Courtesy Dr lmda OtiS)
"':e wiNy linea alb.1l buccalis.
Fig. 23-2. Clusters of fordyce granules WIth a rare Intraoral half (COUrtesy Dr Bill Baker)
Fig. 23-4. Keratotic linea alba buccalis WIth mild leukoedema ICOUrtesy Dr Dale Mllesl
:.J.-S u!oIkoedema of the buccal mucosa in a
Fig. 23-6. P<'ltch-like distribullon of leukoedema;
:..J..
Fig- 23-8. Morsicatio buccarum of the labial mucosa lCourtesy Dr Kenneth AbramoVitchl
:~ff'
o,!,ng prodUCing white plaques
:;' morsicatio buccarum.
bUccal mucosa
53
WHITE LESIONS White Sponge Nevus ,Familial White Folded Dysplasia) 'Figs. 24-1 and 24-2) White sponge nevus is a relatively uncommon entity that usually appears al birth or in early childhood bUI pe~ists throughout life. It is characterized by mucosal lesions that are asymptomatic, white. folded. and spon!!y. Often the lesions exhibit a symmetric wavy panem. The most common location is the buccal mucosa. bilaterally. followed by the labial mucosa. alveolar ridge, and noor of the mouth. This condilion may involve the entire oral mucosa. or may be distributed unilaterally as discrete while patches. The gingival margin and dorsal longue are almost never affected. allhough the soft palate and vcolml tongue are commonly involved. The size of the lesions v:lrics from patient to patient and from time to time. White sponge nevus exhibil.~ no race, sex or gender predilection; however, because of this condition's autosomal dominant pattern of transmission. multiple family members may manifest the disorder. Extraoral mucosal sites may involve the nasal cavity, esophagus. larynx. vagina. and rectum. Concurrent skin lesions exclude the diagnosis. Causation has been attributed to a basic defeci in epithelial maturation and exfoliation. No treatment is required, and the lesions are hannless. Traumatic White Lesions fAcute Trauma, Chemical Burns and Peripheral Scar) fFigs. 24-3 through 24-61 Traumatic white lesions can be caused by a variety of physical and chemical irritants such as friction· al trauma, heat, prolonged aspirin comact, and excessive use of mouthwash or other caustic liquids. In particular. frictional trauma is onen noted on the allached gingiva. It is caused by excessive tooth brushing. movement of oral prostheses. and chewing on the edentulous ridge. With time the mucosa becomes thickened with a roughened white surface. Pain is characteristically absent, and histologic examination reveals hyperonhokeratosis. Severe trauma can produce a white lesion owing to the loss of the superficial layers of mucosal epithelium. Undemeath the white slough there is a raw. red, or bleeding surface. Typically aCUie traumatic lesions appear as punctate white patches with diffuse and irregular borders. Moveable mucosa is more susceptible to trauma than allached mucosa. P-din of severdl days duration is common. Trauma involving the subjacem dermal layers may induce a fibrous healing response or scar. Scars are often asymptomatic. linear. pale pink. and sharply delineated. A thorough history may reveal previous injury, recurrent ulcerative disease. seizure disorder. self-multilating behavior. or previous surgery.
54
Leukoplakia IFigs. 24·7 and 24·81 Leukoplakia a clinical tenn descriptive for a white plaque or patch the oral mucosa that cannot be scraped off and cannot classified as any other clinically diagnosable dise Individuals of any age may be affected; however. majority of cases occur in men between the ages of 45 65. Recent incidence figures indicate that the male female ratio is decreasing, with women being an almost as frequently as men. Leukoplal.:ias are protective reactions against chronic UL tants. Tobacco. alcohol, syphilis, vitamin deficiency, hol'Tlx.al imbalance, galvanism. chronic friction, and candidl have been implicated in the cause of these lesi Leukoplakia<; vary oonsidembly in size, location, and c1i appearance. The preferential sites for leukoplakia are the eral and ventral tongue, floor of mouth, alveolar mucosa. soft paJate·retromolar trigone. and mandibular attached giva. The lesional surface may appear smooth and ho~ neous. thin and friable. fissured. corrugated. venucoid. lar, or speckled. The color can take on subtle variations faintly translucent white lesions to gray or brown-while. A classification system offered by the World H Organization (WHO) recommends tWO divisions for leukoplakias: homogeneous and nonhomogeneous. K homogeneous leukoplakias have been further subdh into erythroleukoplakia. nroular. speckled. and verru~ The majority of leukoplakias (80%) are benign:' remaining cases are dysplastic or cancerous. The cli dilemma is in determining which leukoplakias are p lignam or malignant. especially since 4 to 6% of all I plakias progress to squamous cell carcinoma witma years. High risk sites for malignancy include the flOO£ the mouth, lateral and ventral tongue. uvulo-palatal plex, and lips. Leukoplakias with localized red areas also confer a risk of carcinoma. For example, nonhomogeneous I plakias. particularly oral speckled leukoplakias, rep epithelial dysplasia in about half of the cases and ha\e highest rate of malignant transformation among im leukoplakias. Candida albicQ/ls. a fungal organism associated with oral speckled leukoplakias. may lu\c role in the dysplastic changes seen. The initial step in the treatment of leukoplakia eliminate any irritating and causative factors. then ob",~ for healing. The lesion mayor may not disappear. \Vhea unexplained oral leukoplakia is persistent. biops} mandatory. Multiple biopsy sites may be necessary for fuse lesions. onhomogeneous areas of the lesion always be selected for biopsy.
~rn=
LESIONS
•
1-4- T White sponge nevus affecting the buccal
Fig. 24-2. ThICk whIte plaques of white sponge
- pala:e, and retromolar pad
nevus in S<1me patten! sho\Nn In FIg 24-1 GlnglV(ll margIn remalflS unaffooed
El;. ]-4.3. Frictional ker..tosis associ
Fig. 24-4. White pebbly frictional keratosis from traumatic occlusion.
-h brushing
lLS Traumatic white lesion; white chemICal ;pnn placement ar it biopsy site
2'*-7 Leukoplakia; soft palate Biopsy revealed eratoSI$
Fig. 24--6. Traumatic laceriltJOn at age 2 resulted In this palatal sur.
Fig. 24-8. Leukoplakia of {he floor of the mouth and
ventral tongue. biopsy revealed mild eplthellill dysplasia
55
TOBACCO ASSOCIATED WHITE LESIONS Cigarette Keratosis lFigs. 25-1
and 25-2)
Cigareue keratosis is a specific reaction evident in individuals who smoke noo-fillered or marijuana cigarenes to a very
short length. The lesions. which appro"imatc each other upon lip closure. invoh'c both the upper and lower lip al the location of cigareuc placemenl. These kcr.lIotic patches are about 7 mm in diameter and in\lariably arc located lateral 10 the midline. Raised ",hile papules are evident throoghoullhe pmch. producing a roughened texture and finnness to palpation. Occasionally cigarette ker.l1oses may extend onlo the labial mucosa. but rarely is the vennilion border involved. Elderly males are most commonly affected. Discontinuation of the smoking habit usually brings about resolution. The developmclll of ulcer and crust formation should raise the suspicion of neoplastic transfonnation.
Nicotine Stomatitis 'Pipe Smoker's Palate) {Figs. 25-] and 25-41 Nicotine stomatitis is a response of palatal eClodennal structures to prolonged pipe and cigar smoking. Usually found in middle-aged and elderly males. posterior to the palatal rugae. this lesion shows progressive changes with time. Initially the irritation causes the palate to become diffusely erythematous, Eventually the palate becomes grayish-white secondary to hyperkeratosis. Multiple discrete keratotic papules with depressed red centers develop that correspond to dilated and inflamed minor salivary gland excretory duct openings, 1be papules enlarge as the irritation persists but fail to coalesce. producing a characteristic cobblestone (parboiled) appearance of the palale. Isolated but prominent red-centered papules are common. Whether the lesion arises as a consequence of heat or of tobacco is a mailer of debate. Reverse cigarette smoking produces similar findings. Discontinuation of smoking should result in regression.
Snuff Dippers Patch (Tobacco Chewer's Lesion. Snuff Keratosis) IFigs. 25-5 and 25-61 A wrinkled yellow-white area on the gingival mucosal flexure and mandibular buccal or labial mucosa is indicative of intraoral use of unburned tobacco, Smokeless tobacco may
56
take various fonns (snuff. dip, plug. or quid), leaving characteristic mark al the preferential site of tobacco pi ment. Posterior sites are commonly utilized for dip. pi or quid. whereas anterior sites are preferential for sn Individuals who vary intraoral sites have multiple. I prominent lesions. Male teenagers are most freque affected. largely because of intensive marketing effOfu tobacco companies. Early snuff dipper's patches are pale pink in color. \1i the surface appearing corrugated and wrinkled, A progm sion to white, yellow-white. and yellow-brown may e as hyperkeratosis and exogenous staining occur. Chronic smokeless tobacco use is associated with odontal alterations. caries, epidermal dysplastic chan and verrucous carcinoma. To achieve resolution. cessa of use is recommended. If normal appearance does return 14 days after cessation. biopsy is necessary.
Verrucous Carcinoma (of Ackerman) lOr Florid Papillomatosis' (Figs. 25-7 and 25-8J wany, exophytic, cauliflower-like whitish mass is a v malignant squamous cell tumor that is considered I grade and nonmetastasizing. The buccal mucosa mandibular gingiva are the most common locations. ~ over 60 years of age who use smokeless tobacco are often affected, The disease is rare in persons under years of age. Verrucous carcinoma has a distinctive surface ap ance. Characteristically there is a white keratotic surf with pink-red pebbly papules throughout. Lateral g leads to an increase in mass. and the tumor can ac several centimeters or more in diameter. Large lesiOTb be locally destructive by invading and eroding the uJXkrl ing alveolar bone. Similar-appearing lesions include \ cous epithelial hyperplasia, pyostomatitis vegetans. proliferating verrucous leukoplakia. Recommended treatment is wide surgical exci Radiation therapy is contraindicated. since there is a n anaplastic transfonnalion to squamous cell carcinoma.
':C-J!:OACCO ASSOCIATED WHITE LESIONS
"r-ok:! male WIth Cigarette Smoking
ogarette keratosis.
"'cotine stomatitis prorT'Ilnent on
s
Fig. 25-2. Cigarette keratosis on lab""! mucosa of patJenr In FIg 25-1
Fig. 25-4. Cobblestone appearance of nicotine
;: onto the buccal mucosa
stomatitis In a rt':"VefSe smolo:.er
placement of chewing lobaeeo, snuff djpper~ patch.
Fig. 25·6. Wrinkled appearance of a snuff dippers patch.
.,;.c: ng verrucous carcinoma of the
Fig. 25-8. ExtensJVf' pink nodular verrucous carcinoma; alveolar ridge and palate, (COUrtesy Dr James Cottone)
-:~
many years of tobacco chevving
-~cer
Reddlngl
57
RED LESIONS Purpura (Petechiae. Ecchymoses. Hematoma) (Figs. 26-1 through 26-41 Purpum is a condition characterized by the pooling of extravasated blood. The stimulating factor can be i:urogcnic. (:letitia!. or accidenlallraurna to vascular tissues contained within Ihc dermis or submucosa. In circumstances where trauma b not involved, deficits in the platelets either quantitative or qualitative. dotting factors. or capillary fragility ~hould be suspected. Initially purpura tlppcar bright red. but lend (0 discolor with lime. becoming purplish-blue and laler brown-yellow. Bec,lUse these lesions consist of extr::lVascular blood. they do not blanch 011 pressure. The three types of purpura - petechiae. ecchymoses. and hemalOma are clas~ificd according to size and etiology. Petechiae are pinpoint nonraised circular red spots. The sofl palate is the most common intraorallocalion for multifocal petechiae. Palalal petechiae may represent an early sign of infectious mononucleosis. scarlet fever. leukemia. bleeding diatheses. or blood dyscrasia. They may also indicate rupture of palatal capillaries due 10 coughing. sneezing. vomiting, or fellatio. Suction petechiae under a maxillary denture are not true purpura. They evolve as a result of candidal infection and the resulting inflammation of the orifices of accessory salivary glands. not because of denture-created negative pressure as previously believed. An area of extravasated blood usually greater than lem in diameter is called an ecchymosis (common bruise). Careful physical evalualion may reveal the cause 10 be mechanical tr:mma. hemostatic disorders, Cushing's dis· case. neoplastic disease. primary idiopalhic or secondary thrombocylopenic purpura. or use of anticoagulant drugs such as bishydroxycoumarin. warfarin. or heparin. Hematomas are large pools of eXlravasated blood re,.<>ulting from traumatic vascular severance. They occur most commonly in the oml cavity as a result of a blow to the face, tooth eruption. or rupture of the posterior superior alveolar vein during local anesthetic administration. They are usually dark red·brown or blue in color and tender to palpation. Purpura fade with time and require no specific treatment. Detemlining the underlying cause is the prime consideration.
Varicosity (Varix} IFig. 26-51 A varix is a red· purple flucluant swelling frequently seen in the elderly populalion. The swelling represents a venous dilation caused by reduced elasticity of the vascular wall as a resuh of aging. or by an internal blockage of the vein. The ventral surface of the anterior 1'>'0 thirds of Ihe longue is a frequent location. The lip and labial commissure are other common sites. Labial varices appear dark red 10 blue~purple. They are most commonly single. round, dome-shaped. and fluctuant. Palpation of the lesion will disperse the blood frOnl
58
the vessel. flattening the surface appearance; therefo~ lesions are dia.'iCopy·positive. Varices are benign and asymplomatic. and requiR trealmen!. If they are of cosmetic concern 10 the pat varices can be surgically removed without signifi bleeding. Occasionally they are slightly finn becau~ fibrotic changes. Thrombosis is a rare complication. \\ multiple veins on the ventral tongue are prominent the dition is called phlebectasia linguae, or "caviar tongue_~ Thrombus (Fig. 26-6) The series of events that inel trauma, activation of the clotting sequence. and fonnatl of a blood clot typically results in the cessation of blee
LESIONS
.• '-..II pie red petechiae on the soft palate
Fig. 26-2. Ecchymosis following lip trauma In
it
heparinized pi;Jtient
::>3 l'urphsh-blue hematoma resulting from a
... face
Fig. 26-4. Red intriloral hematoma of patient In Fig.
26-3
2>5 Purple lip varix. ICourtesy Or Unda Otisl
Fig. 26-6. Blue organrLIng thrombus; labldl mucosa. jCourtesy Dr Ed Heslop)
:"'>1 Dome-shaped hemangioma of the ventl",1 :ClJftesy Or Tom Razmusj
Fig. 26-8. Multinodular hemangioma of the buccal
mucosa.
59
RED LESIONS Hereditary Hemorrhagic Telangiectasia fRenduOsler-Weber) (Figs. 27-1 through 27-4) Hereditary hemorrhagic telangiectasia is a genetic disease that is inherited as an autosomal dominant trait. The disease is chardcterired by multiple telangiectasias, which are purplish red macules or slightly red papules represeming pennanently enlarged end-eapillaries of Ihe skin. mucosa. and other tissues. The lesions are usually I to 3 mm in size. lack central pulsation. and blanch upon dia.<>eop)'. After pubcny the size and number of lesions tend 10 increase with age. Males and females are affected equally. Bleeding is a prominent feature of Ihis disease. The lesions of hereditary hemorrhagic telangiectasia are located immediately subjacent to the mucosa and are easily traumatized. resulting in rupture, hemorrhage. and ulcer fonnation. Skin lesions are less subject to rupture because of the overlying cornified epithelium. The mosl common locations on the skin are the palms. fingers, nail beds. face. and neck. Mucosal lesions can be found on the lips. tongue. nasal septum. and conjunclivae. The gingiva and the hard palale are less commonly involved. Complications include epistaxis. gastroinleslinal bleeding, melena. hematuria. cirrhosis. and pulmonary arleriovenous fislUlae. PrecaUlions are recommended wilh Ihe use of inhalalion analgesia. general anesthesia. oral surgical procedures, and hepatotoxic and anti-hemostatic drugs. Rupture of a lelangieclasia may cause hemmorhage Ihat is best controlled by pressure packs. History. clinical appearance. and hislologic features are importanl in making the diagnosis. Sturg~Weber Syndrome
,Encephalotrigeminal
Angiomatosis) fFigs. 27-5 through 27-8) SturgeWeber syndrome is a rare congenital disorder Ihat mani,
~
60
1 \\1\
fests venous angiomas of the leptomeninges of Ihe b ipsilateral macular hemangiomas of Ihe face, neurom lar deficits. and oculo-oral lesions. The macular he gioma of Ihe facial skin. also tenned "pon-wine slain"nevus nammeus:' is the most slriking feature of !he s. drome. The facial hemangioma is well-demarcated. fla slightly raised. and red to purple in color. It blanches pressure. It is present at binh. dislributed along a brandl the lrigeminal nerve. and Iypically eXlends to the pala midline without crossing 10 Ihe Olher side. The ophth division of the trigeminal nerve is most frequently aE No tenderness or innammation is associated \>. ith hemangioma. and it does not enlarge with age. The altered venous blood now caused by an angioma the leptomeninges can resull in cerebral conical dege lion. seizures, mental retardation. and hemiplegia. On I al skull radiographs gyri form calcifications characlc cally appear as double-contoured "tram-lines." Appro imately 30% of patients have ocular abnonnaJities inc ing angiomas. colobomas. or glaucoma. Vascular hyperplasia involving the buccal mucosa lips is the most frequenl oral finding. The palale. gin and noor of the mouth may also be affCCled. Dislribu of Ihe bright red oral palches is to areas supplied b~ branches of the trigeminal nerve. Like facial lesions. palches stop abruptly al the midline. Involvement of gingiva may produce edematous tissue and cause diffi with hemostasis when surgical procedures involving tissues are performed. Abnormal tooth eru macrocheilia. macrodontia. and macroglossia are seq of large vascular overgrowths. In areas of vascular hyper plasia oral surgery should be perfonned in accordance stricl hemostatic measures.
LESIONS
. oe lip tel
Fig. 27-2. Gingival telangiect.'lsias, .>arne patient as In Fig 27-1 With hereditary hemorrhagic telangiectasia.
J • ... telangiectasias; hereditary hemorr· Ii!U:ngiectasla. ICourtesy Dr Iv1argot van Dis)
Fig. 2~-4. Blanching of telangiectasias on diascopy: heredItary hemorrhagic telangiectasia. ICourtesy
_ _....~ •
r ~
_
5
~x ...vlne
stain; Sturge-Weber syndrome,
:? :..i.'rry Skoczylas)
:--1. _'" .ateral hemangioma of the palate;
eMr syndrome.
Dr Margot van Dis)
Fig. 27-6. Unilateral involvement of intraoral hemangioma; same patient as in Fig. 27-5 with Sturge-
Weber syndrome. ICourtesy Dr Larry Skoczylas)
Fig. 27·8. Tram-line gyriform calcifications, lateral ·skull radiograph"; same patient as in Fig, 27-7 with Sturge-
Weber syndrome.
61
RED AND REDIWHITE LESIONS Erythroplakla (Figs. 28-1 through 28-4) Erythroplakia is defined as a persistent velvety red patch that cannot be characterized clinically as any other condition. This term. like "leukoplakia," has no histologic connotation: however. the majority of erythroplakias arc histologically diagnosed as epithelial dysplasia or worse. and thus have a much higher propensity for progression to carcinoma. Erythroplakias may be located anywhere in the mouth. but appear 10 be most prevalent in the mandibular mucobuccal fold. oropharynx and floor of the mouth. The redness of the lesion is a result of 3lrOphic mucosa overlying a highly vascular submucosa. The border of the lesion is usually
well-demarcated. There is no sexual predilection and patients over the age of 60 are most commonly affected. Three clinical variants of erythroplakia have been recognized: (I) the homogenous foml, which is completely red in appearance: (2) erythroleukoplakia, which has red patches interspersed with occasionalleukoplakic areas; and (3) speckled erythroplakia, which contains white specks or granules scattered throughout the lesion. Biopsy is mandatory for all types of erythroplakia, because 91 % of erylhroplakias represent severe dysplasia. C'".lJ'Cinoma in situ, or invasive squamous cell can:illl).mao Close inspection of the entire oral cavily is also required. since 10 to 20% of these patients will have several erythroplakic areas. a phenomenon known as field cancerization.
Erythroleukoplakia and Speckled Erythroplakia (Fig, 28·5) Erythroleukoplakia and speckled erylhroplakia, or "speckled leukoplakia," as some authors prefer, are precancerous red and white lesions. Erythroleukoplakia is a red patch with isolated leukoplakic areas. whereas speckled erythroplakia is a red patch that contains white speckles or granules throughout the entire lesion. A variant red-white lesion thai has a nodular appearance is called proliferative verrucous leukoplakia. Erythroleukoplalda and speckled erythroplukia have a male predilection, and most lesions are detected in patients over age 50. They may occur at any intraoral site, but frequently affect the lateral border of the tongue, buccal mucosa, and soft palale. These lesions are often associated with heavy smoking, alcoholism, and poor oral hygiene. Fungal infections are common in speckled erylhroplakias, Candida a/bicans. Ihe predominant organism, has been isolated in the majority of cases: therefore the management of these lesions should include analysis for candida. The cause and effect relationship of candidiasis and speckled leukoplakia is unknown. but erylhroplakia with leukoplakic regions confers a greater risk for atypical cyla-logic changes. Because of the increased risk for carcinoma, biopsy is mandatory of all red-white lesions. Squamous Cell Carcinoma (Figs. 28·5 through 28-8' Squamous cell carcinoma is a malignant neoplasm of mucosal origin. It is the mOSI common type of oral cancer. accounting for over 90% of all malignant neoplasms of
62
the oml cavity. Oml cancer may occur al any age. but primarily a disease of Ihe elderly: greater than 95% of cancers occur in persons over the age of 40. In Ihe pasL prevalence was much higher in males, but the mak female r.!tio has dramalically decreased in recent YC3f\ approximately 2: I. owing to the increased num~r women who smoke. The exaci cause of oml cancer is unknown. C}to atypism and mutagenesis may be a resuh of multiple f associated with aging and exposure to a variety of bi chemical. and physical agents such as the following: tion with Treponema pa/fidl/m. herpes simplex virus. h papilloma virus, or Candida a/bicans: excessive use tobacco and alcohol: nutritional deficiency states: neglect: chronic trauma: radiation: and immune supp'~"". The most common site for intraoral squamous cell cinoma is the lateral border and ventral surface of tongue. Other intraoral sites, in descending order involvement, are the oropharynx, noor of the mouth. va. buccal mucosa, lip. and palate. The occurrence of mous cell carcinoma of the lip has decreased dramatl in the pasl decade because of Ihe increased use of p tive sunscreening agenls. The dorsal surface of Ihe t is almost never affected. The appearance of squamous cell carcinoma is hI_ variable. with over 90% of the cases having an e.",,""'" kic component, and about 60% showing a leukop component. A combination of colors and surface pal such as a red and white lesion Ihat is exophytic. infil or ulcer.lIed, indicates instability of the oral epilhelium is highly suggestive of carcinoma. Early lesions are asymptomatic and slow-growing. As the lesion de\c the borders become diffuse and ragged. and induratioo fixation ensue. U the mucosal surface becomes ulc the mosl frequent oral complaint is that of a persl "sore" or "irritation:' Not uncommonly, patients may plain of numbness or a burning sensation. swelling. or ficulty in speaking or swallowing. Extension of lesi several centimeters in diameter can result if treatm delayed. permitting large lesions to invade and de vital osseous structures. Spread of squamous cell carcinoma occurs b) extension, or by way of the lymphatiC vessels. Slagl the tumor according 10 size (T). regional lymph nodes and distant melastases (M) affords assessmenl of the eof disease. Surgery and radial ion Iherapy have ben principal forms of treatmenl for oral cancer. The prognosis for oral cancer depends. in large sure. on the site involved, the clinical stage at the u diagnosis, the width of Ihe tumor al its greatest di Ihe palient's access 10 adequate heah,>care, abilit} 10 and mounl an immunologic response. Early treat paramount: therefore biopsy should be initialed if ~ suspicion of neoplasia.
AND REDIWHITE LESIONS
:3-1 Erythroplakia not discernible unlll the
>pressea as seen in Fig 28-2
Fig. 28-2. Erythroplakia with leul
erythroplakia along the ~ub):ngual levedled carcinoma In s:tu. /Courtesy Dr
Fig. 28-4. Erythroplakia of the floor of the mouth: biopsy revealed squamous ceil carCInoma
Erythroleukoplakia; biopsy rt"'VeaJed l
Fig. 28-6. Squamous cell carcinoma of the :orgue
.~
cancerization.
1:;-
e erythroleukoplakla that proved to caronom.:l (Courtesy Dr Robert Cralgj
Fig. 28-8. Speckled erythroplakia; biopsy revealed squamous cell carCinoma (Courtesy Dr Robert (ralgl
63
RED AND REDIWHITE LESIONS Lichen Planus (Figs. 29·1 through 29-6) Lichen planus is a common skin disease that frequently has mucosal manifestations. The etiology and pathogenesis are unknown. although evidence suggests thai lichen planus is an immunologic disorder. possibl)' an autoimmune disease. in which T.lymphocyles destroy the basal cell1ayer of the affected epithelium. Both CD4 and COB T-cell subsets have been identified in the submucosal lymphocyte population. Nervous and high-strung persons are predisposed to Ii~hen planus. The majority of patients are females over the
age of 40. The disease exhibits a protracted course with periods of remission and exacerbation. The skin lesions of lichen planus initially consist of small. flat-topped. red papules with a depressed central area. The lesions may enlarge and become polygonal in shape or coalesce into larger plaques. TIle papules progressively acquire a violaceous hue and surface lichenification, which consists of fine white striae. The lesions usually itch and may change color 10 yellow or brown before resolution. Bilateral distribution on the flexor surfaces of the extremities is common. occasionally involving the fingernails. Patients with characteristic purple. polygonal. pruritic papules on the skin often have concurrent intraoral lesions. Oral lesions of lichen planus may have one of four appearances: atrophic, erosive. strialed (reticular). or plaquelike. More thun one form may affect a single patient. The most frequently affected sile is the buccal mucosa. The tongue, lips. palale. gingiva. and floor of the mouth may also be affected. Bilateral and relatively symmetrical lesions are common. Patients with reticular oral lichen planus characteristically have multiple delicate white lines or papules arranged in a lacy. web~like network known as "striae of Wickham." The glistening white areas are often asymptomatic but of cosmetic concern. They may involve large areas. Atrophic lichen planus results from atrophy of the epithelium and predominantly appears as a red. non-ulcerated mucosal patch. Wickham's striae are often present al the border of the lesion. When the attached gingiva is affected. the lerm "desquamative gingivitis" has been used. Erosive lichen planus occurs if the surface epithelium is completely lost and ulceralion results. The buccal mucosa and tongue are commonly affected sites. Initially, a vesicle or bulla may appear which eventually erodes producing ulceralion. Mature lesions have irregular red borders. a yel· lowish necrolic central pseudomembrane, and an annular
64
white patch often at the periphery. The condition i millently painful and may onset rapidly. All of theSt lures are helpful in differentiating oral lichen planU5 other clinically similar·appearing lesions such as I plakia, erythroplakia. candidiasis. lupus er)'them pemphigoid. and erythema multiforme. The least common type of lichen planus is the • tommie plaque form. This lesion is a solid white plaqIR patch that has a smooth to slightly irregular surface asymmetric configuration. Lesions are commonly fOlD,. buccal or glossal mucosa. Patients may be una.. arr these lesions. In many cases clinical appearance alone can confi diagnosis of oral lichen planus. and a biopsy is not sary. Asymptomatic intraoral lesions can be left Biopsy of the atrophic or erosive form should be formed at the border of Ihe lesion. The oral lesions of lichen planus lend 10 be more tent than those of the skin. A vacation, change in or discharge of psychologically burdensome proble bring about abrupt and dramalic resolution of (he Chronic. symptomatic. erosive lichen planus lesi best managed with lopical or syslemic steroids immunosuppressants. A small number of patients "'1 . lichen planus are diabetic and should be tested for intolerance. Carcinomatous transformation has reported (in less than 100 cases) 10 have an asso<"'-_ with erosive lichen planus and tobacco use. The true and effeci relalionship. however. has yet 10 be esta for squamous cell carcinoma and lichen planus. Electrogalvanlc White Lesion fFigs. 29·7 29-8} Electrogalvanic while lesions closely resemble hypenrophic form of lichen planus. This disorder IS apparent after the age of 30 and frequenlly occurs buccal mucosa. immediately adjacem to a melallic tion. Mild cases are asymptomatic. whereas erosi\e can cause a burning type of pain. Histologically this mimics lichen planus. Electric microcurrents ind dissimilar restoralions is one explanation for thu nomenon. Inlerestingly, lichenoid drug reactions... similar in appearance to electrogalvanic while lesioas: be caused by the systemic application of the same (mercury and gold) found in dental restorations. T consists of replacing the reslOralion with a different tive malerial. preferably gold. porcelain. glass iOOOlDl:E" composite materials. 1be prognosis is excellent.
~:>
AND REDJWHITE LESIONS
.3CeClUS
skin plaque with lichenification on
. re of lichen planus.
• ul denuded patches of erosive lichen
5 Red .. trophic lichen planus on buccal _psy (Courtesy Dr Tom Razmusj
ElKtrogalvanic white lesion that has a _ - '1( dent to the adjacent dass-V alloy
Fig. 29-2. Characteristic V/ickham striae of reticular lichen planus. ICourtesy Dr Birgit Glass)
Fig. 29-4. Erosive lichen planus; same patient as in Fig 29-3.
Fig. 29-6. Plaque form of lichen planus with
a
fevv striae.
Fig. 29-8. Electrogalvanic white lesion opposite Side in the same pallent as seen in Fig. 29-7
65
RED AND REDIWHITE LESIONS Lupus Erythematosus fFigs. 3D-' through 30-41 Lupus erythematosus (LE) exist'" in three ronns: chronic discoid lupus erythematosus (CDLE), which only involves the skin: systemic lupus erythematosus (SLE), in which mulli· pie organ systems are involved: and subacute cutaneous lupus erythematosus. a cutaneoUs varianl wiTh mild systemic symptoms. The cause of all three types is unknown. COLE. the benign form of the disease. is a purely mucocutaneous disorder. II may appear al any age. but predominates in females over the age of 40. COLE is classically characterized by a red bUllerfly rash symmetrically distributed across the bridge of the nose. Other prominenl photosensitive areas of the face, including the cheeks. malar areas. forehead. scalp. and ears. may be involved. The lesions of LE are chronic wilh periods of exacerbation and remission. Mature lesions exhibit three zones: an atrophic center lined by a hyperkemtotic middle zone which is surrounded by an erythematous periphery. Frequently there is hypopigmentation of the lesion resulting from melanocytic damage at the epidermal-dermal junction. Telangiectasias, blackheads. and a fine scale are common dermal findings. The lesions are usually limiled to the upper ponion of the body, particularly the head and neck. Twenty to 40% of patients with LE have oral lesions. These lesions may develop before or after skin lesions develop. Lip lesions are red with a white 10 silvery. scaly margin. A sun-exposed lower lip at the vermilion border is a common site. whereas the upper lip is usually involved as a result of direci extension of dermal lesions. Intraoral lesions are frequently diffuse and erythematous. with ulcerative and while components. Occasionally COLE appears as isolated white plaques. The buccal mucosa is the most frequent imraoral site. followed by Ihe tongue. palate and gingiva. Alternating parallel red and white lines in a radial arrangement are an imporlant diagnostic feature. along with the appearance of multiple lesions on several surfaces. These lesions may mimic lichen planus; however, concurrent ear involvement helps to exclude the diagnosis of lichen planus. Ulcerative lesions are painful and require treatment. Avoidance of emolional stress. cold. sunlighl. and hOI spicy foods is necessary. The use of sunscreens. topical steroids. systemic steroids. and antimalarial agents have proven effective. Patients using antimalarial agents require close ophthalmologic foUowup. SLE. an aUioimmune collagen disease. is characterized by the production of antinuclear and anti-DNA antibodies that participate in immunological1y mediated tiS5ue injury.
66
Patients often complain of fatigue. fever. and JOInt Generalized nontender lymphadenopathy is often Hepatomegaly, splenomegaly. peripheral neuropath. hemalOlogic abnonnalities may also be seen. Strict ance of sun exposure is necessary. since sunburn gel' acute reactions. Involvement of the kidneys and is a common occurrence that may prove fatal. S oral lesions may accompany SLE. but there is little of conversion from discoid to systemic lupus. PatieOB SLE often suffer concurTemly from other autoimmtmr lagen-vascular diseases such as Sjogren's syndromerheumatoid arthritis. Allergic mucositis. candidiasis. plakia. erythroleukoplakia. and lichen planus must br side red in the differential diagnosis of oral LE I~ Biopsy and histologic examination with immunon cence confirms the diagnosis. Precautions are ad\ the denial treatmenl of patients with lupus erythe who may be laking high doses of systemic St because of their predisposition to delayed wound the risk of infection. and the possibility of stressadrenal crisis characterized by cardiovascular co...' These patients are also at risk for cardiomyopath~ requires antibiotic prophylaxis. Uchenold and Lupus-llke Drug Eruption )0-5 through 3o-BI Relicular or erosive lesiOfb in appearance 10 lichen planus and lupus er)"the may occur in association with a variety of systemic tion~. Allhough the appearance may be quite varied.. linear plaques with red margins are common. The may erupt upon immediate or afler prolonged use of .. Persistent innammalOry changes may result in large er matous areas. eventual mucosal ulceT'"dtion. and pam. induced lupus erythematosus is often associated ",iIb tis. fever. and renal disease. Hydralazine and p""........ are the most common instigators of lupus-like dna! lions. Other drugs known to cause lupus-like e include gold. griseofulvin. isonia~.id. mcthyldopa. cillin. phcnytoin. procaillamide. Mreptomycin. and dionc. Drugs known to induce lichenoid eruptioM the following: chloroquine. dapsone. furosemide. mercury. methyldopa. palladium. penicillamine. iaLines. quinidine. thiaLides. certain antibiotics. metals. Consultation with a physician and withdra", offending medication will lead to regression of the substitule drug is usually selected to manage thesystemic problem.
o REDIWHITE LESIONS
---
,,_."''''SU$.
rash; chronic discoid lupus
Fig. 30-2. Red scaly lip les'Orl of chronic discoid
lupus erythematosus (Courtesy Dr James Cottone)
'-19 radial red and white hoes, oid lUpus erythematosus.
Fig. 30-4. Red aldwtvte cur\llhrl6:."W" plaq..Jc; chronic discoid lupus erythematosus. fCourtesY Dr James CextOf"'M?)
pus-like drug eruption fOllOWing the _ am tnptytlne
opposIte buccal mucosa. same paClent
- 'e pliiques and wiae of a lichenoid _..,DOn subsequent to furosemide therapy
Fig. 30-6. Ulcerated lupus.fike drug eruption
as In Fig
30-5
Fig. 30-8. Withdrawal of furosemide reSulted in
complete resolution of lichenoid drug eruption
seen In Fig
30-7.
67
RED AND REDIWHITE LESIONS Acute Pseudomembranous Candidiasis (Thrush) fFigs. 31-1 and 31-21 Acute pseudomembranous candidi-
asis, an opportunistic inft:ction, is caused by an overgrowth of the superficial fungus Candida albicans. It appears as diffuse. curdy. or velvety white mucosal plaques thai can be wiped off.
leaving a red. raw, or bleeding surface. The organism is a common inhabil3m of the oral cavity. gastroinlcslinal1f3et. and vagina. InfanlS whose mothers display vaginal thrush al the time of binh and adults who have experienced an upset in the normal oral microflora due 10 antibiotics. steroids, or systemic alterations such as diabetes. hypoparathyroidism. immunodeficiency. or chemotherapy are frequently affected.
There is no racial or sexual predilection. Acute pseudomembranous candidiasis is usually found on the buccal mucosa. tongue. and soft palate. Clinically the white plaques appear in clusters that have an erythematous border. A peculiar paltern is seen in asthmatic patienls who use a steroid inhaler. The pattern appears as a circular or oval reddish~white patch at the site of aerosol contact on the palate. Diagnosis can be made by clinical examination. fungal culture, or direct microscopic examination of tissue scrapings. A potassium hydroxide (KOH). Gram·s. or periodic acid-Schiff (PAS)-stained cytologic smear will reveal budding organisms with branching pseudohyphae. Topical appJicalion of amifungal medication for 2 weeks usually produces resolution. Chronic Keratotic Candidiasis (Hyperplastic) {Figs. 31-3 and 31-41 Chronic keratotic candidiasis is caused by organisms of the candida sp. that penetrate the mucosal surface and stimulate a hyperplastic response. Chronic irritation. poor oral hygiene. and xerostomia are predisposing factors: thus smokers and demure wearers are commonly affected. Chiefly involved is the dorsum of the tongue. palate. and labial commissures. The lesion invari· ably has a distinctive raised border and a white. pebbly sur· face with an occasional red area: thus the condition may resemble leukoplakia or erythroleukoplakia. The scattered erythematous comlX'nents are a result of mucosal cell layer desuuction. The white "latch of chronic keratotic candidiasis cannot be peeled off. requiring the diagnosis to be made by biopsy. Microscopically the organisms may be identified by routine hematoxylin and eosin stain or. more appropriately. by the PAS stain. With adequate topical application of an anti-fungal agent. resolution usually occurs. In some instances surgical stripping may be required. All patienls with chronic keratotic candidiasis should be followed closely. since this fonn may be related to speckled erythroplakia. a lesion which is often premalignant or worse. Acute Atrophic Candidiasis (Antibiotic Sore Mouth) fFig. 31·51 The use of broad spectrum antibiotics. panicularly tetracyclines. can result in the oral condi-
68
tion tennOO "acute atrophic candidiasis." This fungal tion is the result of an imbalance in the oral eC(K. between Laclobacillus acidophifus and Candida a Antibiotics taken by the patient reduce the Lacrol».. population and pennit candidlll organisms to floun infection produces desquamated areas of surface that appear as diffuse. nonelevated red patches. 8 pain is the most frequent chief &mplaint. The dis of the patches of acute atrophic candidiasis is so indicative of the cause. Lesions affecting the mucosa. lips. and oropharynx often suggest the administration of antibiotics. whereas redness tongue and palate are more common following the antibiotic troches. When the tongue is affected a devoid of filiform papillae is common. It is rare for didiasis to affect the attached gingiva: if this is the finding. then severe immune suppression is a disuna sibility. The diagnosis of a candidal infection sh confirmed by demonstration of budding organL hypha I fOnTIS on a stained cytologic smear. Trea wilh antifungal agents.
5,
Angular Cheilitis 'Fig. 31-6) Angular cheit chronic painful condition involving the labial co caused by Candida albicans. Clinically. angular appears red and fissured. with the periphery of the less erythematous than central areas. Crusting and ish gmnulomatous nodules may be concurrent. Di caused by opening the mouth may limit nonnal oral tion. Predisposing factors and treatment have been ously discussed. Chronic Atrophic Candidiasis (DenStomatitis) fFigs. 31·] and 31-8) Chronic candidiasis is the most common form of chronic "". ._ It is present in 15 to 65% of complete and partial wearers. panicularly elderly females who wear their tures at night; rarely dentate patients may also be The mandible, however, is rarely involved. Misnomcro this disease are the terms "denture sore mouth" and lUre base allergy". Chronic atrophic candidiasis is caused by candida) isms located under the denture base. There are thrtt of mucosa.! alterations. The earliest lesions are red areas of hyperemia limited to the orifices of the minor salivary glands. Progression produces a di~ merna of the hard palate that is sometimes accom epithelial desquamation. Papillary hyperplasia is tbt stage. It may be generalized or restricted to relief Rarely a fourth stage is apparent; the enlarge~nt of _ _ papules to form red nodules on Ihe vault of the . . .~ Effective therapy requires antifungal treatment mucosa and denture base. The role of trauma, sue. rocking action of the denture. may perpetuate the 000","_
ae:
AND REDIWHITE LESIONS
.! .' Thrush In an immunosuppressed p.3tient. : )ol Sl'verman)
Fig. 31-2. Acute pseudomembranous candidiasis in a patient that uses a steroid inhaler, (Courtesy Dr Geza Terezhalmyl
" ...... .-.', ',\
.~
.:.~~
-3 Chronic hyperplastic candidiasis at the ~'e which
extends onto the buccal mucosa
:", Acute atrophic candidiasis limited to
~
,
Fig. 31-4. White keratotic plaques of hyperplastic candidiasis in a deblliated pallent
Fig. 31-6. Angular cheilitis. (Courtesy Dr JC1mes
:"-Dearing area, due to steroid Inhalant
Cottonel
Papillary hyperplasia; the third stage of
Fig. 31-8. Chronic atrophic candidiasis limited to partial denture bearing area ICourtesy Dr Nancy rvlantlch)
-
-"J.! lCourtesy Dr Ken Abramovltchl
69
PIGMENTED LESIONS Melanoplakia fFig. 32-1' Melanoplakia is a generalized and constant dark pigmentation of the oral mucosa. commonly seen in dark-skinned persons (melanoderms). The condition is physiologic, not pathologic, and results from increased amounts of melanin, an endogenous pigment. that aTC deposited in the basal layer of the mucosa and lamina propria. The most common site for observing melanoplakia is the attached gingiva. It often appears as a diffuse, ribbon-like, dark band with a well-demarcated and curvilinear border that separates it from the alveolar mucosa. Characteristically the region is symmetric and asymptomatic. The degree of pigmentation varies from light brown 10 dark brown. and infrequently may appear blue-black. Other sites of occurrence are the buccal mucosa. hard palate, lips and tongue. At these sites the deposition of pigment often is multi focal and diffuse. Melanoplakia should be differentiated from similar-appearing conditions that produce oral pigmentations, such as Addison's disease. Albright'S syndrome, Peutz-Jeghers syndrome, heavy metal pigmentation, and anti-malarial drug ingestion. Tattoo fFigs. 32·2 through 32-51 Tattoos are caused by intentional or accidental implantation of exogenous pigments in the mucosa. The most common intraoral type is the amalgam tattoo, which has been referred to by some as "focal argyrosis:' The amalgam tatoo appears as a blueblack. non-elevated discoloration that is usually irregular in shape and variable in size. It results from the entrapment of amalgam in a soft tissue wound such as an extraction socket or a gingival abrasion from a rotating bur. Deterioration of the silver compounds of the amalgam impart the characterislic blue-black color. Focal discolorations may occasionally appear green 10 dark gray because of the deposition of high copper alloys. Amalgam tattoos are usually seen in the gingiva in posterior arcas adjacent to a large amalgam restoration or gold casting. These lesions are not limited 10 the gingiva and may also be seen on the edentulous ridge. vestibular mucosa, palate, buccal mucosa. and floor of the mouth. The clinical diagnosis of an amalgam tattoo can be confirmed by finding radiographic evidence of the foreign metal in the paradental tissue. The radiographic appearance may vary from no demonstrable particles to pinpoint or globular radiopacities several millimeters in diameter. If radiographs fail to demonstrate suspected metallic particles. a biopsy is required 10 rule out more serious pigmented lesions. Other types of tattoos seen in the oral ca\'ity are the graphite pencil wound and India ink tattoos. The graphite
70
pencil wound appears following Irauma as a focal. gray macule frequently located on the palate. The the lesion can be easily ascertained by questionq patient. Ordinary India ink tattoos are occasional on the labial mucosa of the lower lip. In generaL la hannless and of no clinical significance; however. ~ be indistinguishable from more potentially ominous
Ephelis ,Freckle) fFig. 32-61 An ephelis is a _ dark-brown macule that appears on the lip or skin ~ ing active deposition of melanin triggered by ex sunlight. Unlike some pigmentations, this lesion ""• • essentially unchanged in size with time. darl; response 10 sunlight, and has a predilection for skinned or red-headed persons. A single freckle is m...... ly distinguished from an oral melanotic macule b} tory of a traumatic or inflammatory episode that the development of the latter condition. Microsc the ephelis shows an increase in melanin pigment ,. an increase in the number of melanocytes. Multiple les on the lip should be distinguished from the iden ephelides seen in conjunction with palmar pigmt' and intestinal polyposis of Peutz-Jeghers s~ .....~ Ephelides m3.Y be of cosmetic concern requiring removal; othen,vise. observation is normally reco""'...... Smoker's Melanosis ITobacco-Assoclate-d mentation) {Figs. 32-1 and 32-81 Smoking imparts a characteristic color change to exposed surfaces that is tenned smoker's melanosis. The is not a nonnal physiologic process, but instead principally from the deposition of melanin in lhe layer of the mucosa. The relationship of s melanosis and inflammatory changes that result f~ smoke inhalation. and the absorption of exogeous pi_ has not been detennined. Smoker's melanosis affects older individuals heavy smokers. It appears as a diffuse brown patch centimeters in size. The mandibular anterior gin buccal mucosa are the most frequently affected sj~ susceptible sites include the labial mucosa. palate, floor of the mouth, and lips. The degree of pig........ ranges from light to dark brown and appears to be related to the amount of tobacco consumed. Us finds dark-brown foci asymmetrically distributed out an ill-defined. light-brown patch. Brown-slaiDtd and halitosis usually accompany the condition. 5 melanosis itself is not premalignant; however. the "'...... should closely inspect the adjacent tissues for 'otba co-induced lesions.
NTED LESIONS
M~lanopl.. kia
dlSC/lbuted along the
_ ~~i.fJ. macular _--e? OrosI
amalgam tattoo.
S Focal argyrosis from failed silver point
"
- Smoker's melanosis; lateral regions of the
Fig. 32-2. Ind!3-lnk tattoo. (COUrtesy Dr David Freed)
Fig. 32-4. R
oa'tlClcs bervvren the rlfSl molcV" elM second blC\.lSpd. confirm.ng the atagnoslS Or amalgam tattoo.
Fig. 32-6. Multiple ephelides {frecklesl of the face and lips
Fig. 32-8. Smoker$ melanosis of the weecl mucosa;
same pclclent as seen In Fig 32-7 71
PIGMENTED LESIONS Oral Melanotic Macule {Figs. 33-1 and 33-2) Within the mouth. an increased amount of melanin deposited as a single. flat. well-circumscribed discoloration usually less than I em in diameter is tcnned an oml melanotic macule. These endogenous pigmentations are common in lightskinned individuals between 25 and 45 years old and probably represent jX)Snraumatic or inflammatory pigmentation. a condition analogous to po5linflammalory hypermelanosis on the skin. The most common site is the lower lip close to the midline. Other sites include the gingiva, buccal mucosa. and palate. The color is uniform and may be blue. gray. brown. or black. Biopsy is recommended. unless the lesioo has been present for many years wilhoUi visible change and periodic observation is provided.
Nevus (Figs. 33-3 through 33-61 The nevus is commonly seen on the skin and may. in rare instances. occur in the mouth. Ahhough the histogenesis of the nevus is controversial. authorities suggest that it has a melanocyte or Schwann cell derivation. There are a number of different types of nevi. which are broadly classified as either con~ genital or acquired. Congenital nevi are present at binh and are also known as birthmarks or "garment trunk" nevi. They are usually larger than acquired nevi and have a higher incidence of malignanttl'3nsformation. Acquired nevi. or moles. occur later in life and usually appear as dari;:. slighlly raised papules or dome-shaped nodules. They may vary in pigment. and can be brown. gray. blue. or black. Occasionally nevi are amelanotic and appear pink. Intl'3orally the nevus is a rare finding. They are usually small (only a few millimeters). pigmented, well-circumscribed, dome-shaped papules or nat macules that occur more frequently on the palate and buccal mucosa of females. Their size tends to remain constant after puberty. These asymptomatic lesions do not blanch on pressure. Benign nevi have been classified into four subtypes according to the histologic appearance and location of the nevus cells. which are arranged in nests. or ·'theques.'· In order of decreasing frequency one finds the following nevi: intramucosal nevus. blue nevus. compound nevus. and junctional nevus. The intra mucosal nevus, the most common nevus found in the mouth and the Ixxly. has ovoid nevus cells located in the connective tissue only. This entity is analogous to the intradennal nevus. which appears as a dari;: raised papule on the skin. often seen with a hair growing from iL It is rare, however. to find a hair associated with the intramucosal nevus of the mouth. Usually the intTamucosal nevus is brown, raised. and between 0.4 and 0.8 cm in diameter. The second most common intraoral nevus is the blue ne\·us. The name originates from the typical blue or blueblack color imparted by the spindle-shaped nevus cells located deep in the connective tissue. These cells are
72
derivatives of neural crest cells that fail to migrate region. A small. well-circumscribed blue macule b ical appearance, although the color of the nevus one. with age. The palate is the mOSI common Malignant transformation of intraoral blue nevi been reported. The compound nevus. as the name implies. posed of nevus cells located in the epithelium and_ na propria. Like the two previous nevi. the c nevus rarely undergoes malignant transformal junctional nevus is a subtype of acquired nevus nevus cells at the junctional layer of the epilhelium. lamina propria. These lesions are the rarest I)pe' nevus and usually appear l1al. brown. and less m. The palate and buccal mucosa are common locan On rare occasions the melanolic frecl::le of H (lentigo maligna) is found in Ihe mouth. More 00....the melanotic freckle is seen on Ihe face of pe the age of 50. This lesion is flat. irregularly sha diny gray-brown in color. It may spread superfi horizontal direction and undergo malignant transf: Nevi may be difficult to distinguiSh from IMU nant counterparts; thus all intraoral pigmented should be surgically removed and submi hislOpalhologic examination. especially if they an: to chronic irritation.
Malignant Melanoma IFigs. 33·7 and Melanomas are malignant neoplasms of melan • may occur in the oral cavity. They occur appro twice as frequently in males as in females and ~ sons over the age of 50. Approximalely 30% of ..."". have been reported 10 arise from previously exi mented lesions, particularly ones with a history of Like the nevus. melanomas may be flat or rai pigmenled or pigmented. When pigmented their usually deep and varies from brown. gray. blot black. The most frequent sites for occurrence art ~ illary alveolar ridge. palatal tissues. anterior gin labial mucosa. Inilially melanoma is a small. slightly raised p&its aggressiveness causes rapid growth in all d. Eventually a prominent. non-moveable. dark leslon The main distinguishing clinical features include colors (Ihe combination of red together with blue white is panicularly ominous), change in size. i""I'L_ ill·defined margins, satellite lesions arising at the of the lesion. signs of inflammation. such as a zone of erythema. bleeding and ulceration. fi~ pation. and rock hard regional lymph nodes. . . . .<;Ii malignant melanomas are extremely dangerous _. , , _ serious than their cutaneous counterpart. due to ea" wide metastasis which resulls in a very poor progDD"
"_L
MENTED LESIONS
mOst common 5ne of the melanotic er p
-"le
!3-3 Blue nevus Of the hard palate ICounesy Dr - ch
O\Vfl flat compound nevus "e (Courtesy Dr Dare Mllesl
3:3-5 3
r
on me
33-1 B.n P19memanon. p,npomr satellite 1es1OflS. erythema charactenstlC of malignant _ ......m ... ,Courtesy Dr GeZil Terezhalmyl
Fig. 33-2. Brown melanotic macule of the hard palate
Fig. 33-4. Dark ptgmented blue nevus on the lateral palatal vault fCOUrtesy Dr Tom McDavrd)
Fig. 33-6. Ratse<:! nooule adJ¥erlt to firs! maxillary molar. amelanotic intramucosal nevus. (COUrtesy
Or Curt Lundeen)
Fig. 33·8. vegetatIVe. amelanotlC malignant melanoma; paklle and atveolar ridge (Courtesy Drs AM Abrams (lnd JOhn Tall)
73
PIGMENTED LESIONS Peutz-Jeghers Syndrome (Hereditary Intes-
tinal Polyposis, fFigs. 34-1 and 34-2) PeutzJeghers syndrome is an aUl050ma) dominant condition associated with multiple melanotic mucocutaneous macnles and gastrointestinal jXllyposis. These multiple benign
intestinal polyps are hamartomatous tissue growths Ihal usually occur in the ileum, bUI may also be found in the stomach and colon. Symptoms such as intennillent colicky pain and complaints of obstruction may be concurrent.
Of relative imponance to the dentisl are the muhiple. asymptomatic. melanotic discolor.uions. These lesions are usually small. flat, brown ovals that are prominently located on the skin around the eyes. nose and mouth. as well as on the lips. perineum. oral mucosa, gingiva, and palmar and planlar surfaces of the hands and feel. The mOSI common intraoral locations for these pigmentations are the lips and buccal mucosa. In contrast to their cutaneous counterparts. the inlrnOral spots tend to persist into adulthood, whereas the dermal macules may fade with age. 0 treatment is necessary for the macules, which microscopically contain hyperpigmentation of the basal cell layer and lamina propria. Although the macules are benign findings, they are of considerable clinical significance, since a small percentage of affected patients are prone to develop gastrointestinal adenocarcinoma and are at an increased risk for tumors of the reproductive system. The diagnosis of Peutz-Jeghers syndrome therefore necessitates prompt medical evaluation,
Addison's Disease ,Adrenal Cortical Insufficiency' (Figs. 34-3 and 34-41Addison's disease most commonly results from aUioimmune-induced destruction of Ihe adrenal gland. Other causes include infectious diseases, adrenalectomy. gram-negalive sepsis. pituitary insufficiency. and tumor invasion. Progression of the disease results in anemia. anorexia. diarrhea. hypotension. lethargy. nausea. and weight loss, A complication associated with this disorder is failure of the feedback loop from the adrenal gland to the pituitary gland. This causes an increase in adrenoconicotrophic hormone (ACTH). which induces melanocYle-stimulating hormone (MSH) and the deposition of melanin in the skin. Classically the skin acquires :I bronze tan that persists following sun exposure. Darkening may be initially noted on the knuckles. elbows. palmar creases. and intraoral mucosa. IntraoraHy Ihe disease is characterized by hypermelanosis similar in :lppearance to melanoplakia. The puuern is not unique and may consist of multiple focal blue-black spots or generalized. diffuse streaks of dark-brown pigmentation. Usually the pigmented areas are macular, nonraised, brown, and varied in shape. The buccal mucosa and gingiva are most commonly affected. bUI the pigmentation may extend ontO Ihe tongue and lips as well. Biopsy is nol
74
diagnoslic and serum cortisol tests are recom Replacement therapy with conicosteroids produ~ ual diminution of the hyperpigmentation: thus the of oral pigmentation is a sensitive indicator of t"'~~ effectiveness. Transient changes in pigmentation in ed patient may be an indication of inadequate the~
Heavy Metal Pigmentation (Figs. 34-5
""':0.;-
34-8J Excessive ingestion of heavy metals (bismu mercury. silver) and cenain drugs (antimalarials. chotics. binh control pills) can produce mucoc pigmentalions, Bismuth is commonly found in medications, which if used chronically will result m deposition of the metal in the gingiva. The discol confined to the marginal gingiva. panicularl) I where inflammation is present. Typically the line" appears blue to black in a linear distribution gingival sulcus. A metallic taste and burning m common complaints. Lead poisoning, or plumbism. usually is a result pational exposure to excessive doses of lead used • or plumbing. The most prominent intraoral chan__ early diagnostic sign is a gray-black "lead line" m. from the deposition of lead sulfide in Ihe marginal Spotty gray macules on the buccal mucosa. a coated tremor of the extended tongue. and hypersaii\' other intraoral findings. The condition is reversible sure to lead is eliminated. Mercury poisoning. or acrodynia. can be aeq absorption, inhalation, or ingestion. Although u"",..,~ today. acrodynia was the end-result of treat syphilis earlier in the century. Inadequate mercW) measures such as handling mercury. brealhing vapors. and spilling mercury place dental personnel for acrodynia. like bismuth and lead intoxication. mercul) produces a dark mercury gingival line. In addition. ease is often accompanied by a multitude of Sl symptoms. including abdominal pain. anorexia. ~-=;:;. psychological symptoms. venigo. oral ulcerations.. rhage, a metallic taste, sialorrhea, burning mouth._ adontal destruction. Silver pigmentation, or argyria. is a rare occu~ most often results from prolonged exposure to si ~ laining ocular or nasal medications. Asymptomatic tations accumulate in the sun-exposed areas of tK along with the hair. fingernails, and oral mucosa. gray pigmentation is characteristic. which once ~ irreversible. Nasal inhalation of solutions contaillUl! salts have a propensity for deposition in the palata! imparting a similar color to Ihal seen on the skin. T·....... is immediate withdrawal of the medication. M
""CiMENTED LESIONS
flat. brown pl9menlaOOOS of me bps,
..._ ..... hers syndrome.
Fig. 34-2. Brown macules on £he buccal mtJCQS.Cl. same pattent WIth Peutz.Jeghers syndrome as If1 Fig 34--1
•
Fig. 34-4. Diffuse plgmenlClllon on the buccal mucosa and lOngue, same patient With Addisons disease as In Fig 34-3
:.pIe
J a....o wn pigmentatl9ns apparent on the lips, _'"".~.s disease.
r----~...,
sh lead line dlwitx,.ned alOng
Fig. 34-6. lead line; same paTlCf1t as.seen In Fig 3 4-5
tenor marginal gll1glViI
_
7 Argyria In a pauenr that ChronlCaJly used "y Ilao;al drops (Courtesy Dr Ch<'Irles Morns)
Fig. 34-8. Argyrosis of the palate In ano\tlef pdtlffit 'Nho used nose drops (Courtesy Dr Ch.'lrles Morris)
75
SECTION
v Intraoral Findings by Surface Change
77
NODULES Retrocuspld Papilla fFigs. 35·1 and 35-21 This anatomic structure is not seen in all individuals. It consists Of a finn. round. fibro-epilhelial papule. usually I 10 4 mro in diameter. located on the attached gingiva Iinguallo the mandibular cuspids jusl below or several millimeters below the marginal gmgl'.a. rhe surface mucosa is usually pink. soft. and smooth. Rarely the lesions may be pedunculated and the stalk can be lifted off lhe gingiva by a periodontal probe. This condition is a variation of normal and is frequemly found bilaterally. Some 3U1horities stale thai the retrocuspid papilla is a developmental anomaly that represents a variant form of fibroma. Apparently the reuocuspid papilla is present in most children, but regresses with maturity: lhus the incidence and size decrease with increasing age. The retrocuspid papilla has no sexual predilection. and no treatment is necessary unless interference with a removable prosthesis is
contains dark-staining lymphoid aggregates \Itnent germinal centers.The luminal fluid is yelloa cous. Excisional biopsy should be performed histologic confirmation. Recurrence of Ihe lym Iial cyst is rare. Torus. Exostosis. and Osteoma (Figs.. through 35-81 Tori. exostoses, and peripheral are readily recognizable bony hard nodules that lologically identical. The term used depends OIl appearance, and systemic associations. Bony protuberances of the jaws, localized to_ midline or mandibular lingual attached gingiva. :Ill'e ·'tori". They are the most common intraorallesK. exophytic by nature. Females are most frequentJ_ Tori have smooth rounded contours. nomml-appea slightly pale mucosa. and a ~ssile b..1se. Often ton to have a lobulated surface. Internally they are conical bone with occasional areas of spongy borJ:' Bony outgrowths in alternate locations ~ "exostoses". The facial aspect of the mumandibular alveolar ridge are common sites. I . Ihe palatal alveolar ridge adjacent to maxillary affected. Usually exoslOses are multiple hard no_-, demonstrate crease-like folds belween distina The surface mucosa is firm. taul, and while 10 par Tori and exostoses tend to increase Slowl} in increasing age. but remain asymptomatic unless ""_-=~ Following a traumalic incidem. patients may be about neoplasia and insist that the bony mass is ",....",,-,. that it was not presem prior 10 the injury. RertlO\ ally unnecessary unless prompted by cosmetic. tic. psychological. or traumatic considerations. Osteomas are considered to be neoplaslic are distinct from the developmemat lesions. ton toses. because osteomas have more growlh ~ to be larger. and may be confined to soft tissue with osteomas should be examined radiogra multiple impacted supernumerary teeth. which cate the presence of Gardner's syndrome (see p. autosomal dominant condition is characlerized mas, dermal CYSIS, mulliple impacled and su"""". teeth, and intestinal polyposis with a high p malignant transformalion. The majority of ...""., Gardner's syndrome will demonstT'dte malignaa: by age 40: Iherefore aLI patients with this conma.. close medical management.
•
78
OULES
rs-1 Retrocuspld papill'" appeanng i'lS a pink
-,
-~-
" Iymphoepithellal cyst on the -'"9"e
.....s..e mandibular tori.
_>-.. .
Exostoses apparent at the mucoglngrval 'T'..2\, Ia and mandible
Fig. 35-2. Unusual elefllng of.-. retrocuspid papilla.
Fig. 35-4. Pinkish nodule rn the IIoor of the mouth
rejJfesentlng a lymphoeplthelial cyst.
Fig. 35-6. MultInodular mandibular tori.
Fig. 35-8. Paletta! exostoses. fCOUrtesy Dr Tom McDCMd)
79
NODULES Irritation Fibroma and Peripheral Odontogenic Fibroma IFigs. 36-1 and 36-2) The irritation fibroma is one of the most common benign lesions of the oral cavity. It results from reactive hyperplasia caused by a chronic irritant; thus this lesion is nOI a true neoplasm as the term "fibroma" seems 10 imply. True neoplastic fibromas are a Tarc intraoral finding. Typically the irritation fibroma appears as a welldefined, pale-pink. slow-growing papule that with time enlarges to form a nodule. This smooth and symmetrically round lesion is finn and painless to palpation. Infrequently a leukoplakic, roughened, or ulcerated surface is present. The base is usually sessile. This growth can arise on any soft tissue location in the mouth, including buccal mucosa, labial mucosa, gingiva, or tongue. Histologically an interlacing mass of dense collagenous tissue is found subjacent to thinned epithelium. Fibromas are best treated by removing the source of the irritation together with surgical excision. Fibromas recur infrequently if treated properly. Multiple intraoral fibromas may be associated with the condition tuberous sclerosis (Bourneville-Pringle's disease), which is characterized by seizures, mental deficiency, and sebaceous adenomas that are in fact fibromas. The peripheral odontogenic fibroma is clinically similar to the irritation fibroma, but is characterized by its unique location and tissue of origin. In most cases the peripheral fibroma is found as a circumscribed swelling in the region of the interdental papilla, generally located anterior to the molar teeth. A cup-like erosion of the underlying alveolar bone may be radiographically evident. It probably arises from cellular components of the periodontal ligament. Microscopically, clusters of odontogenic epithelium among dense collagenous tissue is found.
Lipoma (Figs. 36-3 and 36-4) The lipoma is a common dermal tumor, but a rare intraoral finding. This benign neoplasm is composed of mature fat cells surrounded by a thin, fibrous connective tissue wall. Adults over the age of 30 years are commonly affected, and no sexual predilection exists. Imraorally the lipoma appears as a well-circumscribed, smooth~surfaced, dome-shaped or diffusely elevated nodule that is yellow to pale pink in color. Occasionally lipomas may be polypoid, pedunculated. or lobulated. Lipomas are slow-growing submucosal nodules that occur on the buccal mucosa, tongue, floor of the mouth. alveolar fold. and lip. The palate is a rare site of involvement. Palpation reveals a soft. movable. and compressible submucosal mass that has a slightly doughy consistency. Therapy consists of surgical removal, which includes the base of the lesion. Lipomas rarely recur. Lipofibroma (Fig. 36-5) The lipofibroma is a rare benign intraoral neoplasm of mixed connective tissue origin. Microscopically it is a well-demarcated submucosal
80
mass that consists of mature lipid~containing significant fibrous connective tissue componenL the appearance is a blend of a fibroma and Ii generally found on labial and buccal mucosa. Oa the lesion is non~indurated, movable, painless_ firm depending on the lipoid-to-collagen con lesions are slow growing, but if left untreated grow to several centimeters in diameter.
Traumatic Neuroma fAmputatlon Ne {Fig. 36-61 The traumatic neuroma results fl"()d plastic response to nerve damage following se\ large nerve fiber. Intraorally the traumatic ne~ quently encountered in the mandibular mucobucat the region adjacent to the mental foramen. Other include the area facial to the mandibular incison.. lingual to the retromolar pad. and the ventral { _ of the lesion depends upon both the degree of degree of hyperplastic response. Traumatic neuromas are usually very small suring less than 0.5 em in diameter. Visualization ~ cult if the lesion is located deep below normal ant. Neuromas are painful when palpated. Pressure "PI.... neuroma elicits a response often described as all shock." Multiple neuromas discovered on lips. palate may indicate the possibility of multiple endl"". plasia Type lib. Treaunent of the trawnatic neuroma excison or intralesional injection with corticosteroids.. may further damage the nerve and lead to recurrence. Neurofibroma {Figs. 36-7 and 36-81 • proliferation of all the elements of a perip~ including the sheath of Schwann, results in the tumor neurofibroma. They most commonly apper pink nodules. Clinically neurofibromas may be diffuse, or over \000 in number. Solitary nod~ More commonly, multiple large neurofibromas ~ tered, which are associated with neurofibro Recklinghausen's disease). Neurofibromatosis is an autosomal dominaJll characterized by skin pigmentations (cafe-au-lail axillary freckling) and multiple neurofibromas llR""'" skin. oral cavity, bone, and gastrointestinal trna.. ~ nomonic sign of this disorder is Crowe's sign. wbdt of more than 5 cafe-au-Iail spots and axillary ~ Intraoral neurofibromas may be located OIl the cbI:a. buccal mucosa. tongue, and lips. Most soft tissue ..,""...... are asymptomatic; however, those arising within dec;amay produce pain and paresthesia. Diffuse ne"",fib"",'" striking for their firmness and irregular nooular surfxr results in physical defonnity. In some cases ~:::~ undergo sarcomatous change, necessitating close fl tar)' neurofibromas not associated with von Rec"~",,,,,,,,,!! disease have no tendency for malignant transformatil:a
..cOULES
\
iHge nodule; irritation fibroma.
Fig. 36-2. PInk Interdental papule; peripheral odontogenic fibroma.
Lipoma arising at the junction of the hard Ie (Courtesy Dr Dale Miles)
Fig. 36-4. Diffuse lipoma of the lateral margin of the tongue.
.Jo..S. "~yeIIOW1Sh mass; lipofibroma. :J Srgll Glass!
....,
::
Fig. 36-6. PInk traumatic neuroma (near midline) and a wtutlsh papilloma ICounesy Of Jeny ClOffiJ
Fig. 36-8. Neurofibroma of the lateral margin of the
tongue. 81
PAPULONODULES Papilloma (Squamous Papilloma) fFigs. 37-1 and 37-2) Papillomas are the most common benign epithelial neoplasm of the oral cavity. They appear as smalL pink-white. exophytic masses that are usually less than 1 em in diameter. The surface of the papule may be smooth. pink. and pebbly. or have numerous small fingerlike projections. The base is pedunculated and well-circumscribed. Intraoral lesions are Iypically soft. whereas those on exposed areas of the lips arc usually rough and scaly. Solitary lesions are the general finding, bul multiple lesions are occasionally seen. A viral etiology is probable with a recent study implicating human papilloma virus (HPV) Types 6 and 1 J in 35% of the squamous papillomas examined. Because the papilloma is slow growing, any rapidly advancing papillomatous lesion should be suspected to be a more aggressive lesion. The mean age of occurrence of the papilloma is 35 years and more cases have been documented in males than in females. The most common location is the uvulo· palatal complex, followed by the tongue and frenum, lips, buccal mucosa, and gingiva. Other HPV-induced lesions such as the condyloma acuminatum, focal epithelial hyperplasia (Heck's disease). and verruca vulgaris share similar clinical features, but are microscopically distinct. Treatmem is complete excision, including the base. Recurrence is rare. There have been no documented cases of malignant transformation. Verruca Vulgaris (Figs, 37-3 and 37-41 Verruca vulgaris is a common skin growth that seldom occurs intraorally. The etiologic agent is a papilloma virus, Virally induced cellular changes result in the characteristic clinical findings. Typically the lesional surface is rough and raised with white finger-like projections. The white· ness of imraoral verrucae varies depending on the amount of surface keratinization. Pink areas are not unusual at the lesional base. Verrucae are commonly located on the skin, vermilion border. labial and buccal mucosa, tongue, and attached gin· giva. The base of the lesion is broad, but the size is usually less than I em. Clinically a verruca may appear identical to a papilloma, although the clefts are more shallow and the mass more sessile, Viral inclusion bodies are frequently seen histOlogically, Individuals with skin verrucae are more likely to have oral lesions as a result of autoinocula· tion. Occasionally a lesion may regress spomaneously. If not. treatment is complete excision or ablation with a car· bon dioxide laser,
82
Condyloma Acuminatum fVenere.ili fFigs. 37-5 and 37-61 The condyloma acum_ _ transmissible papillomatous growth that may I to the papilloma or fibroma, except for several ing features. The oral condyloma occurs much quently than the papilloma. It is seen more c sexually active individuals and is much more multiple. The warm, moist. intertriginous ~ anogenital sk.in and mucosa are frequent sites of _ Condyloma acuminata are usually multiple. colored pink to dirty gray. The surface may be more often pebbly and resembles a cauliflower. 1ksessile and the borders are raised and rounded. spread may occur among the host and sexual ....."'. When multiple lesions are present. proliferation ai condylomas can form extensive clusters that ma~ a single mass. Any oral mucosal surface rna) be but the labial mucosa is the most common site logically condylomata exhibit parakeratosis. CTypIX ination of comified cells, and koilocytosis. (her condyloma acuminala have HPV Types 6 and 11 sent in the epithelium. Treatment of choice is ... sion, since these lesions have a high rate of =.".,,=~ Occasional oncogenic transformation of longgrowths has been reported. Lymphangioma (Figs. 37·7 and 37-8) L_ giomas are benign tumors of lymphatic channeJJi u. op early in life with no sexual predilection. The) on skin or mucous membrane. The oral cavity is ~ site. The most common intraoral sile is the dorsal a1 surface of the anlerior portion of the tongue. f; the lips and labial mucosa. Small superficial lymphangiomas have irregtbIF lary projections that resemble a papilloma. Tk. and compressible, and vary in color from normal. whitish. slightly translucent. or blue. Deep·seatM cause diffuse enlargement and stretching of me mucosa. Macroglossia. macrocheilia. and cystic are clinical deformities resulting from the diff~ Aspiration or diascopy is mandatory prior 10 excision of a lymphangioma to pre\'ent compLic ciated with the similar-appearing hemangioma. with a large, diffuse lesion often require hopltal . monitor post-operative edema and possible air"..~ tion. Lymphangiomas do not undergo malignant Some lymphangiomas. especially congenital types.. spontaneously during childhood.
;00.
"V'ULONODULES
unculClwd p.nk papilloma on the soft -esy Dr (urt lundC'ffi)
• Sh papilloma WIth surface proJe(fJons
"'-e ,Courtesy Dr Tom .\llcD.3vJd1
lOU""r condyloma acuminata on ventral
fig. 37-2. Firm whitish verruca vUlgaris.
Fig. 31-4. Mulllp'e verrucae vulgaris at commssure o"he bps
Fig. 37-6. MUlliple gray.sh-p,/lt( condyloma acuminata.
Fig. 37-8. Papulonodular surface of a Iymphagioma of the lip In the SClme patlent.?ls In FIg 37-]
83
VESICULOBULLOUS LESIONS Primary Herpetic Gingivostomatitis (Figs. 38-' through 38-31 Herpes simple~ virus (HSV) Types I and 2 belong to the family Herpesviridae. which also includes
cytomegalovirus. varicella zoster virus. and Epstein-Barr and the recently discovered human herpes virus VI. These viruses are ubiquitous in nalUre and infect a wide variety of animal speeies. Approximately 80 to 90% of the adult human population have been infected with HSV. Viral transmission occurs by direct mucocutaneous contact of infected secretions, resulting in over half of a million cases of primary herpetic gingivostomatitis annually in the United States. HSY-l is the causative organism in the majority of cases: however, Type
2 herpes virus. which has a propensity 10 infect the skin below the waist. can cause herpetic gingivostomatitis by oral-genital or oral-oral contactTIle manifestations of the primary infection may be trivial or fulminating. Trivial infections may produce subclinical signs of infection that often go unrecognized, or flulike symptoms. The initial infection of herpetic gingivostomatitis primarily affects children under the age of 10, and secondarily young adults aged 15to 25 years. The acute inflammatory response of the primary infection of HSV usually follows a 3- to lO-day incubation period. The infected individual will complain of fever, malaise, and irritability. Initially. focal areas of the marginal gingiva become fiery red and edematous. The swollen interdental papillae bleed after minUIe ttawna because of capillary fragility and increased permeability. Widespread inflammation of the marginal and attached gingiva develops. and small clusters of vesicles rapidly crupi throughout the mouth. The vesicles burst. fonning yellowish ulcers that are individually circumscribed by a red-halo. Coalescence of adjacemlesions forms large ulcers of the buccal mucosa. labial mucosa. gingiva, palate. tongue. and lips. Shallow erosions of the perioral skin may be apparent. Hemorrhagic crusts of the lips are characteristic. Headache. lymphadenopalhy, and pharyngitis are usually present. A significant problem in patients with primary herpetic gingivostomatitis is the pain caused by the mouth ulcers. Mastication and deglutition may be impared. resulting in dehydration and subsequent elevation of temperature. Vrral culluring. serum antibodies. and cytology are confirmatory. Treatment is supportive and should include acyclovir in severe cases. Primary herpetic gingivostomatitis is a contagious disease that usually regresses spontaneously within 12 10 20 days wilhout scarring. Complications associated with the primary infection include auto-inoculation of other epidennal sites. producing keratoconjunctivitis and herpetic whitlow: extensive epidermal infection in the atopic individual, which is tenned Kaposi's varicelliform eruption; meningitis. encephalitis. and disseminated infections in immunosuppressed patients. Immunity to HSV is relative. and patients previously infected with the virus may be reinfected with a different strain of HSV.
84
Recurrent Herpes Simplex fFigs. 38-4 :.,...,....~ 38-7) Following the initial infection. HSV inti nerve fibers. migrates to a regional neuronal _ becomes stably associated with the nucleus oftilr cell in a latem and undetectable manner. Re virus. replication of progeny panicles. and c renee occurs in approximately 40% of persons the latent virus. Recrudescence is dependent on Or immune mechanisms to eliminate reactivated H5' rences are often precipitated by a triggering eH. sunlight. heat. stress. trauma, or immunosup~ Recurrent herpes simplex (RHS) tends to P'<""'~ ters of vesicles that ulcerate. The vesicles repeated: op at the same site following the distribution of ed nerve. Recurrences on the vermilion bo~ (recurrent herpes labial is) are clinically more "' "". intraoral recurrences (recurrent herpetic st"" -" lesions of recurrent herpes labialis are chara~ appearance of small clusters of vesicles that lesce. and form slightly depressed. yello.... Ihat have distinct red halos. Spread to perioral mono especially if greasy lip ointments are used horizontal weeping of vesicular fluid. Contact fluid with other epidennal structures can result in ulation of the eye (keratoconjunctivitis). finger whitlow). or genitalia (genila.! herpes). In relati\ persons, recurrent herpetic stomatitis is periosteal-bound. keratinized mucosa cons· attached gingiva and hard palate. Recurrences cal mucosa and tongue are infrequent. unless tbr: _ _;:. immunosuppressed. Most patients with RHS complain of pam some individuals experience lillie discomfon. neurogenic symptoms such as tingling. throl,.._: burning often precede the eruption of lesions b) :Sunscreens are effective in the prevention of ':~~:~ Management also includes lysine, vitamin C. UId drugs (acyclovir) in the immunosuppressed.
Herpangina (Fig. 38-8) Herpangina is a infection involving the oral cavity. caused • Coxsack.ie viruses. This infection is seen maiDI dren during the warmer months of summer...... contagious. Young adults are occasionally affecei pangina produces light-gray papillary vesicles ..~ ,..... to form multiple. discrete, shallow ulcers. 1lIC" :::.~~ an erythematous border and are limited to me .a lars of the fauces, soft palate. uvula. and thtDiffuse pharyngeal erythema. dysphagia. and. are common features, as are fever, malaise, head:&.. phadenitis, abdominal pain. and vomiting_ rarely occur. Treatment is palliative and spon,""",". ing occurs within I to 2 weeks.
eo.
::5ICULOBULLOUS LESIONS
_";:~-~-'~_S:'W5!1ng lips, primary herpetic gingivo-
- 3. Prlm",y Infection of herpes simplex typl!' I oreducing pcllnful gingIVitiS
Fig. 38·2. Multiple broken-down herpetic vesicles with red halos, same patient as in Fig. 38-1,
Fig. 38-4. Viru.s-Idden vesICles of rec:urrent herpes labla"s. (Courresy Dr James (ortonej
; Recurrent herpes simplex of the palate
Fig. 38-6. Patlefll In Fig 38-5 twO days later WIth broken down herpetic vesicles.
] Herpetic whitlow. (COUrtesy Dr lmda
Fig. 38-8. Erythematous soft palate witn multiple veSICles; herpangina. (Courtesy Dr Charles Morns)
85
VESICULOBULLOUS LESIONS Varicella fChlckenpox) (Figs. 39·1 and 39-21 Varicella and herpes zoster are caused by the same herpetic virus. varicella lOSler. Varicella is the highly contagious primary infection. whereas herpes zoster is the recurrent neurodermal infection. Typically. young children become infected with the. virus during the latc winter and spring months. Following exposure to the virus and a 2 to 3 week incubation period. mild prodromal features appear. Fever, malaise. and a distinctive red rash on the trunk are the first recognizable signs of Ihis disease. The pruritic rash quickly spreads to the neck. face and extremities, and is followed shonly by the eruption of papules that form vesicles and puslUles. Individual vesicles burst, producing a "dew drop on a rose petiLr' appearance. The first and largest skin lesion is called the "herald spot:' It is often located on the face and. if scratched. may heal with scarring. Intraoral lesions of varicella are few and often go unnoticed. They appear as vesicular lesions that break down and form ulcers with an erythematous halo. The soft palate is the predominant site. followed by the buccal mucosa and mucobuccal fold. Anorexia. chills, fever. nasopharyngitis. and musculoskeletal aches may accompany the course of the disease. Complications are infrequent. and vesicles eventually cruSI over and resolve sponlaJleously within 7 10 10 days. Infection during pregnancy poses a significant risk to the fctus.
Herpes Zoster fShingles, fFigs. 39·3 and 39-4) Herpes zOSler is the recurrent infection of chickenpox. Unknown factors result in reactivation of dormant varicella virus from sensory ganglia and migration of virus along the affected sensory nerves. Viral recrudescence usually affeclS older adulls past age 50, but may be seen in young adulls or children. Prior to eruption. prodromal signs of itching, tingling, burning, pain. or paresthesia occur. Lesions are characterized by acutely painful vesicular eruptions of the skin and mucosa that are unilaterally dis· tributed along nerve pathways and stop abruptly at the midline. Two areas are affected the most: the trunk between venebras T3 and L2. and the face along the ophthalmic division of the trigeminal nerve. Cutaneous lesions of shingles begin as erythematous mncules that are followed by vesicular and pustular eruptions. Crust formation occurs within 7 to 10 days and persists for several weeks. Pain is intense. but usually dissipates when the cruSls fall off. The imraoral lesions are vesicular and ulcerative with an
86
imense red. inflammatory border. A
hemotl~
nem is common. The lips. tongue. and bocc:aI::~:~:: have unilateral ulcerative lesions if the n of the trigeminal nerve is affected. Invohe~ ond division of the trigeminal nerve typical]) po"'o=",. lateral palatal ulcerations that extend up to tu the palatal raphe. Considerable malaise. fe\er. accompany herpes zoster. PatieniS often inlense pain I to 2 days before the viral \"esi~ Herpes zoster usually heals withoul scar~.~~~ within about 3 weeks, but many patienls rna. persistem pain after Ihe lesions have faded. called "poslherpelic neuralgia:' may continue f .~~: 10 a year before regressing. It is resistant 10 . . . t therapy. Patients who are immunosuppressed ae: larly susceptible to shingles and have a hip - : : : rate. In the past the rare occurrence of bilat .. was termed "the death sign" because tho.: inevitably died. Varicella ZOSler virus infeCtl"~OD::'_.~:: ally associated with the Ramsay Hunt S) n zoster. unilateral facial paralysis. and ear e Reye's syndrome (high fever. cerebral edema.. eration. high monalilY. and salicylate use).
Hand·Foot·and·Mouth
Disease (Figs. through 39-8) Hand·foot-and-mouth dise~ contagious disease caused by a number of COl"'.... B viruses. It usually affects children. but ma~ young adults. It typically occurs in spring andh_., the name implies, il produces small ulcerath"e:;:::~~ mouth logether with an erythematous and \ a the dorsal and ventral surface of the hands, fi soles of the feet. Muhiple pinpoint vesicles crust are characterislic. There may be several to 100 pinpoint lesions wilh distinctive erylhe~ Oral lesions of hand·foot·and-mouth diseue~' m. tered mainly on the tongue. hard palate. and labial mucosa. In time they coalesce to form la::areas. The oropharynx is usually unaffected- -.. number of intraoral lesions is usually less than a common symptom. along with elevated 1 malaise. and lymphadenopathy. The diag made by viral culture and serum antibody sllJl:hls.. er. the classic distribulion of lesions on lhe hands, soles of feet, and oral mucosa is diagnoso,;: instances. Healing occurs regardless of lR_-=~ approximately 10 days.
thal7:::
CULOBULLOUS LESIONS
Fig. 39-2. Intraoral vesICle of chickenpox•
.... ]
•
-:eral erup!lon of herpes :zoster along 'r branch of lhe trigeminal nerve
_..., S ~ ill pinpoint lesion of hand-foot-andQueue n a young adult. {Courtesy Drs Birgit
_ , Hand·foot-and·mouth disease of the (C).Jrtesy Drs BIrgIt & Tom Glass!
Fig. 39-4. pC! nfulln(raord' 1e<.lOns of pa{l(>nt in Fig 39-3 w,rh herpes zoster•
Fig. 39-6. Erythematous border surrounding an ulcer; hand-foot·and·mouth disease. (Courtesy Drs Birgit & Tom Glass)
Fig. 39-8. Paontut clusters of vesICles of hand-foot-
and-mouth disease, same priltlent.n 8gs. 39-5 through 39-8 (Courtesy Drs Blrgll & Tom GlasS)
87
VESICULOBULLOUS LESIONS Allergic Reactions (Figs. 40-' through 40-81 Allergy is 3 condition of hypersensitivity 10 certain malerials acquired by repeated exposure 10 an allergen. Hypersensitivity reactions usually produce inappropriate tissue damage as a result of antigen-antibody reactions (increase in antigenic stimuli or a heightened inunune stale). M.anifesl31ions of allergy may be generalized or localized. and may occur at any age. A genetic predisposition 10 allergy and persistenl sensitivity are common features. Hypersensitivity reactions have been classified imo several types according to the following faclors: the speed with which the symptoms occur (immediate or delayed); clinical appearance; and cellular and (issue response (Type I - IgE-medialed immediate hypersensitivity, Type II antibody-dependent cytolOxic hypersensitivity. Type 1II complex-mediated hypersensitivity. Type IV - cell-mediated. or delayed hypersensitivity. and Type V - stimulatory hypersensitivity). Those of clinical significance to the dentist include immediate hypersensitivity Type I reactions (anaphylaclic shock. urticaria. angioneurotic edema. allergic stomatitis) and delayed hypersensitivity Type IV reaclion (contact allergy). Immediate allergic responses such as anaphylaxis are histamine-mediated and occur within minutes of exposure to antigens. When the condition is localized to superficial blood vessels. IgE-mediated histamine release results in vasodilation. increased capillary permeability, tissue swelling. and pruritis. Typically. individual wheals. also known as urticaria or ·'hives". arise following the ingestion of cenain foods such as shellfish. citrus fruits. chocolate, or systemically administered drugs. Angioedema is a hypersensitivity reaction characterized by the accumulation of serum within tissues, brought about by histamine-mediated vasodilation. Hereditary and acquired fonns exist. with the fonner more serious because of possible visceral involvement. Swelling is the most prominent feature of angioedema. It appears rapidly and lasts for 24 to 36 hours. Sensations of warmth. tenseness, and itchiness are concurrent. The perioral and periorbital tissues are commonly affected. Angioedema is often recurrent and unpredictable. If an allergen can be identified, withdrawal of the agent and administration of antihistamines is recommended. Allergic stomatitis, also tenned "allergic mucositis:' is an oral Type 1 hypersensitivity reaction to a systemically administered drug or food. l1le oral manifestations of drugrelated eruptions are varied and may be clinically similar to erythema multiforme, lichen planus. Of lupus erythematosus. Intraorally a dry, glistening. red area is usually apparent. Focal white areas may be adjacent. TIle fonnation of multiple vesicles that desquamate and produce fibrin--covered ulcers eventually results. An erythematous. inflammatory border and a painful. burning sensation are common. The response
88
may be limited to the buccal mucosa, gingiva.. li~ 01 or may involve the entire oral cavily. Conc~ ..... lesions are possible. Treatment requires witlJdra, allergen and administration of antihistamines. Generalized anaphylaxis is an immediatt hypersensitivity reaction that can be life·tlm~ laryngeal tissues are involved. It results fro"m:.;_;,::~~ antibody interaction that produces mast cell <: and the release of vasoactive amines and medi histamine. In fulminant cases, a generalized m=..., . vascular penneability and smooth muscle con~ es urticaria. dyspnea. hypotension. laryngeal ~::.: vascular collapse. Mild localized immediate h)l ity reactions are treated with antihistamines. epinephrine is required to effectively manage 5e'u:" ali zed anaphylactic reactions. Treatment sh include the elimination of the allergen. Delayed hypersensitivity (Type IV) is a res immune system to a locally or systemicall~ allergen thai usually develops slowly and reachei mum size 24 to 48 hours after antigenic r Topically applied allergens such as latex glo\1:5 cal disinfectants may produce a delayed hy~ response evident as itchy, erythematous skin tes.a lact dermatitis) that eventually become inflamed ated at the site of contact. Another form of delayed hypersensitivit) ISo stomatitis (stomatitis venenata). which may ocxw intraoral mucosal site. It characteristically produc:es rna at the site of contact with the topical Reactions 10 lipstick or sunscreen preparations the lips to appear red, swollen. fissured. or drl. sation of burning may be present. The gingiva can also show signs of delayed tivity. Plasma cell gingivitis produces diffusel) ......''''~ and fiery red gingiva because of the flavoring in some toothpastes and chewing gums. Often die ...,"'~ commissures are involved. resulting in cheilitis. Antiseptics. antibiotic lozenges, topical "''''...~ eugenol preparalions. and mouthwashes may produ.;l.. lar burning lesions. These appear on the alveolar _""'_ dorsum of the tongue. or palate as erythemalous are covered by a gray-white pseudomembrane. restorations and partial denture frameworks 11m _ heavy metals such as coball, mercury. nickel. oralso induce delayed hypersensitivity reactio&.. mucosa adjacent 10 the restored area. Usuall~ cz: red and ulcerated. and bums. Allergy to the ff:=~:~"; in dentures. once thought 10 be a common 0 now known to be rare. Immediate localized hypersensitivity is m,,,,,,!,ol,,,,t antihistamines, whereas delayed hypersensiti\ treated with corticosteroids.
",_""""Z
.'ESICULOBULLOUS LESIONS
-~I
~ 'leal r
on the cheek Immediately following of Chinese food: Type I
~sitivity.
~
{Courtesy Dr Michele Saunders)
Fig. 40-2. Lichenoid drug-eruption. Ulcerations resolved following discontinuation of thlClllde therapy.
...;..3 S-ee-song-Induced palatal erythema, Type IV sensitivity. (Courtesy Dr Carson Mader)
Fig. 40-4. Fingers of a dental ",ssistant with contact dermatitis; 'TYpe IV hypersensitivity.
.....:-5 ,.. :er':l!
Fig. 40-6. An erythematous reacrion to benzocaine:
Sit
,:,,-"nICI iln.
.....;_"! - ~ nflammed atl
contact stomatitis.
Fig. 40-8. Contact stomatitis to nickel In the adjelCent GIst alloy
89
VESICULOBUUOUS LESIONS Erythema Multiforme fFigs. 41-' through 41-4) Erythema multiforme is a self-limiting disease of the skin and mucous membranes. [\ commonly affects young adults, particularly males, bUI may affect children and the elderly as well. Low-grade fever, malaise. and headache typically precede the emergence of lesions by 3 to 7 days. Erythema multiforme has an unknown etiology; however, recent evidence suggest thai circulating immune complexes that provoke complement-mediated cytopathic effects, combined with lymphocytic and neutrophilic stimulated vascular injury. may playa pathogenic role. Precipitating factors include bacterial, fungal. and viral infections such as herpes simplex and Mycoplasma pneumoniae. emotional stress, and allergy, especially to sulfaand barbiturate-containing drugs. In about 50% of the cases no causative factor has been identified. Although there is great variation in the clinical appearance of the disease. as the name "multiforme" suggests, stomatitis and cutaneous lesions are the most prominent features. The hallmarks of this disease are the red-white. concentric, ring-like macules tenned "target," "bulls-eye." or "iris" lesions that rapidly appear on the extensor surfaces of the anns and legs, knees, and palms of the hands. The trunk of the body is classically exempt from lesions, except in the most severe cases. Initially the skin lesions are small, red, circular macules that vary in size from 0.5 to 2.0 cm in diameter. Then the macules enlarge and develop a pale white or central clear area. Shortly thereafter the lesions fonn vesicles and bul~ lae. The vesicles may go unnoticed until they rupture and become confluent. The ulcers fonned are large, raw. and shallow, with an erythematous border. A necrotic slough and a fibrinous pseudomembrane typically cover the ulcers. Urticarial plaques that do not break down may also be present. Imraorally, red macular areas, multiple ulcerations, and erosions with a gray-white fibrinous surface may be seen. They are limited to the buccal mucosa, labial mucosa. palate. or tongue. or involve all of those areas. Rarely is the gingiva involved. Dark. red-brown, hemorrhagic crusts are characteristically present on the lips, which aids in making the diagnosis. Lesions are usually short-lived and last about 2 weeks. Erythema multifonne rarely persists for more than I month. Oral lesions without cutaneous lesions
90
have been reported. Recurrent and chronic fonns Pain is the most common symptom. which rTU~ fere with normal oral activity. Oral hygiene neglected, resulting in secondary bacterial ini Treatment consists of topical palliative rinses and.. instances. low dose systemic steroids. CampI" resulting from erythema multifonne are uncomnx. the disease progresses to its major fonn, Stevenssyndrome.
Stevens-Johnson Syndrome {Figs. 41·5 th~.. 41-81 The severe fonn or major variant of erythema fonne is tenned "Stevens-Johnson syndrome," named two investigators who firs! described the clinical ~:a:: of the disease in the early 19205. It frequently affecu and young adults, predominantly males. The oral Stevens-Johnson syndrome are similar to those of"'..... multiforme, but there is more widespread invohcutaneous and stomatologic structures, together ... constitutional signs including fever, malaise. "'. . . cough. chest pain. diarrhea. vomiting, and arthralgia.. The classic clinical triad of Stevens-Johnson ~ consists of eye lesions (conjunctivitis). genital lesKa anitis. vulvovaginitis), and stomatitis. In addition the characteristic target skin lesions on the face, abdomen that later develop into painful "weepinglobullous lesions. Like erythema multifonne, the gingiva is less affected by desquamating bullae than the non-k.~ mucosa. Extensive ulcerative and hemorrhagic lesm. lips and denuded areas of oral mucosa are imense:1); and usually prevent affected patients from eating . . lowing. Inadequate nutritional intake, dehydration. itation are common sequelae that necessitate hospiiw...... Significant morbidity and mortality may oc portive therapy is not provided. Treatment consists venous fluid and nutritional therapy, short-tenn .. steroids. and palliation consisting of oral anestheDc agents that coat and protect the lesions. and mouthwashes. Secondary infection is managed wi.s oties. the ensuing fever with fluids and amipyrebO' condition has a longer duration than erythema m but usually resolves within 6 weeks. Fatalities ta.. documented in sulfa-induced Stevens-Johnson S)nd_.
00_.
::5ICULOBULLOUS LESIONS
•
-~rge( ~ Tom
>·1.
lesion; erythema multiforme. McDavldj
-1.1·3• ...·w : pie erythematous ulcers on the d(l(sum
"i-.
.&
Fig. 41-2. Ulcerated lips. erythema multlforme. (Courtesy Dr John McDowell)
Fig. 41-4. Ulcers of erythema multlforme on ventral
..-.g...e erythema multlforme. (Courtesy Dr
tongue. same patient In Figs 4' -2 through 4 r-4
::x".,\rell)
(Courtesy Or John McDowell)
1-5. Stevens-Johnson syndrome. (Courtesy 'cDavld)
, T-7 severe conJunctMtrs and weeping SIon Stevens.Johnson syndrome.
Fig. 41-6. Extensive palatal ulcerations of StevensJohnson syndrome In.si'lme pallent as In Fig 41-5
/Courtesy Dr Tom McDavldl
Fig. 41-8. He'TlOlTaglC and crusted lips of chid seen In Fig 41-7 Who has Steven.s-Johnson syndrome.
91
VESICULOBUUOUS LESIONS Pemphigus Vulgar;s jFigs. 42-1 through 42-41 Pemphigus is a pOieniially falal. vesiculobullous disease which has been categorized into four types: \'ulgaris and \'egetans. which have inlr30ral manifestations. and foliaceous and er:,.thematosus, which are nOI believed to produce oral disease. The most imponant aspect of this condition is early recognition of the oral lesions. which usually precede skin involvement by several months. In fact. or"l.I lesions may be the only manifestation of the disease. Diagnosis during the early stages greatly enhances the initiation of conicosleroid and immunosup'pressive therapy and. therefore. the long-tenn prognosis. Vulgaris. the mosl common type of inlraoral pemphigus. usu311y develops between the ages of 30 and 50. It may be seen in younger or older patients. but rarely does it develop in patients beyond 60 years. It is seen with equal frequency in males and females and is usually encountered in lightpigmented patients of Jewish or Mediterranean origin. Pemphigus vulgaris is probably an autoimmune disorder involving a reaction of IgG to an intercellular subtance. resulling in epithelial cell-to-cell separation. ACUie and chronic fonns exist. Ihe slow chronic fonn being the most common. The most prominent clinical fealUTt of pemphigus is the rapid development of mulliple bullae that tend to rupture and leave erosions of the skin and oral mucous membranes. When there is syslemic involvement. severe debilitation may resull in death. Early mucocutaneous lesions consist of "weeping" bullae or gelatinous plaques that are clear and shimmering. TIle bullae are extremely fragile and rapidly disintegrale. hemoJfhage, and crust. They tend to recur in the same area and later spread 10 adjaceOl regions. Light lateral pressure applied to a bulla will cause it to enlarge by extension (Nikolsky's sign). A characteristic and consistent finding is the appearance of a whitish superficial covering. which is the roof of a collapsed bulla Ihat can easily be stripped away. Cases that show predominantly desquamative areas that affect the gingiva have been clinically tenned "desquamative gingivitis." Pemphigus may appear as an epithelial slough with white tissue folds. an aphthous or traumatic ulcer or. in circumslances in\'olving multiple areas of the lips, buccal mucosa. tongue. gingiva. palate. and oropharynx, the condition may resemble erythema multifonne. Individual lesions orten have circular or serpiginous borders. whereas extensive erosions of the buccal mucosa are red and raw. and have diffuse irregular borders. Frequent eruptions may be superimposed over healing lesions so that periods of remission are absent. The longue is less commonly involved than the lips, buccal mucosa. and gingiva. Thick hemorrhagic cruSts and fetor oris are characteristic of extensive lesions. Patients wilh pemphigus are often dislUrbed by the severe pain associated with the condition. The diagnosis of pemphigus is confinned by a positive
92
Nikolsky's sign. biopsy. and immunofluorescent techniques. Prior to steroid therapy, dehydration ticemia were fatal complications of pemphigus.
Benign Mucous Membrane ICica Pemphigoid and Bullous Pemphigoid (FIgSthrough 42-8) Pemphigoid is a chronic. self-I mucocutaneous disease that is slightly more commor oral cavity than pemphigus. but is associated with morbidity and mortality. Two types that produce oral lesions may be seen in the mouth: benign mucc:.. brane pemphigoid and bullous pemphigoid. Bullous pemphigoid. which is the least com~ two. affects both the skin and the oral cavity. and sexual or racial predisposition. Skin folds locate
ph..,..
'UICULOBULLOUS LESIONS
, &2-1. T'oung child with extensive erosions of _ .....,;·,gus vulgaris.
·tJ-). SuperfICIal clear bullae of ~mphigus Courtesy Drs Tom McDavId and Martrn Tyterl
Fig. 42-2. up involvement of child In Fig 42-1 with
pemphigus vUlgaris.
Fig. 42-4. Ruptured and herr\o(rhagic bullae; ~mphJ gus vUlgaris. (Courtesy Drs Tom McDavid and Martin Tyler)
.oLI-S :JesquamativegIf'lQMtis"; benign mucous _ _"',ne pemphigoid.
Fig. 42-6. DesquamatIVe 911lQival patCheS of benign mucous membrane pemphigoid.
..._'~lu-7., O'sltys sign suggestive of benign embrane pemphigoid; same patient In
Fig. 42-8. Corneal scarring; benign mucous membrane pemphigoid.
,~
-rough 42-7
93
, ULCERATIVE LESIONS Traumatic Ulcer jFigs. 43-1 through 43-31 Recurrent oral ulceration is a common condition resulting from several etiologies. trauma being the most common cause. Ulcers may occur at any age and in either sex. Likely locations for traumatic ulcers arc the labial mucosa. buccal mucosa. palate, and peripheral borders of the tongue.
Tmumatic ulcers may result from chemicals, heal. electricity. or mechanical force, and are often classified according to the exact nature of the insult. Pressure from an ill-fitting denture base or flange, or from a partial denture fmmework:. is a source of a decubitous or pressure ulcer. Trophic, or ischemic ulcers. occur particularly on the palate at the site of a previous injection. Dental injections have also been implicated in the traumatic ukemtions seen on the lower lip by children who chew their lip after dental apJXlintments. In addition to faClitial injury, young children and infants are prone to traumatic ulcers of the soft palate from thumb sucking, called Bednar's aphthae. Ulcers may be precipitated by contact with a fractured tooth, a partial denture clasp. or inadvertent biting of the mucosa. A bum from food or drinks that are too hot commonly occurs on the palate. Other traumatic ulcers are caused by factitial injury from inappropriate use of fingernails on the oral mucosa. The diagnosis of these conditions is simple and is often obtained from a careful history and examination of the physical findings. The appearance of a mechanically induced traumatic ulcer varies according to the intensity and size of the agent. The ulcer usually appears slightly depressed and oval in shape. Initially an erythematous zone is found at the periphery, which progressively lightens because of the keratinization process. The center of the ulcer is usually yellow-gray. Chemically dam<:tged mucosa. such as that with an aspirin burn. is less well-defined and contains a loosely adherent. coagulated surface slough. Following removal of the traumatic influence, the ulcer should heal within 2 weeks. if not other causes should be suspected and a biopsy perfonned. Recurrent Aphthous Stomatitis IMinor Aphthae, Aphthous Ulcer) /Figs. 43-4 through 43-61 Recurrent aphthous stomatitis (RAS) is classified into three categories according to size: minor aphthae, major aphthae, and herpetifonn ulcers. Approximately 20% of the JXlpulation is afflicted with minor aphthae, or "canker sores" as they are commonly referred to by patient~. They may be seen in anyone, but females and young adults are slightly more susceptible. Familial patterns have been demonstrated and persons who smoke are less frequently affected than non-smokers. Factors that precipitate aphthae include atopy. trauma. endocrinopathies, menstruation. nuuitional deficiences, stress, and food allergies. Although the etiology is unknown, current studies suggest an immunopathic process involving ceIl-mediated cytolytic activity in response to HLA or foreign antigens. The L-fonn of streptococcus has been suggested to playa causal role in the fonnation of aphthous ulceration. 94
Minor aphthous ulcers have a propensi~ t mucosa that is situated over minor salivary gland labial and buccal mucosa are frequently affec1l:lw.. ulcers arc rarely seen on heavily keratinized : : : : the gingiva and hard palate. Occasionally. prod" toms of paresthesia or hyperesthesia arc reponed Minor aphthae appear as shallow, )eIlO'l\-,.. ulcers usually about 2 to 5 mm in diameter_ :\ -.,._ et)·thematous border surrounds the fibrinous P'~-="'" brane. No vesicle foonation is seen in this di~ tive diagnostic feature. Ulcers that occur mucobuccal fold often appear more elongated.. Burning is a preliminary complaint that is intense pain of a few days' duration. Tender lar. anterior cervical. and parotid nodes are OI1et particularly when the ulcer becomes secon~ :~;;~ Aphthae are invariably. recurrent. and the occurrence varies. Most persons exhibit singk or twice a year. beginning during childhood cence. Occasionally the ulcers appear in crops. less than five occur at one time. Patients Voulcers may have periods of several months I ulcers are constant. Persistent ulceration!' extremely painful and usually have a ragged More extreme measures may be required 10 treat those patients. Minor aphthous ulcers spontaneously without scar foonation within I..;. Although no medication has been totall) the treatment of aphthous stomatitis. patients ded to antibiotic suspensions and coagulating. and anti-inflammatory agents.
""""'=.
Pseudoaphthous Ulcer (Figs. 43-7 Pseudoaphthae is a term coined by Binney recurrent, aphthous-like mucosal ulcers of which are associated with nutritional deficiea. Studies indicate that 20% of patients with ",=-~~1iI thous stomatitis are deficient in folic acid, iron.. B!2' Pseudoaphthae are frequently cone inflammatory bowel disease. Crohn's disease. erance, and pernicious anemia. Pseudoaphthae resemble aphthous ulcers. t.. acteristically more persistent. There is a slight for females between the ages of 25 and 50. 1k depressed, rounded, and painful. The bof'de=,. raised and firm. but induration is seldom Alterations of the tongue papillae may clue the cian of an underlying nutritional deficienc) SDk is slow, and patients may complain of never ulceration. Chronic and persistent disease evaluation for nutritional deficiencies. inchJdia!: logic studies. If the laboratory results are al:inomlk medical referral is required.
RATIVE LESIONS
.;. 3-1 :Jenture-flange-induced traumatic ulcer.
Fig. 43·2. Traumatic ulcer; same patient as In Fig 43-1.
.1.3-3 Tr.1umatlc ulcer due 10 the Ingestion of
Fig. 43-4. Oval aphthous ulcer on CllVeolar mucoXl
'oed ,Courtesy Dr Donna Wood)
·3-S Aphthous ulcer WIth promn"lent red
Fig_ 4]-6. A ckJsler of .phthaul ulcers
mucosa. (Courtesy Dr Tom Schiff)
-3-7 -:. oe band of erythema SUrrounding a '" ~ pa,lent wrCh Crohn'S disease. OonnaWoodJ
Fig. 4]-8. Pseudoaphthous ulcer of Crohn'S disease. (Courtesy Dr Donna Wood)
95
ULCERATIVE LESIONS Major Aphthous (Peridadenitis Mucosa Nec-
rotica Recurrens IPMNRJ, Sutton's Disease. Scarifying Stomatitis. Recurrent Scarring Aphthous Ulcer) (Figs. 44-1 through 44-4) Major aphthous is an exaggerated variant of minor aphthous that produces larger and more destructive ulcers that last longer and reCUT more frequcnlly. The etiology is unknown; some suggest that an immune defect is involved. Others speculate Ihal the large ulcer is a severe fonn of recurrent aphthous slOmatitils. which results from the coalescence of several smaller ulcers. Young female adults with anxious personality traits are most commonly affected. Major aphthous ulcerations are often multiple. They involve the soft palate, tonsillar fauces. labial mucosa. buccal mucosa. and tongue. occasionally extending onto the attached gingiva. Characteristically the ulcers are asymmetric and unilateral. The most prominent feature is the large si7-e together with a depressed. necrotic center. A red raised innammatory border is common. Depending on size. Lraumatic innuences, and secondary infection. ulcers may last from several weeks to months. Because the ulcers erode deep into the connective tissue. they heal with scar formation and tissue distonion. Muscle destruction can result in tissue fenestration. and if the periodontium is involved, loss of tissue altachment may occur. Extreme pain and lymphadenopathy are common symptoms. Healing can be accelerated and scarring reduced with the use of steroids. Ulcers similar to those of PMNR are seen with some frequency in association with cyclic neutropenia. agranulocytosis. and gluten intolerance. Ulcers located on the tongue may strongly resemble carcinoma. The presence of scarring is of diagnostic importance to rule out malignancy.
Herpetiform Ulceration (Figs. 44-5 and 44-61 Herpetifonn ulceration is a type of recurrent focal ulcerafion of the oral mucosa that clinically resembles the ulcers seen in primary herpes; hence the name herpetifonn. This condition. however. is probably a variant fonn of recurrent aphthous ulceration. The prominent feature of the disease is the numerous, pinhead-sized. gray-white erosions that enlarge. coalesce. and become ill-defined. Initially the ulcers are I to 2 mm in diameter and occur in clusters of 10 10 100. The mucosa adjacent to the ulcer is erythematous. and pain is a predictable symptom. Any pan of the oral mucosa may be affected by herpetifonn ulcerations, but panicularly affected is the anterior tip of the tongue. margins of the tongue. and labial mucosa. The smaller size of these ulcerations distinguishes them from aphthae, while their absence of vesicles and gingivitis together with their recurrent nature distinguishes them from primary herpes and other oral viral infections. Virus cannot be cul-
96
tured from these lesions. and the ulcers are not CO""", The first episode of herpelifonn ulcerat occurs in patients in their late twenties. lO)ean peak incidence of aphthae. The duration of tbr variable and unpredictable. and the etiolog) h:aI detennined. Recurrent herpetifonn ulceratj especially well to tetracycline suspensions. and tion often regresses spontaneously after several ~ Beh~et'$ Syndrome 'Oculo-OraJ-Geni dromeJ 'Figs. 44-7 and 44-8) Beh,et'.s •
named for the Turkish physician who first de.scr' ulcerJ.tive disorder. principally involves three SJle'I:" oral cavity. and genitals. For this reason it has beaI rized as a triple~symptom complex with ulcerati\~ tat ions. In its fully developed Slale. cutane arthritis of the major joints. gastrointestinal neurologic manifestations. and thrombophle seen, though rarely are all components preseO! m patient. The etiology remains unknown. but .a hypersensitivity reaction. possibly involving HlA immune complexes. and vasculitis. has been su Be~et's syndrome is two to three times ~ in males than in females, with an onset bel',l,'een 20 and 30. Persons from Asia. the Mediterrat'Jll.":llr and Great Britain are most commonly affected. Eye manifestations of Be~t's syndrome u-0 _ phobia. conjunctivitis. and chronic recurrent hypopyon that occasionally leads to blindness. festations may be concurrent with or occur yean and genital ulcers. Skin changes are characterized taneous nodules and macular and papular e"". .vesiculate, ulcerate. and encrustate. Genital involve the mucosa or skin. and tend to be smaUer common than the oral lesions. Oral ulcers. the most prevalent lesion of Be drome. may be the initial sign of the disease. One_ crops of aphthous-like ulcers on the buccal mucosa are characteristic; however. any oral mu.. may be involved. Similar to aphthous. the ulcm shallow. and oval, with the size of the ulce~ Small lesions tend to occur more frequentl~ u.. lesions. A serofibrinous exudate covers the swfax margins are red and well-demarcated. Complaiar. are frequent. and recurrent periods of exace remissions are characteristic. Patients with linuIc.. cutaneous involvement are managed sympton..."".-'" topical and systemic steroids. Protracted diseasethe neuro-ocular structures requires the care of a Azathioprine, cyclophosphamide. thalid colchicine have been used successfully in sel All of these agents have potentially serious sidt
LL-l j:I~lstent ulcers on marginal and attached P
~3_
Painful major ..phthous of the gingiva.
~5 "~ul[lple
herpetiform ulcerations of the OS<'! (Courtesy Dr Geza Terezh
_ ~7 foung male with tonsillar ulceration of .-..x:etJl syndrome. ICourtesy Dr Geza Terezh
Fig. 44-2. Multiple tongue ulcers in patient with m.. jor ..phthous.
Fig. 44-4. Large irregular ulcer of the soft palale; same patient with major aphthous as in Figs. 44-1 through 44-1
Fig. 44-6. Coolescing herpetiform ulcerations; same patient
Fig. 44-8. Multiple genit
ULCERATIVE LESIONS Granulomatous Ulcer IFigs. 45-1 and 45-21 Two common granulomatous infections thai may produce oral ulcers are tuberculosis (TB) and histoplasmosis. These are rare lesions thaI are usually found in older adults after the disease is far advanced. Underlying disorders such as AIDS resull in a younger population group being affected. Because pulmonary lesions oflen precede oral lesions. the pulmonary complain! of persislent cough is an imponanl historic finding. Dissemination of organisms from the lungs 10 the mOUlh via infected sputum can resull in oral infection. Oral TB and histoplasmosis infection are characterized by ulceralion. These ulcers may occur on any mucosal surface: however. tuberculous lesions occur preferentially on the dorsum of the tongue and labial mucosa at the commissure. The clinical picture varies and the ulcer may resemble a traumatic ulcer or epidermoid carcinoma, particularly when the lesion is located on the lateral border of the tongue. Lesions on the alveolar ridge often resemble a granulating extraction site. The center of the granuloma+ tous ulcer is yellow-gray or even bluish. necrotic, and depressed several millimeters. The peripheral region of the ulcer is undulating or lumpy and has been described as "cobblestoned:' The margin of the lesion is irregular. welldemarcated. and undermined. odular and vegetative components are often seen in conjunction with the ulcers of histoplasmosis. Cervical lymphadenopathy is a common finding. Depending on the location and irritating factors. some patients rarely complain of pain and the discovery may be an incidental finding; other patients experience severe, unremiuing discomfon. Tuberculous and histoplasmosis lesions are contagious. and active organisms can be transmitted under appropriate conditions. A biopsy or culturing is required to confirm the diagnosis. Histologic features and special stains demonstrate the presence of the causative organisms. Treatment of the primary lung problem is with specific long-term antibiotics; for TB, streptomycin is usually followed by isoniazid (INH); for histoplasmosis. amphotericin B is administered. The primary lung problem should be treated prior to dental treatment. Squamous Cell Carcinoma (Figs. 45-3 through 45-6) Squamous cell carcinoma often appears as an ulcer. In the early stages the condition is usually small, nonpainful. and non-ulcerative: however. the persistent nature of the disease results in neoplastic proliferation that soon exhausts the blood supply. resulting in surface telangiectasia and eventual ulcer formation. Older ulcers tend to be large and crateriform. covered by a central yellow-gray
98
necrotic slough. Red, raw foci are frequenL ders are firm, raised. and sometimes fungatJ.a!. Carcinomas mlly occur anywhere in I.bC" most common siles are the posterior third margin of the tongue and the floor of Associated features may include pain. nu,n>i_ _ plakia. erylhroplakia. induration. fixallGa. phadenopathy. Metaslatic Iymphadenopath) ~ c.....~ ized by nonpainful rubbery or hard nodes m. ale the base and maned together. Excessive use .
Chemotherapeutic Ulcer IFigs. 45-7 Patients receiving immunosuppressant c- _
dru,,_,
of serious illnesses. including OfB:an ~~~~~~ aUlOimmune condilions. and neoplasia. nta) ulceralions and stomatitis. Side effects of the peutic drug may be directly or indirectly oral mucosa. Antimetabolites such as me~ the replication of rapidly reproducing cell,. _ _""'"'" oral epithelium, whereas alkaloids such b ~ phamide induce leukopenia and secondar) uJoc: The chemotherapeutic ulcer. an early sign m ...., . , . ity. appears during the second week of the~ persists for 2 weeks. These ulcers may occur mucosal sile. The lips. buccal mucosa. tongue.. ~ mouth. and palate are affected most frequeml __ area is red and bums. The surface epithelium K ulcer forms that is usually large. deep. painful. The margins of the ulcer are irreglI-E. characteristic red inflammatory border is om because of the lack of an inflammatory re host. If the pain becomes severe and the inta1:e nutrition and fluids is impaired. a reduction ia may be necessary. Culturing is highly recommended for allleslca of their propensity for infection with gram-nepIl" isms and fungi. and because of the likelihool. ulcers may represent recrudescence of latent plex virus. Topical anesthetics are used to mi.... r toms. whereas oral hygiene measures. includuJr bial agents such as chlorhexidine. are criti secondary infection. soft tissue necrosis. aDd necrosis. Consultation and open communie.at:D the physician and the dentist can help reduc.e ""...... and promote oral comfort.
-.."ii
=-
CERATIVE LESIONS
,"
.IS-I Granulomatous ulcer on anterior tongue .' .,Q!)aetmum lubfrCUjOSIS (Courtesy Dr _ " noz)
Fig. 45-2. Granulomatous ulcer on the dorsum of the longue; histoplasmosis {Courtesy Dr Michael Huber)
Fig. 45-4. FfOQr-Qf-lhe-moulh ulceraoon; squamous
cell carcinoma. {Courtesy Dr Robert Craig)
Fig. 45·6. Squamous cell carcinoma In the same pallenl as In FIQ 4S-S (COUrtesy Dr Tom McD
-'5--7. Chemotherapeutic Induced ulceration '"'II(
patient (Courtesy Dr Tom McDavid I
Fig. 45-8. Chemother..peutlc ulceration of the buccal mucosa caused by methotrexate therapy_ (Courtesy Dr Jerry Cioffil
99
SECTION
v Sexually Related and Infectious Conditions
101
SEXUALLY RELATED AND INFECTIOUS CONDITIONS Traumatic Conditions (Figs. 46-1 and 46-21 Injury to the lingual frenum lind fellatio syndrome are common oral conditions associllled with sexual activity. Ulceration of the lingual frenum may occur when the longue is mechanically abraded against the incisal edges of the mandibular incisors during orogenilal sexual activity. A while fibrinous exudate and an erythematous border are commonly seen. A hislory of cunnilingus confirms the diagnosis and abstinence is recommended to pennil healing. Chronic irritation may lead to secondary bacterial infection, development of leukoplakia, a tr::lUmatk fibroma. or it may permit ingress of the human papilloma virus. Fellatio. a sexually traumatic condition, produces erythema and submucosal hemorrhage most commonly seen at the junction of the hard and sort palate. Initially isolated bright red petechiae appear. which eventually become a confluent patch that bridges the palatal midline. The purpuric lesion is painless and nonulcerative, does not blanch on diascopy. and clinically resembles the petechial patch produced by infectious mononucleosis; however. lymphadenopathy and fever are characteristically absent. Petechiae darken and fade away in about a week. Sexually Transmitted Pharyngitis 'Figs. 46·3 and 46-4J Venereal organisms such as herpes simplex virus Type 2. Neisseria gonorrhoeot'. and Chlamydia Ira· choma/is may cause pharyngitis by transmission from direct contact with infected genital or oral secretions or lesions. Herpetic stomatitis (Type II) is most prevalent after sexual activity begins. usually occurring in persons between 15 and 35 years of age. Limited reports indicate that primary HSV-2 infection produces a prominent pharyngotonsillitis and fever while inflammation of the gingivae may be less severe than HSV-I primary infection. Multiple small vesicles are usually apparent in the early stages; the vesicles collapse to form ulcers that resolve in JO to 21 days. Gonococcal pharyngitis may produce a diffuse erythematous throat. small pustules in the tonsillar area. or an erythematous and edematous patch involving the throat. tonsillar area. and uvula. Burning is the initial symplom. followed by increased salivary viscosity and halitosis. Other oral manifestations include the following; painful. discrete ulcerations of the oral mucosa: fiery red and tender gingiva with or without necrosis of the interdental papilla; tongue ulceration: and glossodynia. Penicillin G. tetracycline, and ceftriaxone regimens have been used effectively to treat this condition. C. /rochomads may also cause a sore, "lumpy" throat. mild pharyngitis, and tonsillar inflammation with pustule fonnatiOfi. TIle treatment of choice is tetracycline.
Infectious Mononucleosis (Figs. 46-5 and 46-61 Infectious mononucleosis is a relatively benign lymphocytic infection characterized by fatigue, fever. malaise.
'02
pharyngitis, stomatitis. and occasional jaundice. commonly caused by the Epslein Barr virus chieOy in adolescents and young adults. This d low contagiousness and transmission is proba _ exchange of virus-contaminated saliva during deqt Oral lesions are often the earliest manif~ infectious mononucleosis. Multipk red palatal located at the junction of the hard and soft palate ........or ing (he first few weeks of infection. These I~ brown and fade after 7 to 10 days. Acute u1cerati\'t tis. pharyngeal ulcerations, and erythematous n tonsillitis are frequently encountered during (he of the infection. Bilateral posterior cervical 1),,,,,,",_ thy is a consistent finding. Blood analysis re\eal~ lymphocytosis. atypical lymphocytes. and the heterophile antibodies. Trealment is supper: includes bed rest. soft diet. analgesics. and Recovery usually occurs within I 102 montM. SyphJlls IFigs. 46-7 and 46-S1 Syphilis is a disease caused by an anaerobic spirochete, Trt'po......... lidum. The haJlmark of primary oral syphilis u. painful chancre. which represents a granulomatolb..,c;. to vascular obliteration. Chancres may affect a:rry tissue; however. the lips are the most com involvement, followed by the tongue. palate. tonsillar areas. Oral syphilis is usually obsened adult males. The syphilitic chancre initially appears as a that elevates, enlarges. erodes, and becomes ul=_. lesion is usually punched-out. indurated, 2 to 3 em ",;:~ (er. and without a red inflammatory border. The .. covered by a yellowish, highly infectious serous ..."". ." Palatal erythema or an asymptomatic. reddish ulca the initial lesion. along with swollen, non-tender. "".. riorcervicallymph nodes. Chancres typically penIk 4 weeks and heal spontaneously, which may caU!t -::::lO:to erroneously believe thai no treatment is n~ latent period of 4 weeks to 6 months, the sec~ syphilis appears in which the patient rna) headaches. lacrimation, nasal discharge. sore """"'.. generalized arthralgia. together with lymphade vation of temperature, and weight loss. A painless.. rical. nonpruritic skin rash with notable maculo-"",..",,¢ mar-plantar eruptions soon follows. Concurrent ora of secondary syphilis appear as oval red macules, 1*""'::;:' lis, or isolated or multiple mucous patches (paID"" low highly infectious ulcers surrounded by an ery halo). The borders often are irregular and re=.... tracks." Tertiary syphilis occurs in infected paos--. years after OOl1treatment of secondary syphilis. It Iy characterized by palatal perforation and neurolop. toms. Parenteral penicillin G remains the drug of,",r==JIo: treating all stages of syphilis.
,=
,=
SEXUALLY RElATED AND INFECTIOUS CONDmONS
~t;
46-1. Traumatic ulcer of the lIngual frenum Dr James COttone,
Fig. 46-2. Condyloma acuminatum of the lingual frenum. (Courtesy Dr Marden J\lder)
r'9 46-3. Herpes type-II Induced tonsillitis. esy Dr James Cottonel
Fig. 46-4. Herpes type II-induced pharyngitis.
;<:;: 46-5. Pdk'ral pe1ect'l
Fig. 46-6. ExudatIVe tomlI!IUS. same patient W1m
46-7. SyphilitIC chancre of primary syphilis; labla' )ure ICounesy Drs laurie Cohen and JOhn COKe)
jCourtesy Dr James CotlOne)
infectious mononucleosis as rn Fig 46-5 {Courtesy Dr Geza TerezhalmyJ
Fig. 46-8. Snail track mucous patch of se
103
HIV INFECTION AND AIDS Acquired immune deficiency syndrome (AIDS) is a communicable disease caused by the human immunodeficiency virus (HIV. HTLV.III) first reported by the Centers for Disease Control in 1981. The virus is harbored in the blood. tears. saliva. breastmilk. spinal fluid. vaginal secretions and seminal fluid of infected persons and is predominantly spread by sexual contact, by blood or blood products. or perinalally. Infeclion may resuil by exposure to the virus through participation in high risk activities such as sharing needles willi intravenous drug users; having unprotected sexual activity involving exchange of infected bodily fluids; being a recipient of infected blood or blood products; or being accidentally exposed to infected materials. Individuals infected with HIV. as determined by seroconversion. usually manifest persistent generalized lymphadenopathy (PeL) followed by AIDS-Related Complex (ARq, which is characterized by lymphadenopathy. weight loss, fever. dial'Thea. fatigue, skin anergy. oral candidias~s. hairy leukoplakia. and herpes virus recrudescence. Progressive changes in immune regulation caused by T-cell lymphopenia and reduced helper T-cell (OKT4/LEU3a) function results in full-blown AIDS, characterized by opponunistic infections and susceptibility 10 cenain fonns of cancer. At present there is no curative treatmem available for AIDS, and infected persons eventually succumb to the disease. The oral manifestations of HIV infection are often numerous and concurrent. Recognition of the oral features associated with HIV infection should warrant patient referral to a physician.
Oral Bacterial Infections fFigs. 47-' and 47-4) Oral bacterial infections in patients infected with HIV usually involve the periodontal tissues. Examples of these infections include acute necrotizing ulcerative gingivitis (ANUG). HIV·gingivitis, and HI V-periodontitis. ANUG is common in HIV-infected patients. It is char- . acterized by sudden onset of fiery red. swollen. painful, bleeding gingiva and a fetor oris. The interdental papillae appear "punched-out." ulcerated. and covered by a grayish necrotic slough. Treatment involves debridement alone or combined with metronidazole therapy if constitutional signs such as fever, malaise, and anorexia are present. HIV gingivitis is characterized by chronic gingival erythema that occurs equally in the maxilla and mandible despite the absence of apparem local factors. Initially. small. red. punctate. muhifocal petechiae of the attached gingiva appear. which later fonn noncoalescing. distinctive red linear bands of the marginal and auached gingiva. Spontaneous gingival bleeding and lack of response to conventional therapy are common. The etiology is uncer+ tain. but it has been proposed that immune defects, in par+ ticular PMN abnonnalities. may playa role.
104
~""';;;~;
HIV periodontitis is an extremely rapid process that produces a loss of periodontal an. in days. It initially manifests in the amerior sues. radiates to the posterior areas with time. distinct propensity for occurence in the incisor teeth. This bacterial infection is characterized spontaneous gingival bleeding. interdental ..,,..~ and cratering. gingival edema and intense eT)~ gingival recession. extremely rapid and irregm. (up to 10 mm in 6 months). delayed wound spread to adjacent mucosa. Aggressive peri""_~ sures are required to limit this disease. In the HIV-infecled patient. bacterial flora the oral cavity can be found. The most COlTlllXa bacteria are respiratory and colifonn flora. t
-01_
often produce diffuse. erythematous. and ulcera:d. of the tongue that results in symptoms of Antibiotics are effective. but overgrowth of,,",""';" isms may occur as a result.
Oral Fungal Infections 'Figs. 47-5 ane Candidiasis, in a variety of clinical presen.w.... most common infection of the mouth affecting dIr surfaces of patients with AIDS. and is often thr. ~::::~: manifestation. Candidal infections are usuall) .: nature and may appear red. white. flat. raised. or Any oral mucosal surface may be infected. -:=-:,;~: palate, tongue. and buccal mucosa are the lDOSI sites. Symptoms of infection may include mild burning. or altered taste. Types of candidiasis ~:~::: domembranous candidiasis. erythematous (a didiasis, hyperplastic candidiasis. and angular Pseudomembranous candidiasis is charaac=;; creamy white plaques that upon scraping reveal.! or bleeding mucosal surface. A KOH-stained SlDeZ' gal culture reveals the typical morphology of C''''''.... cans. The erythematous or atrophic fonn clin' as a diffuse red area, usually located on the ~ tongue. At this location the condition is associ3tCd loss of filifonn papillae and is tenned "medim glossitis." A diffuse. erythematous contact I sponding in size and shape to the tongue lesK. apparent on the palate. Chronic hyperplastic c:::~~: late stage of candidal infection, clinically appean. white keratotic plaques on the buccal mUCOR. plaques cannOl be wiped off. Topical antifungal agents are almost alwa)'-s ......_ the treatment of oral candidiasis; however. me __0::.."'" may be chronic and recurrent, and may be pmh.;; esophageal candidiasis. Infrequent oral fUn,!g~21~:~::- associated with AIDS are geotrichosis and his:
INFECTION AND AIDS
.: 7-1. ?'Uncned-out Interdental paPillae of 19 ulceratIVe gingIVItis; Hlv-posrnve patient.
Fig. 47-2. Pun
as In Fig 47·1
" .'·3. ~on
«; ~7-5. Median rhomboid ~e patient. ~Courtesy Dr
glossitis In
-r; 41-7. Acute pseudomembranous Qindidiasis In a pauent WIth AIDS.
,,
Fig. 47-4. RadlographlC €\Ildence or rapid bone loss; bottom r ms liIken 6 months after lOP films; HIV penodontl[l$
Fig. 47-6. Atrophic undidi..sls
i'!(
posrenor extent
of pal.?l€' overlYing the glosS'lIS seen (Cour.:esy Dr Ed Heslop)
'n
Fig 47-5
Fig. 47-8. Acute pseudomembranous undidia,!, In same AIDS patl{'nt as In Fig 47-]
105
HIV INFECTION AND AIDS Oral Viral Infections IFigs. 48-1 through 48-61 Herpes viruses (herpes simplex, varicella zoster, cytomegalovirus. and Epstein-Barr) figure prominently in oral disease in the AIDS patient. Herpes simplex virus (HSV) infections usually appear on the lips as herpes labialis or within the mouth on keratinized epithelium as recurrent intraoral herpes. The recurrent infection forms smalL round vesicles that rapidly erupt. leaving shallow yellow ulcers bordered by a red halo. Coalescence of adjacent vesicles into large ulcers is common. Unlike patients with normal immune funclion. patients with AIDS may have herpetic infections on mucosal surfaces lypically ascribed to aphthous stomatitis such as the tongue and buccal mucosa. HSV recurrences are often more frequent. more persistent. and more severe in patients infected with HIV. Varicella zoster virus (VZV) recrudesces more frequently in HIV-infected persons than in the ordinary population. The clinical appearance is similar in both groups, but the prognosis is worse for patients with immune suppression. VZV produces multiple vesicles commonly located on the trunk or face thai are usually self-limiting and unilateral. Cephalic vesicles are found along a branch of the trigeminal nerve. either extraorally or intraorally. Vesicle eruption, coalescence. ulcer formation. and scabbing are characteristic of the condition. Deep searing pain is the premiere symptom. which may persist as post-herpetic neuralgia. Therapy with acyclovir is sometimes used in an attempt to accelerate healing and to mitigate symptoms. The prevalence of C}'tomegalovirus (CMV) approaches l(}()% in HIV-positive homosexual males and approximately 10% in children with AIDS. The virus has a predilection for salivary tissue and can be recovered from the saliva of persons infected with HIV. Inflammatory changes associated with CMV and HIV-infection include unilateral and bilateral parotid gland swelling and xerostomia. Oral manifestations of human papilloma virus (HPV) are frequently found in persons infected with HIV. So far, over 65 serotypes of HPV have been identified. A variety of mucocutaneous lesions are HPV-induced, including squamous papilloma. verruca vulgaris, focal epithelial hyperplasia (Heck's disease). and condyloma acuminatum. The condyloma acuminatum, or venereal wart, usually appears as a small, soft, pink to dirty gray. exophytic growth that has a cauliflower-like surface. These lesions are often multiple and recurrent, and coalesce to form large. sessile, pebbly growths. Condyloma acuminata can be found on any mucosal surface. particularly the ventral tongue. gingiva, labial mucosa. and palate. Transmission is
106
most likely by direct contact resulting in contagioa:l from anal or genital sites, or by self-inoculation. "Ii consists of local excision together with simultanelXil cation of all lesions of infected partners. Hairy leukoplakia is a raised. corrugated. poart, cated white lesion on the lateral border of the tongue. associated with the Epstein-Barr virus and HIV. Early lesions appear as discrete, white, vertican~ plaques on the lateral borders of the longue thai ~ bilateral, whereas older lesions may cover the eOla and dorsal surface of the tongue and extend onto . . mucosa and palate. The lesions are asymptomatic. rubbed off, and often are of esthetic concern to ~ Histologically one sees hyperkeratotic hairlike ~ koliocytosis, minimal inflammation, and candidal . Histopathologic confirmation of hairy leukoplakia II tant, because the diagnosis predicts the devel"",,,,,.. AIDS within 80% of those affected in I to 3 yean. Oral Malignancies {Figs. 48-7 and 48-81 No...:;; sarcoma is the most common malignancy assoc' HIV infection. It is a tumor of vascular prolife affects the cutaneous as well as the mucosal tissue. ology is unknown. but viral factors (possibly eM\ ated with angiogenesis have been suggested. mately 20% of all AIDS patients are affected: the lence is about 30% in HI V-infected homosexual rI1IIIIa. Kaposi's sarcoma is characterized by three stages.. _",~, the malignancy is an asymptomatic red macule. enlarges into a red-blue plaque. Advanced lesions lobulated, blue-violet nodules that ulcerate and cao_,,The hard palate at the lateral areas is the mosl COllUDlill tion, followed by the gingiva and buccal mucosa. the lesions are multifocal, uncomfortable, and esthe pleasing. Treatment is palliative. utilizing radiatioo and chemotherapy. Clinically similar-appearing l~ can be ruled out by biopsy are erythroplakia. heman_ purpura. and atrophic candidiasis. Non-Hodgkins B-cel! lymphoma and squa carcinoma are associated with H1V infection. p a result of abnormal immune surveillance which enhanced neoplastic proliferation. Non-Hodgkim. phoma often appears as a diffuse. rapidly prolifi purplish mass of the palatal-retromolar compleL mous cell carcinoma is most frequently found as a white or ulcerated lesion on the lateral border tongue. Many of the usual co-factors. such as age, alcohol abuse, and poor oral hygiene. are HJV-infected persons.
fn=_
lV INFECTION AND AIDS
If:.
48-1. Per51stent recurrent herpes labialis In
Fig. 48-2. Recurrent herpes simplex In a pallent with AIDS.
_~,;;a;,,
r ~8-3. Un~lC!'al palatal ulcerauons of herpes aest:e'r ran HIV'positlve patient. (Courtesy Dr • '1eg.i1rd)
_
"
Fig. 48-4. PapdlOma-vlrus-induced condyloma acumin..ta In a HIV.positive patient.
48-5. White corrugated patches; hairy
Fig. 48-6. H.dry leukoplakia; XJmc pdtlent dS In Fig
oplakla in an HIV.posltlye patient.
48-5
C8-7. Early purple macule and mature purpliSh :~ Kaposls saKoma In an AIDS patient. 5-, Dr \o1lCheal HUbef)
Fig. 48-8. Noduiar non-Hodgkins lymphoma In a
patient With AIDS. (Courtesy Dr George Kaugro)
101
EVIATIONS TION
ENGLISH
LATIN DERIVATIVE
at pleasure
ad libitium
before meals
ante cibum
after meals
post cibum
water
aqua
a day. daily
dies
£\Nice a day
bis in die
three times a day
rer in die
four times a day
quater in die
hour
hora
at bedtime
hora somni
every hour
quaque hara
every three hours
quaque tertia hora
every four hours
quaque quarta hara
every six hours
quaque sexta hara
do not repeat
non repetatur
as needed
pro re nata
immediately
statim
label
signetur
with
cum
drops
guttae
tablet
tabella
capsule
capsula
every day
quaque die
"'
Appendix II
THERAPEUTIC PROTOCOLS ESICS
ANALGESICS
ENT RATIONALE: relief of the symptoms of mild to pain associated with oral
,":::te .3
ns.
Acetaminophen Tylenol® 325 mg
Rx
AspIrin 325 mg. Butalbnal 50 mg. Caffiene 40 mg Fiorinal rabs
Disp.:
40 Tablets
5ig:
Take I to 2 tablets q.4 h. p.r.n. pain.
Rx
Dihydrocodeine bitarrrate 16 mg. Aspirin 356.4 mg. caffeine 30 mg Synalgos-DC Capsules (Wyeth)
Oisp.:
40 Tablets
5i9:
Take I to 2 tablets q.4 h. p.r.n. pain.
Rx
Oxycodone HCI 5 mg. Acetaminophen 325 mg
McNeil)
Tylenol 325 mg (McNeill 100 Tablets Take 2 rabIes q.4 h. p.r.n. pain not to
exceed 12 tabs in 24 hours.
Acelylsallcytic I\cid Bayer Asp.nn 325 mg (Glenbrook)
100 TClblets
Take 2 tablets q,4 h. p.r.n. pain.
Percocet® Tablets {Dupont)
Ibuprofen '.Iotrln 400 mg IUpjohn/
Disp.:
25 Tablets
51g:
Take I tablet q.4 h. p.r.n. pain.
laO Tablets
Take 2 tablets q.4 h. p.r.n. pain.
Rx
Oxycodone He! 4.5 mg. Oxycodone Terephthalate 0.38 mg. Aspirin 325 Percodan/!) Tablets /Dupont)
aproxen
mg
Disp.:
25 Tablets
Sig:
Take I CClblet q.4 h. p.r.n. pain.
Rx Acetaminophen with Codeine 30 mg Tylenol with Codeine No.3
Meperidine Hel 50 mg, Promethazine HCI 25 mg Mepergan Fonis ® CapSUles /Wyeth)
Disp.:
25 Tabrets
30 Tablets
5ig:
Take I tablet q.4 to 6 h. p.r.n. pain.
Rx AspIrin with Codeine 30 mg Empirin with Codeine No.3 (!) Tablets Burroughs WelJcome)
Hydrocodone bitartrate 5 mg, Acetaminophen 500 mg Lonab 5 Tablets IRussl
Disp:
30 Tablets
30 Tablets
5ig:
Take I tablet q.4 h. p.r.n. pain.
aprosyn~ 375mg
/Synrexl
50 Tablets Take 2 tablets t.i.d. p.r.n. pain.
T. e 2 lablets q.4 h. p.r.n. pain.
ake 2 tablets q.4 h. p.r.n. pain.
115
Appendix II
THERAPEUTIC PROTOCOLS ANTIHISTAMINES
TOPICAL CORTICOSTEROIDS
TREATMENT RATIONALE: For the relief of the symptoms of anxiety and anxiety~related skin eruptions.
TREATMENT RATIONALE: For adjunctive treatment and temporal')' relief of symptoms associated with ora inflammatory and ulcerative lesions.
Rx
HydroxyzIne Atarax lXl 25 mg Tablets IRoerigl
Disp.:
50 Tablets
5ig:
Take 2 lablets q.i.d. p.r.n.
Rx
Diphenhydramine hydrochloride Benadryl 25 mg fWarner-tilmbertJ
Disp.:
25 Tablets
5i9:
Take I tablet q.i.d.
116
Rx
Beramethasone valerate ointrne"'T 0.1 % Vallsone l!:l fScheringJ
Disp.:
15 gm (45 gm) tube
5ig:
Apply w mouth sores after bedtime.
Rx
Fluocinonide gel 0.05% tide>< (Symex)
Disp.:
15 gm 130 gm/ tube
5ig:
Apply to mouth sores after meats bedtime.
Rx
Hydrocortisone acetate oinunen;. 05% Orabase HCA (COlgale-h:
Disp.:
5 gm tube
5i9:
Apply to oral lesions after mealS bedtime.
Rx
Triamcinolone acewnide oinrl'TleT 0.1% Kenalog in Orabase 15ql.o::I::
Disp.:
5 gm tube
5i9:
Apply to ulcerated area after meats" at bedtime.
Rx
Dexamethasone elixir Decadron
Disp.:
100 mJ bortle.
5ig:
Rinse with I teaspoonful q.l.d minutes then expectorate.
meas:
~;;:
Appendix II
THERAPEUTIC PROTOCOLS UNOSUPPRESSIVE AGENTS
ORAL ANTIMICROBIAL RINSES
JMENT RATIONALE:
TREATMENT RATIONALE: To reduce the pathogenic microbial flora often associated with the inflammatory signs of oral disease.
.ard'junetive treatment and temporary of symptoms associated with severe f1ammatory and ulcerative lesions. Prednisone Medro/ ® 4 mg Dasepak 2/ s rUpjahn)
Rx
Chlorhexidine gluconate 0.12% Peridex ® Oral Rinse (Procter & Gamb/e)
Disp.:
480 ml bortle
Sig:
Swish J teaspoonful for I minute then expectorate. Peform twice daily morning and evening after rooth brushing. Avoid earrng or drinking for 30 minutes.
Rx
Tetracycline HCf Tetracyn ® 250 mg (Pfizer/
Disp.:
40 Capsules
Sig:
Dissolve 1 capsule in 1 teaspoon of warm water. then swish the solution for 3-5 minutes and swallow. Repeat q.i.d.
Rx
Tetracycline HCI Achromycin V ® /25 mg/5m/ (Leder/e)
Disp.:
60 mr la/so available in 16 fI oz)
Sig:
Rinse with 2 teaspoonsful for 3 minutes and swallow. Repeat q.i.d.
I dosepak 12/ t.3bs) Take graduated daily doses according to the manufacturerS directions listed
on the dosepak.
Prednisone I 0 mg 36 Tablets
Take 1 tab t.i.d. for 10 days. then
diminish dose by I tab every 2 days for the next 4 days.
Azathiopnne Imuran SO mg (Burroughs WellcomeJ 30 Tablets
Take a single dose of 50 mg once daily. (Patients nor improved in '2 weeks mClY be refractory to this drug).
-:..~~: Chronic immunosuppression with ~ ne increases the risk of neoplasia. prescribing this drug should be familiar nsk as well as the serious mutagenic
"'ematologic consequences to both men oomer1.
117
Appendix II
THERAPEUTIC PROTOCOLS FLUORIDE THERAPY
TOPICAL ORAL ANESTHETICS
TREATMENT RATIONALE:
TREATMENT RATIONALE:
To prevent dental caries in susceptible patients.
Relief of the symptoms associated minor irritations of the mouth.
Rx
Stannous ftuonde 0.4%
Rx
Disp.:
4.3 ft
519:
Apply 5 to 10 drops in a carrier and place carrier on teeth daily for 5 minutes.
Ol
Rx
Oral ftuorlde 0.125 mg Luride «l per drop ICa/gateHayt)
Disp.:
60 ml bertIe with dropper
Sig:
Apply 2 drops per day" IBirth to 2 years) Apply 4 drops per day" 12 to 3 years) Apply B drops per day" 13 to 12 years) "in the mouth of the child
DiphenhydramIne HCI Benadryl ® elixir' 2.5 mg/5 rn Davis}
~
Disp.:
4 ft Ol
Sig:
Rinse with 1 tablespoon a.c. an:: pain.
Rx
Benadf}'l
Disp.:
4 fJ 02 of each, mIx equal parts
51 9:
Rinse wirh I rablespoon for 2 ........... a.c. and p.r.n. pain.
Rx
lidocaine HCI 2% Xylocaine ® viscous soluoon -
Disp.:
4 fI
Sig:
Rinse with I teaspoon a.c. and p rpain. Expectorate after rinsing.
Rx
Orabase with Benzocaine IColga:rHayti
Disp.:
5 gm 115 gm)
Sig:
Apply to affected area a.c. and p pain.
Ol
r..,
Appendix II
THERAPEUTIC PROTOCOLS XIETY AGENTS TMENT RATIONALE: the management and short·term relief symptoms of anxiety. Chlordiazepoxide LJbrium III 10 mg {Rochel
20 Tablets
NUTRIENT DEFICIENCY THERAPY TREATMENT RATIONALE:
To replace deficient nutrients necessary for homeostasis.
Rx
Ferrous sulfate 250 mg
Disp.:
100 Tablets
5i9:
Take I tablet t.i.d. for I month, then r€'-assess patient'> hemoglobin.
Rx
Folic acid 0.4 mg
Disp.:
30 Tablets
5i9:
Take I tablet daily for I month, then re-assess patients folic acid level. .,.
Take I tablet twice daily.
Diazepam. Valium ® 5 mg IRoche)
20 Tablets Take I tablet 2-3 times daily. and J tablet , hour before dental
appoIntments AlpraxoJam )(.;nax ® 025 mg [UpJOhn) 20 Tablets Take I tablet twice daily.
*Caution: Medical supervision is advised.
Rx
Water soluble bioflavinoids 200 mg with ascorbIC acid 200 mg Peridin-e lID 400 mg (Beutlich)
Disp.:
100 Tablets
51 9:
Take I tablet t.i.d. for 2
weeks.
Busprrone Buspar ® 5 mg {Mead JohnsonJ 20 Tablets Take 1 tablet twice daily.
119
Appendix II
THERAPEUTIC PROTOCOLS ANTIHISTAMINES
SALIVA SUBSTITUTE
TREATMENT RATIONALE: To reduce the effects of histamine-mediated hypersensitivity and temporary relief of the symptoms associated with minor oral irritations.
TREATMENT RATIONALE: For the relief of a dry mouth.
Rx
Carboxymethyl cellulose 0.5% solution.
Rx
Disp.:
8 fI 02
51g:
Use as a rinse p.r.n.
Rx
Moi-stir l8:l (Kingswood)
Disp.:
120 ml with pump spray
51 9:
Use as a rinse p.r.n.
Rx
Xerolube (Scherer)
Disp.:
180 ml with pump spray
5i9:
Use as a rinse p.r.n.
Phenylpropanolamine HCI 25 mg and Brompheniramlne Maleate HCI 4 mg Dimerapp (Roblnsl
Rx
Salivart (!!) (Westport PharmJ
Disp.:
40 Tablets
Disp.:
75 ml with pump spray
519:
Tak.e I tablet q.4 h. as needed.
519:
Use as a rinse p.r.n.
Rx
Terfenadine Sefdane ® 60 mg (Merrell Dow)
Oisp.:
30 Tablets
51 9:
Tak.e 1 tablet twice a day.
Rx
Astemizole Hismanal (!l 10 mg (Janssen)
Oisp:
25 Tablets
519:
Take I tablet once a day.
Diphenhydramine HCI 8enadryl 25 mg (Parke-Davis)
Disp.:
40 Tablets
5ig:
Take I tablet every 6 hours as needed.
Rx
Brompheniramine Maleate Hel Dimetane
Disp.:
40 Tablets
51 9:
Take 1 or 2 tablets every 6 hours as needed.
Rx
120
--
Appendix II
THERAPEUTIC PROTOCOLS UNGAL THERAPY ~TMENT RATIONALE:
ANTI·FUNGAL THERAPY
Rx
NystatIn ointment Mycost.3tin ointment ® 100,000 I.U. ISquibb!
Disp.:
15 gm (30 gml tube
Si9:
Apply liberally to affected area 4 to 6 times daily.
Rx
Nys[CItin-neomycrn sulfate-gramrcidintriamcinolone acetamide TreS"'tin ® IRugby)
Disp.:
15 gm 130, 60 gml tube
Si9:
Apply liberally to affected area 3 to 4 times daily.
Sninate pathogenic fungal organisms , iO
reestablish the normal oral flora. Nystatin vaginal tablets Nil,,,,, II!> I 00,000 W.ILederle!
90 Tablets DIssolve , tablet as a lozenge 5 rimes dally for I4 consecutIVe days.
Remove denturef5) jf applicable.
Clorrimazole Mycelex Troches ® 10 mg (Miles Pharm) 60 Tablets DIssolve I tablet as a lozenge 5 times dally for 14 consecutIVe days.
Remove denture/5J jf applicable.
ANTI·VlRAL THERAPY TREATMENT RATIONALE: To prevent and/or treat oral herpetic infections.
Kewconazole Mzera! (g) 200 mg (Janssen PharmJ
Rx
Acyclovir ointment 5% Zovirax @ (Burroughs WelicomeJ
14 Tablets
Disp.:
15gm
Sig:
Apply ta oral lesions with a conon tip applicator 6 times a day.
Note:
Treatrnenr should begin during the earty /prodromal! stage of the recurrence.
Rx
Acyclovir Zovirax ® 200 mg (Burroughs Wet/come)
Disp.:
50 CapSUles
S;9:
I capsule q.4.h. for 5 to 10 days.
Remove denture(s/ if applicable.
Note:
Treatmenr should begin during the early stage of the recurrence In the immunosuppressed patient
Nystatin topical powder Mycosratin (B) ropical powder 100,000 W. ISquibb)
Rx
L·lysine Enisyl ® 500 mg (Person & Covey)
15 gm squeeze bottle
Disp.:
100 Tablets
Apply liberally to tissue side of clean denrure p.e. Soak the clean denture in a suspension of I teaspoon of powder and 8 oz. of water over night
Sig:
Take 4 tablets q.4.h. until symptoms subside.
Note:
Treatment should begin during the early stage of the recurrence.
Take 1 tablet daily for 2 weeks.
Nystatin Mycostatln Pastilles (!I 200.000 U fSquibb! 60 Tablets Dissolve 1 pastille in mouth 4 times daily as a lozenge for 14 consecutive days.
121
Appendix II
THERAPEUTIC PROTOCOLS SEDATIVElHYPNOTICS
ANTIBIOTIC THERAPY
TREATMENT RATIONALE: To produce a "sleep-like" state for the effective management of an oral disease or condition.
TREATMENT RATIONALE: To eliminate pathogenic bacterial organisms that cause oral infection.. Rx
Phenoxymethyl PeniCillIn Penicillin V 500 mg Tablets
Disp.:
40 Tabs
51 9:
Take 2 tablets immediately eTC tab q.6 h. 1 hour before I1'lea$..
Flurazepam Dalmane ® I 5 mg (Roche)
Rx
PeniCllhn V Porassium lIqUId PeniCillin VK liquid 125 mgI5
Disp.:
30 Tablets
Disp.:
200ml
519:
Take) tablet h.s.
51 9:
Child should tClke ! teaspoorT:
Rx
Temazepam Res£Onl ~ I 5 mg (sandoz)
Rx
Amoxicillin Amoxil ® 500 mg /Beecharr'
Disp.:
30 Tablets
Disp.:
40 Tabs
51 9:
Take 1 tablet h.s.
51 9:
Take I 500 mg tablet q.8 h
Rx
Chloral hydrate Noctec ® 500 mgt 5 ml ISquibb)
Rx
OlcloxaciUin Sodium Dynapen II!> 500 mg ISnstol
Disp.:
I pim
Disp.:
40 Tabs
5i9:
Take 1 teaspoon before bedtime or 30 minutes before surgery.
51 9:
Take 1 500 mg tablet q.8 h
Note:
For penicillinase-resistant lnfec:xr
Rx
Trimethopnm 80 mg and Surfamethox.3zole 400 mg &:lctrim ® /Rochel
Disp.:
40 Tabs
5ig:
Take
Note:
For infections involving Esche'c"" Hemophilus influenzae, Kl Enrerobaaer species.
Rx
Triazolam HalClon ® 0.25 mg /Upjohn)
Disp.:
30 Tablets
5i9:
Take 1 tablet h.s.
Rx
122
J
tablet q.12 h.
Appendix II
THERAPEUTIC PROTOCOLS
Metronidazole Flagyl ® 500 mg 15earlel
40 Tabs
ANTIBIOTIC THERAPY - BACTERIAL ENDOCARDITIS PROPHYLAXIS TREATMENT RATIONALE: To prevent bacterial endocarditis in
patients with rheumatic, congenital, or
Take 2 tablets immediately then 1 tablet q.6 h. until gone.
other acquired valvular heart disease who are undergoing dental procedures.
For a febrile patient with acute necrotizing ulcerative gingivitis involving anaerobic bacteria.
Rx
Amoxicillin, 500 mg
Disp.:
9 tabs (4.5 grams)
5;9:
Take 6 tabs (3 g). orally! hr before dental procedure. then 1,5 9 6 hr after the initial dose.
Note:
Standard regimen for the prevention of bacterial endocarditis in adults and children> 66 Ibs; (30 kg)
Rx
Amoxieillin. 250 mg
Disp.:
By weight
Sig:
Take 50 mg/kg. orally. 1hr before dental treatment, followed by half the original dose 6 hr after the original dose.
Note:
Standard regimen for the prevention of infective endocarditis in children < 66 Ibs (30 kg). The following weight ranges may also be used for the initial pediatric dose of amoxicillin < 15kg, 750 mg; 15 to 30 kg. 1500 mg; and> 30 kg. 3000 mg.
Rx
Erythromycin"- ethylsuccinate. 400 mg
Disp.:
3 Tabs
Sig:
Take 2 tabs orally, 2 hr before dental treatment, followed by half the original dose 6 hr after the initial loading dose.
Erythromycin ethyJsuccinare 400 EEl ® 400 mg (Abbott!
56 Tabs Take I 400 mg tablet q.6 h. Continue for 7 days. Tetracycline Hel Achromycin V ® 250 mg (Lederle)
56 Tabs Take
J
tablet q.i.d. Continue for 7 days.
Cephalexin Keflex ® 250 mg (Distal .
...
56 Tabs Take 2 tablets q,6 h. Continue for 7
days.
CTERIAL ENDOCARDITIS PHYLAXIS Clindamycin By weight J0
mg/kg I hr prior to dental treatment, followed by half the original dose 6 hr after the initial loading dose For the prevention of infective endocarditis in children allergic to penicillins
OR
Rx
Clindamycin, ) 50 mg
Disp.:
3 Tabs
Sig:
Take 2 tabs orally. I hr before dental treatment, followed by half the original dose 6 hr after the initial loading dose.
Note:
For patients allergic to penicillin.
~erences in absorption and bio-availability require changes in dosing vvhen using different fams of erythromycin.
123
Appendix II
THERAPEUTIC PROTOCOLS ANTIBIOTIC THERAPY - BACTERIAL ENDOCARDITIS PROPHYLAXIS HIGH RISK PROTOCOL - ADULT
ANTIBIOTIC THERAPY - BA ENDOCARDITIS PROPHYLAXIS HIGH RISK PROTOCOL - CHILD
Rx
Ampicillin
Rx
AmpICillin
Disp.:
2g
Disp.:
By weight
519:
2 9 1M or IV 30 min prior to dental treatment.
Sig:
50 mglkg 1M or IV 30 mIn pncl'" dental treatment
PLUS
PLUS
Rx
Gentamycin
Disp.:
Byweighr
Si9:
1.5 mg/kg 1M or IV 30 min prior to dental treatment
THEN
Rx
Gentamycin
Disp.:
By weight
51 9:
2 mg/kg 1M or IV 30 min prlOf treatment
1.5 g. AmoxicjIJjn. orally 6 hr ilfter Initial dose
THEN One haff the initial dose 6 tv Be'"
OR
The parenteral regimen may be repeated 6 hr after initial dose Note:
Note:
For maximum protection agaInst bacterial endocarditis in adults at risk.
For prevention of bacterial endal:m::= in children under 66 lbs {30 kg
ALTERNATIVE INTRAVENOUS REGIMEN - ADULT
ALTERNATIVE INTRAVENOUS REGIMEN - CHILD
Rx
Vancomycin Vancocin fUlly) in parenteral solution
Rx
Vancomycin Vancocin (LJllyJ in parental SClksUa"1
Disp.:
Ig
Disp.:
By weight
Si9:
Slowly administer I g over I hr intravenously beginning I hr prior to dental procedure.
51 9:
20 mg/kg IV given slowly ""'" • beginning I hr prior to dental procedure
Note:
For prevention of bacterial endocarditis in penicillin-allergic. high-risk adult patients undergoing dental procedures.
Note:
For prevention of bacterial enooc...; in penicillin.allergic. high-risk cr undergoing dental procedures
124
III
TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS LESIONS
ease 's granules
Age
Sex
Any
M-F
Any
-..skatio .-..curum
..._ ..u· c white
M-F
Melanoderms
"""'''',e keratosis Elderly
Treatment None reqUIred
White wiJI/Y line of vilf}'Ing length located on Eliminate buccal mucosa. bilaterally lesionS are bruxism and nomender. smooth to palpatJon. and do nO[ clenching. rub off Variable onset; per<;lsts With oral h.3bits.
Graytsh-lNtllle patch of variable size located OIl buccal None reqUired mucoSCl Ibllaterally). labial mucoSCl, and soft palate, LeSions Clfe nontender. smooth to palpatiOn Clnd dlSClppear when the mucosa is stretched Leukoedema becomes more evident WIth Increasing age
M-F
Eliminate AsymmeUlc white plaque located on buccal mucosa and labial mucosa. often blaterally, (heft! lesions are nonleoder. rough to palpaoon. and ~p chewing peel slighrty when rubbed. YanabIe onset perstStS habit. WIth cheek Of lip biting habtt
M-F
Solitary or confluent rc'llSed while plaques that None required rTlCly appear on buccal mucosa. labial mucosa. alveolar ndge. floor of the mouth. ancllor soft palate, lesions are nontender; rough to palpation, and do f'IO( rub off Onset at blrth. perSists for I.fe
M-F
White surface slough (eschar) usually located on Eliminate the less-keratinized alveolar mucosa Palilte irritant, common for food -burns- lesions are tender to topical palpation i1nd rub off leaving a raw or bleeding anesthetics surface. Onset within hours of trauma; regression and in I to 2 weeKs analgesicS.
lesions
oplakla
Clinical Characteristics VhlItlsh-yeUow granules clustered In plaques located on buccal mucosa (bllaterallyl. labial mucosa. retrOfllCllar pad. lip. auached gingIVa. tongue. and frenum lesJons are nonteoder. rough to palpation. and do flO{ rub off 0"lSet after puI:lel'ty. ~ for ~fe
Any
Mba buccalis Any
oedema
Race! Ethnicity
21 (MFJ
M
Any
White patch tNt VClrit's in size, hOmOgeneity, and BiOpsy and texture High fisk lOCations include tlocr of the histologic mouth, vemral tongue. lateral tongue. and examinatIOn uvulo-paJatal complex_ lesions do not rub off Close and usually are nontender. Onset occur<; after follow-up prOlOnged contae[ WIth an indUCing agent mandatory. persists as long as the InduCing agent is present. WhIte pebbly CIrcular patches localed on upper Use filtered and lower Nps lkiSSlng 1es1Of1S1, Keraloses are Clgarmes. firm. non!ender; and do not rub off Onset II"l conjunctIOn WIth a PfOlOnged clQ
"'"00
127
Appendix III
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS WHITE LESIONS
Disease
Age
Sex
Race! Ethnlcity
Nicotine stomatitis
40-70
M
Any
Snuff dipper): patch
Verrucous c.ardnom.a
Teenage and adult
Over 60
M
Any
M
Clinical Characteristics White cobblestoned papules located on hard palate. exCluding the anterior third. Papules have red centers. are nontender. and do not rub off. Onset is vanable to degree of smolong. lesIons are long-standir19.
Corrugated whitlsh-yellow patch lOCated on rrucobuccal fold, most prominent unilaterally. Patch IS rough. nonlender and does nol rub off. long-standing habit precedes lesion, patch persists with continuation of habit.
128
lsee Red and/or RedMlhite Lesions)
..,.
"""' " ...,..
Papuloncx.lular whilJsh-red mas.s located on buccal mucosa. a~r ridge, gtngNa Lesion is firm nomendef; rough to palpation, and does not rub off. Long..standir19 tobacco habit precedes onset lesion enlarges unless treated.
Squ.amous cell c.arclnom.a
Sroc
~~?~.
t""e"I
·
"'
DE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS USIONS
Disease
Age
Sex
Clinical Characteristics
Race!
Treatment
Ethnicity Purpura
M-f
My
Red spot or palCh consistlf"IQ of extravasated
blood
mat onsetS soon after uaurna
El,mInate under~ng
Le'irDnS do not blanch upon diascopy and size problem varies /petechlae < ecchymosis < hematoma). Petechiae common on soft palate; other purpurae typically occur on buccal/labial mucosa, depending on SIte at whICh blood IXJOIs LesIOrn fade awcry
v.icosity
~mbus
ngloma
""'" 55
""'" 30
ChildadOleSCent
F
M-f
F
Reddlsh-purple papule or nodule located on None venual tongue. lip. or labial mucosa. lesions are necessary asymptomatic and blanch upon diaSCOpy. Surgery for Varicosities increase in size and number with esthetics. increasing age and are persistent
Red to blue-purple nodule kxated on labial SurgICal mucosa, lip. or tongue. leslOl1S are firm and rerTlCl'laJ and may be render 10 palpatiOn. OnSet after traumatic histologiC bleed, lesion is diascopy negatIVe and persists examination. until treatment. OCcasionally thrombi will jf persistent or spontaneously regress symptomatic.
Red (0 purple. soft smooth-surfaced or multtnodular exophytIC mass located on dorsal tongue. buccal mucosa. or glnglVa lesions are diascopy positive. Onset early in life; perSistS until treated. OCcasionally hemangiomas will spontaneously regress.
If present Since youth. no funaJonal disability, and no changes in size. shape. or color; no ueatment IS
necessary. OCherwJse. surgery/ histologic e.
Post-puberty
M-f
MJltlfocal red macules located on palms. fingen. None reqUired. nail beds. face. neck. conJunctIVa. nasal septum. Monitor for lips. tongue. hard palate. and gingIVa. LesJOns hefTlO(rhage are present at birth. become more Visible at and/or puberty. and increase in number with age. anemia Telangiectasias lack cenual pulsation. blanch upon dIaSCopy. and If they rupture severe bleedJOg may result
Birth
M-f
Syndrome associated WIth seizures. mental deficits. None reqUired. gyriform calCifications, and a red to purple flat or Elective slightly raised facial hemangioma. Vascular lesion surgery for often affects lips. IabiaVbuccal mucosa. gingiva esthetics along branches of trigeminal flefVe. Abnormal ()(a1 enlargements may be concurrent.
~sls
2MS and
M
JOUComa
over 60
"'ifteditary
-.onhaglc jectasla
e-weMr tyftdrome
.Jewish. AsymptOfTla!JC red macule of mucocutaneous Mediterranean structures that enlarges and becomes raised or HIV·infected and then darkens in color. Advanced lesions are red--blue-violet nodules !hat ulcerate and cause pain. The hard palate. gingIVa. and buccal mucosa are the most common oral Iocaoom.
PalliatIVE'. conSisting of radiation therapy. laser surgery. chen'lOtherapy.
"'.
combinatIOn thereof
129
Appendix III
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS RED AND REDIWHITE LESIONS
Disease Erythroplakia
Age
Sex
Race/ Ethnicity
Over 50
M>F
Any
Erythroleukoplakia Over 50 & speckled erythroplakia
Squamous cell carcinoma
Over 50
M
21 M:F
Any
Any
Clinical Characteristics Red pi.l[ch of vanable size located on any oral mucosal site. High risk areas Include floor of the mouth, soft palate--retromolar trigone, I<Jter<'li border of tongue. Erythropl<1kias do not rub off and are usually asymptomatic. Lesions onset after prolonged contact with carcinogens, duration is varl<1ble. Regression IS rare. Red pi.ltch with multiple foci of white. Nontender. do not rub off, often superficially Infected With candida. Common locations include lateral tongue, buccal mucosa, soft pal."te, and floor of the mouth. Onset after prolonged exposure to carcinogens Regression unlikely even If inducing agent IS removed. Red, red/white, or ulcer commonly located on lateral tongue, ventral lOngue, oropharynx, floor of the mouth, gingiva, buccal mucosa, or lip. Carcinoma often asymptomatic until It becomes large, indurated, or ulcerated. Onset after prOlonged exposure to carcinogens. Persistence results in metastasis, usually apparent as painless, firm, matted, fixed lymph nodes
T
.....
......... c.a.
I
"" " " """' CJc«
c ""}G
Lichen planus
Over 40
F
Any
Purple, polygonal, pruritic papules on flexor surfaces of skin: occasionally finger nails are affected, Intraoral lesions are often symptomatk: and consist of white linear papules, reddish, patches and ulcerated regions of mucosa. Metted surfaces are often bilateral. Most common locations include buccal mucosa, tongue, lips, palate, gingiva, and the floor of the mouth. Lesions onset with stress; persist for many years with periods of remission and exacerb<1tion,
Electrogalvanic white lesion
Over 30
F
Any
Reddish-white patches that resemble lichen pl<1nus . . " . , . located on buccal mucosa adjacent to metalliC restorations Lesions do not rub off and are usually tender or cause a burning sensation eli&> Onset after weeks to years of exposure to metallIC ca..sn; restoration; duration is variable depending on "> rt:SCOR the persistence of the allergen.
Lupus erythematosus
Over 40
F
Any
Reddish butterfly rash on bridge of nose, MaculoT".,... papular eruption with atrophic central areas rnaj involve the lower lip, buccal mucosa, tongue and =uc;; palate. Intraoral lesions invariably have red and white radiating lines emanating from the lesion Lesions do not rub off, but are tender to palpatIOn. Onset often after acute sun exfXlsure, Lesions persiSt and require drug treatment.
,....-
'"'
130
~ixlll
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS AND REDlWHrTE LESIONS
Disease
Age
l.ichenold &
Adult
pus-llke '*Y9 eruption
c.ndldl~sis
Sex
Race/" EthnlcJty
Clinical Characteristics
Treatment
Red-white patches that resemble lichen planus and lUpus Often the lesions are atrophic or ukerated Centrally. Buccal mucosa, bilaterally. is the most common site. Onset is variable and may be weeKs or years after an allergic medication IS begun. Regression occurs when the offending drug is eliminated.
Withdraw offending drug and substiMe
Variable appearance: white curds. red patches, white patches with red margins. Any oral soft tissue 5lte is susceptible: hoI.Yever; the attaChed gingiva is rarefy affected. Onset is often coincident with neutropenia, and/or immune suppression. lesions persist until adequate anufungal therapy is provided
MUfungai
medication,
_apy
Eliminate diabetes,
en""
crinopathy, immune-
suppression.
13.
Appendix III
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS PIGMENTED LESIONS
Disease
Age
Me'anoplakJ41
Sex
Race! Ethnicity
M-F
Melanoderrns
Clinical Characteristics GeneralIZed C()flStant daI'k patch located on attached gIngIVa and buccal mucosa PIgmentation vanes from light brown to dart brown and IS often drffuse. cuMllnear. asymp!Omauc. and does not rub off Melanoplaklo3 pl"esent at bKth and pefSlSts fOf fe
Tanoo
Teenagers adults
M-F
Ephelis
Any
M-F
Smoke,~
Older adult
M-F
DIffuse brown patch of several centlfnetE!fs. lJSl.0I on posteric:N' buccal mucosa and soft palate HIStory of heavy tobacco s~ng precedes development of the lesion. Features may decrease with discontinuation of the habit Melanosis is asymptomatIC and nonpalpable
O,al melanotic m.-eule
25 - 45
Slight male predilectIOn
Asymptomatic brown [0 black macule usuali)' IocClted on Io\rver lip near mldlrne, also OC~ on palate. buccal mucosa. and gingIVa Onsel IS posHnnammatory and (he l€SIon perSIstS UJ"Iti treatment.
Nevus
Any
F
Any
Melanoma
25-60
M
caucasians.
Amalgam !attoo IS the most common type of Intraotal tattoo Appears as a blue-black macule on gingIVa, edentulous ndge. vestibule. palate. or buccal mucosa. RadiographS may demonstrate radiopaque foci. lesions are asymptomatic, do nOl blanch. and persist for life.
Ught·skinned persons
melanosis
especially IIghl-skinned
proons
1J2
~
''''''''
Ught to dark brown macule !hat appears on facial skin. elC(remities. or lip following sun elCposure Ephelides are Initially small but may enlarge ana coalesce lesions are nontender Clnd do not bW'lCt' or rub off
Nevi are highly variable in appearance. They r'T'la'r E."""" be pink. blue, brown, or black. but do not l:lIanc1' =XC!I!t upon diascopy They usually appear as a blursn ~~~'-= or brownIsh smooth-surfaced papule JocatecJ Clf'I I! the palate. Other common Sites Include the tu::ca mucosa. face, neck. and trunk_ Many lestOns are present at birth. They increase in size and ~ WIth Increased age.
Panless. slightly raISed plaque (l( patCh that has multiple colors. especially foci of brown. black. gray. Of red. In·defined marglfls. sate(I:le lesions and InftammatOl)' borders are charaeterrstIC They are usually located on maxillary alveolar ndge, palate, antenor gingJYc'l. and Iablal rrucosa 30% aflse from pre-exJsting plgmenlaUOl'lS A recent change In size. Shape. or cOlOr IS particularly ominous.
=
.te:lpendiX III
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS ENTED LESIONS
Disease
Age
Sex
Race!
Clinical Characteristics
Treatment
Ethnlclty -.-utz:.J~hers
syndrome
Child. young adult
Multiple, asymptomatiC melanotic oval macules. Oral: none prominently located on the skin of the palmarl required. plantar surfaces of the hands and feet around Gastrothe eyes, nose, mouth. lips. and perineum. intestinal IntraoraUy. brown dIscoloratIOns occur on the evaluation buccal mucosa. labial mucosa, and glnglVCl. and geneoc lesions do not Increase in siZe, but cutaneous counseling lesions often fade WIth age; mucosal pigmentatJO/l persists for life, Colickly intestinal symptoms are prObable
Diffuse inuaoral hypermelanotre palC~ occunng Sy5temK in conjunction Wllh bronzing of the skin, corticosteroids. especiaily of the knuckies, elbows, and palmar creases. Patches are nontender. nonraised, and vanable In shape. The buccal mucosa and glnQiva are most commonty affected. Onset of the disorder is insidious and associated with adrenal gland hypofunction. Patlenl may complain of gClstrointestlnal symptoms and fatigue.
Adu'
Blue-black linear pigmentation of marginal gingrva, prominemty viewed along arJterior gingiva. Spotty gray macules may be apparent on buccal mucosa, Neuralgic symptoms, headache, hypersalivation are common. Argyria: blue-gray skln pigmentation. especially In sun-exposed areas.
Terminate exposure {O heavy metal. medical referral. Oral lesions require no treatment.
13'
AppendIx 1/1
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS PAPULES AND NODULES
Disease
Age
Sex
Race! Ethnicity
Clinical CharacteristIcs
Retrocuspid
Child. young adult
M-F
N1y
Smooth-surfaced pink papule, 1 to 4 mm In diameter, located on the lingual attached gJngM!I apical to the marginal gingiva of the mandibular cuspds. These papuJes appear early In life. are often found bilaterally, and regress as the paoert' ages. The rerrocuspid papilla IS firm to paJpaoon. asymptomatIC. and nonhemorrhaglC
Any
Welkircumscribed, soft, fluctuant yellO'NiSh swelling that ranges in size from a f~ millimeters up to I cm, Common locations for this nontender cyst include the lateral neck JUS[ anterior 10 the sterno-cleidomastoid muscle. tIoor of the mou!h. lingual frenum, and ventral tongue lesion onsets dUring chrldhood or adolescence and persists until ueatment.
Any
Torus: bony hard nodule or mulnnodular mass located on !he palate at the midline. or mandibular lingual afveolar ridge. Exostosis .nos • bony hard nodule, often multiple. located on buccal/labial alveolar ridge. Osteoma: bony hard nodule located adjacent to the jaWS. often embedded In soft ossue /oJ1 3 !}'PeS 0( Ieslons are firm. asympwmauc lunless uaumatizedl. slow gr'O'Nlng. and Ion9"standing. Osteomas have !he greatest growth polenClaL
papilla
LymphoepitheJial Child. cyst young adult
Torus, exostosis,
!\dult
F
and osteoma
fibroma
Mult
Upoma
Ovec 30
Upoflbrorna
134
Ovec 30
M-F
M-f
T",-",==
...,..,,==
-
Jrrltation fibroma: smoo[h.surfaced, pink. firm. symmetric papule or nodule that anses at a Site of chronic irritation, such as the buccal mucosa. labial mucosa, and tongue. The gingwa is the most common location for the peripheral odont~ genic fibroma. Both Jesioru; have sessile bases. are nontender. and nonhemorThagJC
""""'"
Welkircumscribed. smooth-surfaced. domeshaped, yellowish to pink nodule commonly located on buccal mucosa. lip. tongue. floor of the mouth, soft palate. or mucobuccal fold lesion is Slightly doughy upon palpation and groINS Slowly.
""""'"
Welkll"cumscribed, smooth--surfaced, domeshaped. ptnkish nodule commonly located on buccal Of labia, mucosa. lesion IS painless. movable. and rather firm. Slow grcrwth and persistence are characteristic.
""""'" """"l' twa
boo<So
-9'~
'"'QDIMdix III
IDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS 'llt'PULES AND NODULES
Disease
Age
Sex
Race!
Clinlca' Characteristics
'h'eatment
Ethnlclty Tlo1umo1tlc ftflIroma
~ro'ibroma
Any
Over 25
Childhood
M-f
Small. slightly raised, firm, pressure-sensitrve papule Excisional that is commonly located in the mandibuiar biopsy and mueobuccal fOld near the mental foramen, histologic facial to mandibular IncisorS, Nnguaf retromolar eJlamrnatlon, regions, and ventral tongue VisualizatIOn of the If lesiOn recurs lesion may be difficult if the neuroma is subjacent COrticosteroid to normal-appearing mucosa, Palpation elicits injections may an 'electric shock' sensation. Onset occurs be effective. subsequent to trauma; lesions persist until treated
Firm pink: nodules that Clre often deep-seated. These rumors are loCated in skm. bones. Q( lI1tTaoraIIy - buccal mucosa, tongue, CJ( lips lesions are nontendef but movable. Contll1l..JE"d enlargement can lead to defCJ(mity Multiple lesions and slon pigmentations are associated with von Recklinghausen'S disease lneurofibromatosis).
ExcisionaJ biopsy. histologIC eJlammtion and fOllO'vv-up fOf malignant transformation In cases of
neurofibromatosis
P;apllloma
30s
llIBTuColI vulgaris Chlldh/xld young adult
Condyloma
M
M-f
20 - 45
M
Childhood. adolescent
M-f
~mlnolltum
phollnglomi!l
Small. pink:. pebbly, slow grO'Ning papule located on LMJIa. soft palate, longue, frenum. lips. buccal mucosa. CJ( gingiva The base IS pedunculated and welKircumscribed. whereas the surface is most often rough to palpatIon,
Excisional biopsy and histok>glC examination.
Rough. VoIhitis~nk: papule located on the skin of Excisional the hands. and perilablally on the lips, labial biopsy and and buccal m..x:osa, and attaehed gingiva. Lesions histologic are skwgro..ving and have a sessile base. examination. Verrucae may regress spontaneously or spread to adjaCent mucocutaneous surfaces.
Small, plnk-to
Excisional biopsy and histologiC examination.
Soft. compreSSible. pinkish-white swelling that Surgical may be superficial or deep-seated. Superficial excision; lesiOns resemble papillomas; deep-seated lesiOns depending on cause diffuse enlargement. lymphangiomas size and may occur In neck IcystK: hygroma). dorsallocation. lateral tongue. lip. or labial rruc:O$Cl. long-standing surgery may lesions can cause functional problems or regress require g""",,,1 spontaneously. anesthel:JC
135
Appendix III
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS VESICULOBUUOUS DISEASES
DIsease
Age
Sex
Race!
ClinIcal Characteristics
Ethnlclty Primary Infant Child, herpetic: young adult glng Ivostomatltls
Multiple vesICles that rupture, coalesce. and f(l(lTl ulcers of the tip. buccal and labial mucosa. gingiva. palate. and tongue. Ulcers are painful and initially are small, yellOW. and have red
M-F
inflammatOf)' borders. Onset is rapid. several days after contaCt WIth person haroorrng the virus lesiOnS persiS! for 12 to 20 dayS
Recurrent herpes simplex
Herpangina
Adult
Child.
MUltiple small vesiCles that rupture and ulcerale These lesiOns occur repeatedly at same site, usually the lip. hard palate. and attached glngN
M-F
D.ter 55,
My
M-F
over 35 in HIV+
Hand-foot· and-movth disease
Child.
young adult
Allergic reactions JmmecUate
Any
Vesicles on skin and face that after rupturing resemble a "deo.v drop_' Intraorally ulcers may be seen on soft palale. buccal mucosa. and rrMJcobuccal fold. Skin lesions crust over and heal with 5Gl{ formation. CondltJOn otten accompanied by chills. fever nasophal)'fl9ltJi. and malaise. Spontaneous healing occurs in 7 to 10 days. Unilateral vesicular and pustular eruptions that develop over I to 3 days. lesions occur along dermatomes and especially along the trigeminal nerve tract. lesions are vesicular. uicerative. intensely paInful and commonly affect me lip. tongue and buccal mucosa extendIng up to the mIdline Neuralgia may persist after healing
M-F
~
:~:~: ~
Crops of mUltiple small yellO'Nish ulcers that ocas on palm and sole of hand and foot. Inuaorally the tongue•.hard palate, buccal and labial mucosa are affected. Total number of lesions may approach 100. Healing occurs spontaneous~ IJ1 about 10 days. Red swellings or wheals that occur perioral~ or en ~ lips. buccal mucosa. gingiva. lips, and tongue ~ Contact wim allergen usually precedes epISOde by a f(W ITllnutes to hours. warrnd1. tenseness.
and itchiness are concurrent L.esions regress If the allergen is withdrawn.
136
(J'
rrMJltiple discrete .shallovol ulcers lesions have etythematouS border and arE' bmlled to anlenor pillars. soft palate. lMJIa. and tonsils. PharyngltlS. headache. fever; and lymphadenitis are often concurrent. lesiOns heal spontaneously Within 1 to 2 weeks.
Child
Herpes zoster
::~~
light gray paprllary vesicles that rupture formtng
M-F
youngaduJt
Chicken pox
~
~ndixlII
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS VESICULOBUUOUS DISEASES
Age
Disease Allergic reKtJons delayed
Erythema m"ltJforme
Sex
Any
Race! Ethnicity Any
Clinical Characteristics
Itct¥ erythemal:ous lesions tllat may eventuaty ulcerate May occur on any cutaneous or mucocutaneous surface. IntraOl"alty me lips, gingiva, alveolar mlJCOsa. tongue. and palate are affected. Erythema develops slowty over 24 to 48 hours Fissuring and ulceration may result.
Young adult
M
My
Treatment ""gen; """""' " corueo· steroids.
Skin - rilrget lesions. Oral- hemorrhagic crust of the Topical lipS: painful ulcerations of me tongue. buccal mucosa. Attached gingiva rarety affected. Headache. kJv.J-grade fever; and previous resplratory infection often precedes lesions.
analgesics. antipyretics. flUIds. cO!1icosteroids. amibioocs to prevent
>e
Slight SteYens.Johnson Child. syndrome young adult preference
Skln - target lesions. Eye - conJunctivitis. Genital- Topical balanitis. Oral - hemorrhagic crust of the lips: analgesics. painful ulcerations and weeping bullae of the antipyretics, tongue. buccal mucosa, Attached gingiva rarely fluids. affected. Stevens-Johnson syndrome is the corricofulminant form of erythema mu/tlforme. steroids. Eating and swallO'Nlng often are impaired. antibiotics to
for males
"''''''''' >e
Pemphigi"s v"lgarJs
30-50
M-f
light skinned
persons. Jev.nsh
"'" """"persons
a.nlgn mucous Membrane
pemphigoid
Over 50
2:1 F:M
Multiple skin and mucosal bullae !hat ruptUre. hemorrhage. and cruSt lesions tend to recur In the same area. have cIrcular or serpiginous borders. and tend to spread to adjacent areas. Nikorsky sign positIVe. CO/lapsed bullae is a common sign. Dehydration can occur if lesions are extensive.
Medical referral. sy'itemic steroids. and oral topical steroids.
Bullae on skin folds. ingUinal and abdominal areas. Oral topical Corneal lesions can lead to scarring. Bullae often steroids. are hemorrhagic and persist fOf days then Medical desquamate. lesions occur on the gingIVa. palate referral and and buccal mucosa. systemic steroids rf severe; rule out cOl"neal involvement and internal malignancy.
137
Appendix III
GUIDE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS ULCERATIVE LESIONS
Disease
Age
Sex
Race!
Cllnlca' Characteristics
Ethnlcity Traumatic ulcer
My
SymPCOrrt.:lliC. yellow-gray ulcer of variable SIze and shape, depending on IndUClrlg agent_ Ulcers are often depressed and usually oval 111 shape with erythematous border Commonly located on labial and buccal mucosa. tongue at the borders. and hard palate Duration is I to
2 weekS.
Recurrent aphthous stomatitis
Young adult
F
Srnau yellowlsh oval ulcer WIth red border. Icxat:eo ~:;~;= on movable non-keraClnlled mucosa. COfm'lC:W1 : SItes Il1Clude labial mucosa. buccal mucosa. tIoc.Ir ::::of the mauCh. longue. and occ.asK>nally soft palCtt aJ...Ir: UlCers are lender and may be associated WIth a tender ~ph node lesions onset raptdly and disappear in 10 10 14 days without SG3f tormaoon
Pseudoaphthous ulcer
25 - 50
F
DepresSed yellowish round
20 days.
;~~~~ ':;s_ ::oc:il
•
... 2
,e~
Major aphthous Young
138
F
Asymmetric unilateral ulcer with necrotic and depressed center. Ulcers have a red inflammatory border and are extremely painful. located on soft palate. consillar fauces. labial mucosa, buccal mucosa, tongue: may extend onto attached gingiva. Rapid onset. Underlying tissue is often destroyed. lesions heal In 15 to 30 days with scar forrrt.:ltion. Recurrences are common.
~=::~
.ac:oendix III
DE TO DIAGNOSIS AND MANAGEMENT OF COMMON ORAL LESIONS RATIVE LESiONS
Disease
Age
Sex
("petirorm
20,
M
20-30
3: I (MF)
~e,atlon
Chemo-
ttwraPMItlc ulcer
OIer 50
15to30and older adult
ClinIcal CharacteristIcs
Treatment
Multiple pmhead-$ized yellOWIsh ulcer$located on Tetracycline movable non-keratinlzecl mucog, Common $ite$ rime<;. include anterior tip of tongue. labial mucog. and floor of the mouth No ve<;icle formatIon. Ulcers are painful and may be associated WIth several tender lymph nodes le$ions ome( rapldly and dlo;appear in 10 [0 14 day!: WIthout $car formatIOn.
Asian, Eye - conjunctivitis. irins; Genital - ulcers; Oral Mediterranean, painful aphthc:ll.5-1ike ulcers on labial and buccal Anglo mucosa. S1un - maculopapular r.Nl and nodular eruptIOnS. Oral ulcers are often an initial Sign of the disea$e onset. Mhritis and gastrointestinal complaints may be concurrent. Recurrences, exacerbations. and reml$$iom are likely.
Topical and
systemic steroids
Asymptomaoc, cobblestoned ulcer that usually BiOpsy. occurs on dorsum of tongue, or labial histologic. commi$sure. Cervical lymphadenopathy and examination. primary respiratory complaint often is concurrent. Tuberculosis Onset of oral disease fol~ lung Infection of streptomycin $everal weeks to monthS duraDon Oral ulcer and isoniazid. may per$i$t for months to years If underlying ~ disease not treated. AlI~delCil B.
Sr"any'omatovs Older adult "Ice, 'nlbercYlosls. plasmosisl
SqlUlmous cell urdnoma
Race! Ethnlclty
2:1 MF
M-F
Nonpalnful yeUovvish ulcer WIth red indurated bc:lrders commonly located on pasterll)( third of the lateral border of tongue. Vffiual tongue. lips. and floor of the mouth. AssoclCltec! features may nclude numbness, leukoplakia, erythroplakia. induration. fixation. fungation. and lymphadenopathy. Caronoma has a sk:rw' ~ and is often notICed after a recent Increase In sIZe
Surgery. rachaoon
IrregUlar ulcerations of the lips, labial and buccal mucoo;a. tongue. and pal
Antimicrobial rinses to prevent seconda
therapy, and/or chemotherapy.
1J9
Appendix IV
SELF-ASSESSMENT QUIZ 1. fFig. 49-)) This soft tissue swelling was observed on the gingiva of a 7-monch-old infant. The infant's mother sCates that during the past several days the lesion has slowly increased in size. Aspiration yielded a straw-colored fluid. This lesion is most likely a: A. congenital epulis of the newborn B. congenitallymphangioma C. mucous retention phenomenon D. gingival eruption cyst E. traumatic hyperplasia
6. 'Fig. 49-5) This raised soft tissue leslm ~~~~ the patient"s lower lip. In the central region 01 appears translucem. Palpation reveals the I~ and fluctuant. The differential diagnosis for should include: lympangioma hemangioma varix D. mucocele E. all of the above
A. B. C.
7_ ,Fig. 49-5) The most likely diagnosis
of"'o===-
A. Iympangioma
B. hemangioma 2. (Fig. 49-2) This dome-shaped papule on the ventral surface of the tongue is soft and fluctuant. Although the lesion is painless. the lesion occasionally fluctuates in size. A history of trauma was confinned. The most likely diagnosis for this lesion is a(n): A. fibroma B. lymphoepithelial cyst C. mucous retention phenomenon D. accessory salivary gland tumor E. bulla of pemphigoid
3. 'Fig. 49-31 A 34-year-old man who is a member of the wind section of the symphony arrives at the dental clinic for evaluation of a sore lump on his palate. He states that he was unaware of the swelling until 4 days ago, when the reed of his clarinet contacted the lesion. Palpation reveals the mass to be very finn. This patient most likely has a(n): A. B. C. D. E.
periapical abscess incisive canal cySt necrotizing sialometaplasia adenocarcinoma of the palate traumatic ulcer of the palatal torus
4. 'Fig. 49-41 A healthy 9-year-old male appears at the dental clinic with this soft tissue mass. It has been present for 3 weeks. but has progressively increased in size. The patient claims that moderate bleeding occurs every time he brushes. so he has avoided brushing that area for the last several days. All the adjacent teeth are asymptomatic and test vital. Periapical radiographs of the area reveal no abnormalities. This lesion shows features of malignancy. A. troe
B. false
C.
vanx
D. mucocele
8. (Fig. 49-6) A 45-year-old woman appe3Ba clinic with this pink: smooth-surfaced papuk_ II
diameter and is linn and nonfluccam. 11le ... ~~':.::.~"~~: present for several years and has slowl) IflCleasot The lesion is most likely a(n): irritation fibroma peripheral odontogenic fibroma C. parulis D. pyogenic granuloma E. lipoma A. B.
9. (Fig. 49-7) This asymptomalic speclkd ~ _ . . , . patch of the tongue was found in an el~ admitted to heavy alcohol and tobacco au.e n ••"",. was aware of the lesion's presence but \10m :~::~ the duration. The lesion was finn 10 palpanca likely diagnosis of this lesion is: A. B. C. D. E.
an accessory salivary gland tumor traumatic erythema candidiasis squamous cell carcinoma lichen planus
10. (Fig. 49·81 This asymptomalic le~.~:.:~~:: ered in a 45-year-old woman who has had jo removed from her trunk over the last se\ tenn that best describes this lesion is: A. B. C. D.
macule papule plaque patch
5. (Fig. 49-4) The most likely diagnosis for the lesion described in question 4 is:
11. (Fig. 49...a) The most likely diagnosn
A. B. C. D. E.
A. melanoplakia B. melanotic macule C. blue nevus D. intramucosal nevus E. malignant melanoma
irritation fibroma peripheral odontogenic fibroma peripheral giant cell granuloma peripheral fibroma with ossification pyogenic granuloma
142
=11I ~-.
Fig. 49-1. COUrtesy Dr Barney Olsen
Fig. 49-2.
Fig. 49-3.
Fig. 49-4.
Fig. 49-5. Courtesy Dr Nancy Manuch
Fig. 49-6. Courtesy Dr CUI1 Lundeen
Fig. 49-7. Courtesy Dr.James COUonE'
Fig. 49-8. Courtesy Dr Mcnear VIti
143
Appendix IV
SELF-ASSESSMENT QUIZ 12. IFig. 50-11 A 66-year-old man presents 10 the dental clinic complaining of pain associated with Ihese lesions on his tongue. He states that the lesions cropped up overnight and the discomfort he is experiencing is limiting his abiliIy to swallow. Although the patient has had a history of intraoral ulcerations. he says thai he has neyer before had one in this location. The most likely diagnosis for this condition i~: A. B. C. D. E.
recurrent herpes simplex aphthous stomatitis traumatic ulceration herpangina pemphigoid
13. (Fig. 50-2) This ulcer appeared 8 days ago in a 31year-old homosexual man following a yacation in the Carribean. He claims that the lesion began as a vesicle. but enlarged oyer the last seyeral days. and is now quile painful. The regional lymph nodes on that side are tender 10 palpation. This lesion is most likely a: A. B. C. D. E.
traumatic ulcer recurrent aphlhous ulcer re<:urrent herpetic ulcer syphilitic ulcer granulomatous ulcer
14. (Fig. 50-31 Two months 3fter you treated the patient in Figure. 50-2 he returns to the dental clinic for an operatiye appointment. Your examination reveals scauered white plaques on the lateral border of the tongue and persistent anterior and posterior cervical lymphadenopathy. A low grade fever is also concurrent. This patient demonstrales clinical features most consistent with: A. B. C. D. E.
lichen planus lupus erythematosus infectious mononucleosis syphilis HIV infection
15. {Fig.50-3) The condition affecting Ihis patient's tongue is most likely: A. B. C. D. E.
coated tongue hairy tongue hairy leukoplakia leukoplakia erythroleukoplakia
16. {Fig. 5041 A 34-year-old H1V-posilive man appears at the dental clinic complaining of a burning tongue. Clinical examination reveals an isolated area on the dorsal surface of the tongue that is red and denuded. Bacterial and fungal cultures are obtained. Forty-eight hours later the fun-
144
gal cultures are reponed to be negathe: lite ~::::~~ tures are positive for gastrointestinal flora. Tbe causali\'e organism is: A. Escherichia coli B. Strepw("(x'cus mlllans
C. S,reprococclis I'iridans D. Actinomyces I'iscnms E. Treponema pallidum
\\.oman~~p<~....-~~~~
17. fFig. 50-51 This 28-year-old dental clinic with the chief complailll of a tion in my mouth and throat:' She has no plaint of dryness. Review of her medical hi~ recent upper respiratory infection which ",as ~ l4-day course of amoxicillin. Imraorally one fi ::~~ red patches on buccal mucosa. soft palate. ar:d pharyngeal wall that are tender to palpation. ThM~ is most likely: A. B. C. D. E.
lichen planus pemphigoid pemphigus acute atrophic candidiasis chronic atrophic candidiasis
18. (Fig. 50-61 These linear white plaques \\oCR ered in a 50-year-old woman during a routine ~ ination. The patient claims she has been under stress lately because of family problems. The ~-::~ asymptomatic and do not rub off. The most Iil..t. sis is: A. B. C. D. E.
lupus erythematosus lichen planus candidiasis frictional keratosis none of the above
19.IFig. 50-11 A 45-year-old black woman appe:r dental clinic with a swelling of the palate thai has ly enlarging over the past severnl months. 1lle Iesit'. less but finn to palpation. The condition is most A. B. C. D. E.
periodontal abscess palatal abscess palatal torus pleomorphic adenoma malignant accessory salivary gland tUrTl(W
20. fFig. 50-81 This 53-year-old woman camedenial clinic because of burning, painful gingi\a. . sional biopsy was performed, and during the initial _ _m: Ihe gingiva began to slough. The biopsy report i'-:~: thai the epithelium was separating from the lamma below the basal cell layer. The most likely diagnosu A. B. C. D. E.
pemphigus pemphigoid lichen planus lupus erythematosus erythema multifonne
Fig. SO-I.
Fig. S0-2. Courtesy Dr
Fig. S0-3. COUrtesy Dr WilCheaI VII
Fig. SG-4. Courtesy Dr Sol SIlverman
Fig. SO-So
Fig. SG-6.
Fig. SO-7.
Fig. 50-8. Courtesy Dr Nancy M
\1Ic:heal Vitt
145
Appendix V
GLOSSARY -\bdomen: That pan of the body lying between the thorax (chest) and pelvis.
Anomal.v: Deviation from normal. Anorexia: A lack or loss of appetite for food.
-\cute: Having severe symptoms and a short course. Anterior: Located toward the front (opposite of posferior). -\drenal gland: A small endocrine gland located near the kidney that secretes endogenous glucocorticosteroids. \\ihich conlrol digestive metabolism; mineralocorticoids. lo'h.ich connol sodium and potassium balance: sex hormones: and catecholamines (epinephrine and norepinephrine). which aller bloext pressure and hean function.
Antibiotic: A chemical compound that inhibits the growth or replication of certain forms of life. especially pathogenic organisms such as bacteria or fungi. Antibiotics are classified as either bioslatic or biocidal.
.\drenalectomy: Surgical removal of the adrenal gland.
Antibiotic sensilivily: Testing a suspected organism to see if if is sensitive to destruction by one or more specific antibiOlics.
.\Junctional: Not functioning or working. "genesis: Complete absence of a structure or pan of a structure due to an absence of the tissue of origin in me embryo.
.\IDS: Acronym for Acquired Immune Deficiency Syndrome. reserved for patients infected with HJV (Human Immunodeficiency Virus). It also refers to the tenninal stage of the disease. .\..Ilergen: A substance capable of inducing hypersensitivity or an allergic reaction. .\malgam: An alloy used to restore teeth. composed mainly of silver and mercury.
Antibody: A protein produced in the body in response to stimulation by an antigen. Antibodies react specifically 10 anligens in an auempt to neutr.dize these foreign substances. Antigen: A substance, usually a protein. that is recognized as foreign by the body's immune system and stimulates formation of a specific antibody to the antigen. Antipyretic: A drug or substance used for the relief of fever. Aplasia: Absence of an organ or organ part due to failure of development of Ihe embryonic tissue of origin. Arthralgia: Pain in one or more joints.
-\melogenesis: The formation of the enamel portion of the toom. .\mputation: Strictly. this term refers to the removal of a limb such as an ann or of an appendage such as a finger. With reference to a neuroma, however, amputation means a tumor of nerve tissue due to the severing of a nerve. -Ulalgesic: A drug or substance used for the relief of pain. .\.nalogous: Having similar properties. "naplastic: Pertaining to adult cells that have changed irreversibly toward more primitive cell types. Such changes ure often malignant. .\.nergy: A total loss of reactivity to specific antigens.
Aspiration: 1lle withdrawal of fluid, usually into a syringe. Asymptomatic: A lack of symptoms or complaints by the patient. Atherosclerosis: A condition consisting of degeneration and hardening of the walls of arteries due to fat deposition. Atopy: Hypersensitivity or allergy due to hereditary influences. Atrophic: A normally developed tissue that has decreased in size. Atypical: Pertaining to a deviation from the normal or typical state.
"ngioma: A tumor made up of blood or lymph vessels. .\.nodontia: Congenital condition in which all the teeth fail to develop.
Autoinoculation: To inoculate with a pathogen such as a virus from one's own body. An example would be to spread herpes from your own mouth or lips to your finger. 149
Appendix V
GLOSSARY Autosomal dominant: The uppearun<.:e in offspring of one of two mUlually antagonistic fealures in association with one of the 22 pairs of chromosomes in humans Ihat is not concerned with sexual determination. Bacterial plaque: A collection of bacteria. growing in a deposit of material on the surface of a tooth. that is capable of causing disease. Bilateral: On bOlh sides of Ihe body. Biopsy: Excision of living tissue for the purpose of examination by a pathologist.
Cirrhosis: A chronic disease of the liver charactimJElo< degenerative changes in the liver cells. the de""'....,. connective lissue. and other changes. The resuh the liver cells .'Stop functioning and Ihe flov. of through the liver decreases. There are man) ""_.,,, cirrhosis. including infection. toxic subst~ chronic alcohol abuse. Cla\'icle: The collar bone. connecting the shoulder (scapula) to the chest bone (sternum). Coagulation: The process of cloning. usuall) of Cloning is the natural means by which a patiea bleeding when a vessel has been severed.
Bosselated: Covered with bosses or bumps. Bruxism: A habit related to stress or a sleep disorder. characterized by grinding one's leelh. Bulimia: An ealing disorder characterized by frequent periods of excessive food consumption followed by the purging of the ingested food by vomiting and/or the use of laxatives. Bulla: A circumscribed, fluid..-containing, elevated lesion of the skin more than I crn in diameter. Carcinogen: An agent thai induces cancer. Carcinoma: A malignant growth made up of epithelial cells that are capable of infillration and metastasis. Carcinoma is a specific form of cancer.
Collagen: A protein present in the connective 1Issar: body. Coloboma: A developmental defect Ihal may affen ous pans of the eye, characterized by a mlssJn~ I*'" the structure affected. For example. a coloboma lower eyelid means a missing pan of the lower~..... Commissure: The junction of the upper and lo\o\tt the comer of the mouth.
_.,.or.
Complement: A series of enzymatic proteins in serum that. in the presence of a specific sensitiza. destroy bacteria and other cells. CI through C9 aK' nine components of complement that combme antigen-antibody complex to produce lysis. Concretion: A hardened mass such as calculus.
Cellulitis: A spreading. diffuse. edematous, and sometimes suppuT1uive (pus-producing) inflammation in cellular tissues. Cervical lymphadenopathy: Abnormally large lymph nodes in the neck, often caused by lymphocyte replication in response to a disease state. Chemotaxis: Taxis or movement in response to chemical stimulation. Chemotherapy: Treatment by chemical substances Ihal have a specific effect on the microorganisms causing the disease. This term is usually reserved for the treatment of cancer wilh the use of drugs, thai inhibit rapidly reproducing cells. Side effects are possible. Chronic: Persisting over a long time: when applied to a disease, chronic means that there has been little change or extremely slow progression over a long period.
150
Concurrent: One or more conditions. events, or fi_"'~ occurring at the same time. Congenital: Present at. or existing from the time of Constitutional symptoms: Symptoms affecling die body, such as fever, malaise, anorexia. nausea.. lethargy. Cornified: A process whereby a tissue has beuxue or has thickened its outer coating. Culture: The propagation of an organism in a ......... conducive to growth. Cyst: A pathologic epithelium-lined cavity. us taining fluid or semisolid material. Cytologic: Pertaining 10 the scientific study of celh..
C~lOpathic:
Pertaining 10 or chamclerized by palhologic changes in cells.
mesoderm and Ihe innermost layer is the endodenn. EClOdennal structureil include the skin, hair, nails, oral mucous membrane, and the enamel of the teeth.
Debilitation: The process of becoming weakened. Dt'Ciduous tooth: The primary denlition. or baby leeth. The normal number is 20.
EClopic: Located in an abnonnal place. The ectopic tissue or slruclure mayor may nm be nonnal. Edema: Abnormal amounts of fluid in the intercellular spaces. resulting in visible swelling.
Deglutition: The process of taking a substance through the mouth and throat into the esophagus. Deglutition is a stage of swallowing.
Emanate: To gi"e off or flow away from.
Dehydration: The removal of water from a substance. Prolonged fever and diarrhea cau~e dehydrotion.
EmbrJonic: Pertaining to the earliest stage of development of an organism.
Dtntallamina: 'The embryonk: tissue of origin of the teeth.
Encephalitis: Inflanunation of the brain.
Oe\'elopmenlal: Pertaining to growth to full sir'c or maturity.
Endocrinopathy: A disease or abnormal stale of an endocrine gland.
Diascopy: The examination of tissue under pressure through a transparenl medium. For example suspected ,ascular lesions are examined by pressing a glass slide over an abnormality to see if the reddish tissue turns white. Since blood flows through vascular lesions. pressure causes them to tum white. thus helping to confirm the diagnosis. Distal: Farlhest from a point of reference. In dentistry, distal describes the surface farthest from the midline of lhe patient.
Endodermal: Pertaining to the innermost of the three primitive genn layers of an embryo. Endodennal structures include the epithelium of the pharynx. respiratory tract (except the nose), and the digestive tract. Epistaxis: Bleeding from the nose. Epilhelium: The cellular makeup of skin and mucous membranes. Epulis: A nodular of lUmerous enlargement of the gingiva.
Dorsal: Directed toward or siluated on the back surface (opposite of venlml). Dysplasia: An abnormality of developmenl characlerized by the loss of normal cellular architecture. Dysplastic: Penaining to an abnormality of development. This term is often used 10 describe the appearance of abnormal. premalignant cells under the microscope. The cells begin to lose their normal maturation pattern. and have abnormally shaped, hyperchromatic nuclei. O~'spnea:
Erosion: The wearing away of teeth through Ihe aClion of chemical substances, or a denudation of epithelium above the basal cell layer. Eruption: An emergence from beneath a surface. For teelh. eruption means Iheir growlh imo Ihe oral cavity: it may also refer 10 the development of skin lesions. Er)'themalous: Characterized by a redness of the tissue due to engorgement of the capillaries in the region. El),thematous lesions blanch on diascopy.
Labored or difficult breathing.
Ecchymoses: Large reddish-blue areas caused by the escape of blood into Ihe tissues, commonly referred to as a bruise. Ecchymoses do not blanch on diascopy. Ecosystem: The interaction of living organisms and nonliving elements in a defined area. Ectodermal: Pertaining to the outennost of the three primitive genn layers of an embryo. The middle layer is the
Erythroplastic: Characterized by a reddish appearance. This tenn implies abnormal tissue proliferation in the reddish area. Eschar: A slough of epithelium oflen caused by disease. trauma. or chemical bum. Esthetic: Penaining 10 the appearance of oral or dental structures or the pleasing effect of dental restorations or procedures. 151
•
Appendix V
GLOSSARY Etiolog)': The cause or causes of a disease. or the study lhereof. E"erted: Folded or turned outward. Exacerbation: An increase in severity.
Frenum: A fold of mucous membr:me that I movement of an organ or organ pan. For e\ lingual frenum limits longue movement. and the frenuli limit lip movements.
Exanlhematic: Characterized by the development of an eruption or rash.
Frontal bone: This bone fonns the pan of the sisting mainly of thc forehead. The frontal bone sponds to the fronl pan of the skull and conwn.. _ space called lhe frontal sinus.
Excisionul biopsy: To completely remove a mass of tissue for the purpose of scientific analysis.
Furcal: Pertaining to or associated with lhe pan of a rooted tooth where the roolS join the crown.
Exophytic: An outwardly growing lesion.
Ganglion: A collection of cell bodies of neurons ou...~ the central nervous system. A ganglion is esse terminal through which many peripheral cireui neet with !he central nervous syStem.
Extensor surface: Since the anns and legs can be extended or tensed by the appropriate extensor or tensor muscles, the anlerior surface is referred to as the extensor surface and the posterior surface is referred to as the tensor surface. Extirpate: To completely remove or eradicale. Extremity: A limb of the body. for example an ann or leg. Exudate: Material that has escaped from blood vessels into tissue or onto the surface of a tissue, usually because of inflammation.
Gastroenterologist: A medical specialist whose fi disorders of the stomach and intcstine, Gastrointestinal: Penaining to the stomach and in Genetic counselling: A form of patient counsell "'which the transmission of inherited traits is disc Gingivectomy: Surgical removal of gingival tissue.
Fascial plane: Spaces between adjacenl bundles of fascia thaI cover muscles. Infection often spreads along these planes.
Glaucoma: A disease of the eye charaCteriZN increased intraocular pressure. This condition is asymplomatic and, if not recognized or treated. blindness.
Fenestration: A perforation or opening in a tissue.
Glossal: Pertaining 10 or associated with the lOngue.
Fetor oris: An unpleasant or abnormal odor emanating from !he oral cavity.
Glucose: A form of sugar that is the most imponant hydrate in the body's metabolism.
Field Cancerization: Malignant growths occurring in mulliple sites of the oral cavity. Oflen the oral tissues have been exposed to a carcinogen for a long time.
Glucosuria: The presence of an abnonnal quantit> 0( case in the urine. A sign of diabetes mellitus.
Factitial: Self-induced. as in factitial injury.
Fissure: A narrow slit or clef!. Fluctuant: Strictly. this tenn describes a palpated, wavelike motion that is felt in a fluid-containing lesion. In this text, lhe teon is frequently used to describe a soft. readily yielding mass on palpation.
Granulomatous: Penaining to a well-defined area th:a developed as a reaction to the presence of living orp isms or a foreign body. The tissue consists primaru, histiocytes. Gravid: Pregnllnt. Halitosis: An unpleasant odor of the brellth or expired __
Fontanelle: One of several soft spots on the skull of infants and children where the bones of the skull have not yet completely united. In these areas the brain is covered only by a membrane beneath the skin.
152
Hamartoma: A tumor-like nodule consisting of a ml of normal tissue usually present in an organ but ell in an unusual arrangement and/or an unusual site.
Hapten: An incomplete allergen. When combined with another substance to fonn a molecule. a hapten may stimulate a hypersensitivity or allergic reaction.
Hyperdontia: A condition or circumstance characteri7..ed by one or more extra. or supemumemry teeth. Hyperemia: 1lle presence of excess blood in a tissue area.
Hematopoietic: Penaining to the production of blood or of lts constituent elements. Hematopoiesis is the main funclion of the bone marrow. Hematoma: A large ecchymosis or bruise caused by the escape of blood into the tissues. Hematomas are blue on the skin and red on the mucous membranes. As hematomas resolve they may tum brown. green. or yellow_ Hematuria: The presence of blood in the urine. Hemihypertrophy: The presence of hypertrophy on one side only of a tissue or organ. For e:r;:ample. in facial hemihypertrophy one half of the face is visibly larger than the other. Hemoglobin: The Iron-contammg pigment of the red blood cells. Its function is to carry o:r;:ygen to the tissues. One of the causes of anemia is a deficiency of iron. causing patients to look pale and feel tired. Hemolysis: Generally speaking. this tenn refers (0 the disintegration of elements in the blood. A common fonn of hemolysis occurs during anemia and involves lysis or the dissolution of red blood cells. Hemorrhage: Bleeding: the escape of blood from a severed blood vessel. Hemostasis: The stoppage of blood flow. This can occur naturally by dOlling or anificially by the application of pressure or the placement of sutures. Hereditary: Transmined or transmissible from parent to offspring: detennined genetically. Hiatal hernia: Protrusion of any structure through the hiatus of the diaphragm. Affected patients are prone to indigestion. Histiocyte: A large phagocytic cell from the reticuloendothelial system. The reticuloendothelial system is a network made up of all of the phagocytic cells in the body. which include macrophages, Kupffer cells in the liver. and the microglia of the brain. Histology: The microscopic study of the structure and form of the various tissues making up a living organism.
Hyperglycemia: The presence of excessive sugar or glucose in the bloodstream. Hypermenorrhea: Excessive uterine bleeding of unusually long duration at regular intervals. Hyperorthokeratosis: Keralin is the outermost layer of epithelium as seen under the microscope and is seen in TWO forms: onhokeratin and parakeratin. Orthokeratin has no visible nuclei wilhin the outer layer. whereas in parakeratin nuclei are present. HyperoTlhokeratosis is the presence of excess onhokeratin. Hyperplasia: An increase in the size of a tissue or organ due to an increase in the /lumber of constituent cells. Hypersensitivity: Generally this term means an abnonnal sensitivity to a stimulus of any kind. The term. ho\\ever. is often used with specific reference to some form of allergic response. Hypertension: High blood pressure. Hypertrophy: An increase in the s;:e of a tissue or organ due to an increase in the size of constituent cells. Hypocalcifteation: Less than normal amount of calcificalioo. Hypodontia: The congenital absence of one or several teeth as a result of agenesis. Hypoplasia: Incomplete development of a tissue or organ: a tissue reduced in size because of a decreased number of constituent cells. Hypopyon: Pus in the anterior chamber of the eye. Hypotension: Low blood pressure. Ileum: The distal or tenninal portion of the small intestine. ending at the cecum. which is a blind pouch fonning the proximal or firsl pan of Ihe large intestine. Ilium: The lateral or flaring part of the pelvic bone, otherwise known as the hip. Incisional biopsy: The removal of a portion of suspected abnormal tissue for microscopic study.
153
Appendix V
GLOSSARY Incisive papilla: A slightly ele\'ated papule of nonnaltissue on the palate in the midline immediately posterior to the central incisors. lmmedi
Lamina propria: The layer of conneclive tissue- _ _'" ately beneath the epithelium of the oral mucosa. Laryngeal: Pertaining 10 the larynx. which is a pan: 01 airway. It is located between the pharynx at the ""'..... the oral cavity and the trachea at the beginnlOl lungs. The larynx contains the vocal cords. ~hida audible sounds. Lateral: Pertaining to or situated at the side.
Infant: A human baby from binh to two years of age. Infarct: A localized area of ischemic necrosis resulting from a blockage of the anerial supply or the \'cnous drainage of tissue. Ischemic necrosis is dead tissue resulting from an inad~ equ
154
Leptomeninges: The two more delicate componenb meninges. the pia mater and the arachnoid. Lesion: A site of slructural or functional change ill tissues that is produced by disease or injury. Leukoplakia: A white patch thai cannOI be rubbed , , - that does not clinically represent any olher condu-. Lipid: Fat or fany: a naturally occurring subsrantt up of fatty acids. Lobulated: Made up of lobules. which are smaller sions of lobes. Many structures are divided IIlto and lobules. such as the brain. lung. and sali\ at) p-*Some pathologic lesions are described as Job...... when the lesion is divided into smaller pans. Lymphadenitis: Innammation of lymph nodes g:
A variety of leukocyte or white blood that is important to Ihe immune reponse and that in lhe lymph nodes. Lymphocytes can be large or and are round. nongranular. and classified as eilher TB-lymphocytes.
Macrocheilia: Abnormally large lips. Macrodontia: Teeth that are considerably larger than I10mIIl Macule: A spot or stain on the skin or mucous ~ that is neither raised nor depressed. Some exampks macules include cafe au lait spots. hyperemia. ery~ petechiae. ecchymoses. purpura. oral melanotic ~ and many others illustrated in !his atlas.
\lalaise: A conslitutional symptom thai describes a feeling of uneasiness. discomfort. or indisposition. \Ialignant: A neoplastic growth that is OOt usually encapsulaled. grows rapidly. and can readily metastasize. \laSlication: Chewing.
M)'elogenous leukemia: Leukemia is cancer of the white blood cells: in this instance the predominating leukocytes. or while blood cells. are myeloid or granular (polymorphonuclear leukocytes). Nasophar)'ngitis: Inflammation of the nasopharynx which is the back of Ihe nasal complex and upper throat. Sore throat. posl-nasal drip. and fever are common signs.
\ledial: Sirualed toward the midline (opposite of lateral). \Ielena: Darkened or black feces that are due to the presence of blood pigments: a sign of intestinal bleeding. :\Ieningitis: Inflamm3lion of the meninges. which are Ihe three membranes covering the brain and spinal cord (Ihe dura mater. arachnoid. and pia maier). Meningitis pro· duces both mOlar and mental signs such as difficulty in walking and confusion.
Neocapillary: New growth of capillaries. which are the smallest blood vessels and connect small arterioles to small venules. Necrosis: The death of a cell as a resull of injury or dis-
me. Neoplasia: Characlerized by the presence of new and unconlrolJed cellular growth.
\lesenchymal: The meshwork of embryonic cOllnective lis· sue in the mesoderm that gives rise 10 the connective tissue of the body. blood vessels. and lymph vessels.
Neoplasm: A mass of newly formed tissue: a tumor.
\lesial: Toward the front. anterior. or midline. The mesial surface of teeth is the side of the tooth closest to the midline. The five surfaces of teeth are mesial. distal. occlusal or incisal. labial or facial. and lingual or palatal.
Neuropathy: Any abnOnllality of nerve tissue.
\Ielastasize: To spread or travel from one pan of the body to anOlher: a tenn usually reserved to descri~ the pread of malignant tumors. \licrodontia: Teeth Ihat are considerably smaller than normal. \tineralized: Characteri7..ed by the deposition of mineral. often calcium and other organic salts in a tissue. The term "calcified" is used when the mineral content is known 10 be calcium. whereas the term "minemlized" is more general and does not specify the exact nature of the mineral. \Ionoc)'tic leukemia: Leukemia is cancer of the white blood cells: in this instance the predominating leukoc)·tes. or white blood cells. are monocytes. \Iorpholog)': Descriptive of shape. form. or structure. or lhe science thereof.
Neurogenic: Originaling in or from nerve tissue.
Neutrophil: A medium-sized white blood cell with a nucleus consisting of three 10 five lobes and a cytoplasm containing small granules: one of a group of white blood cells called granulocytes. the others being eosinophils and basophils. Neutrophils make up about 65% of the while blood cells in normal blood. Also known as polymorphOlluciear leukoC)1e. PMN.or"poly." Neutrophil chemotaxis: Taxis or movement of neulTophils in response to chemical substances or agents. Ne\'us: A small tumor of the skin containing aggregations or theques of nevus cells: a mole. It may be flat or elevated, pigmented or non-pigmented. and mayor may not contain hair. Nodule: A circumscribed. usually solid lesion having the dimension of depth. Nodules are less Ihan I em in diameter. Noncaseating: A lissue-degeneralive process that forms a dry. shapeless mass resembling cheese. Occipital bone: One of the bones that make up the skull; a thick bone at the back of the head.
\Iucopurulent: Consisting of bOlh mucous and pus. \Iutagenesis: The induction of genetic mutation.
Oligodontia: Presence of fewer than the normal number of teeth.
155
Appendix V
GLOSSARY Oncugenic: C.pable of cau~ing tumor fannation. Opportunistic microorganism: Microorganisms Inat usually aren't pathogenic. but become '>0 under certain circuml>lanccs. such as an environment allcrcd by the aClion of antibioticl> or long term steroid therapy. Opportuni~tic microorganisms C
Organism: Any viable life foml. sucn as animals. plants. and microorganisms. including bacleria. fungi. and ,·iruses. Otorhinolaryngologist: An car. nose. and tnroat specialist. Palliati\'e: Treatment or the relief of symptoms. nOlthe cause of a condition.
Pedunculated: ils base.
A
tissue mass originating b) a
S1
Periapical: Pertaining to or localed at the ape... I of a tOOlh. Perirurcal: Pertaining to or located at the furcum tooth: below the eEJ where the roots fuse togelhtt' Perilabial: Pertaining to the region around or near Ibt Perineum: The lower surface of the trunk: \\'hen a""..." is lying down with legs spread apart. the perineum area from thc base of the spine to the anal region genital area and. finally. to Ihe crest of the mons pI'L Perioral: In the proximity or or around the oral
ca\l~
Pallor: Paleness of the skin or mucous membrane; an absence of a healthy color. This sign often accompanies constitutional symptoms and anemia.
Periorbital: In the pro:;:imity of or around the orbit.... is the bony socket of the eye.
Palpate: To feel with the fingers or hand.
Peripheral: Pertaining to the outer part. such or margin.
I'apule: A small mass. without the dimension of depth. thai is smaller than I cm in diameler. When described as pedunculated. a papule is on a stalk: when described as sessile. a papule is anached at its base and does not have a stalk.
Permanent denlition: Succedaneous (adult) tceth.... follow Ihe primary lecth. Since there are no replanments for the pennanent teeth. they musl last a Ii~ There are 32 pennanent teelh.
Parturition: The delivery of the fetus from the 11100her: to give birth.
Petechiae: Liule red spots. ranging in size from pm to several millimeters in diameter. Petechiae con, extravasated blood.
Patch: Similar to a macule but larger: a large stain or spot. usually neilher raised or depressed. which may be textured.
Physiologic: Refers to nonnal body function (oppos,ltt pathologic).
Palent: The condilion of being open: this ternl is often applied to ducts. vessels. and passages to indicate thai they are not blocked. Pat hognornonic: Uniquely distinctive of a specific disease or condition: usually consists of signs or findings Ihal when present and recognized. enable the diagnosis to be made.
l\.)
tht ec5!"c
Pilocarpine: A drug used to stimulate salivary flo\\, or produce constriction of the pupil of the eye. Plaque: An area with a flat surface and raised edges. Platelet: One of the elements found in circulating blood.. plalelet has a circular or disk-like shape and is s hence Ihe tenn platelet. Platelets aid in blood coa tion and clot retractioo.
Pathologic: Pertaining to or caused by disease. Polydipsia: Excessive thirst. A sign of disease. Pathosis: An abnonnal stale or condition. Pol~'poid:
Parietal bone: One of the bones that makes up the skull: there is one parietal bone on each side of the skull, fonning Ihe skull's tOp and upper sides.
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A polyp-like protruding growlh with a base tha equaJ in diameter to the surface of the mucosal lesion.
Pol}'uria: Excessive amounts of urine. A sign of diseast
Posterior: Directed toward or situated at the back (oppotte of anterior). Primar~
mar)
tooth: Deciduous (baby) tooth; there are 20 priteeth.
Prognathism: A developmental deformily of the mandible that causes it to protrude abnormally. Pruritis: Itching.
Relinopath)': A disease or abnormality of the retina of the eye. The retina cannot be seen without special instruments. and is thai pan of the eye which receives and transmits visual information coming in from the pupil and lens onto the brain via the optic nerve. Renal Failure: Inability of the kidneys to function properly. A patient whose kidneys fail completely will die without renal dialysis or a kidney transplant. One of the causes of kidney failure is prolonged hypertension (high blood pressure).
~udoh~'phae:
Long. filamentous foons that can be seen under the microscope when Cal/dida albicafls. a fungal microorganism. assumes its pathogenic form.
Pulse: A patient's heartbeat. as felt through palpation of a blood vessel.
Punctate: Spotted: characterized by small points or punctures. Purpuric: Pertaining to purpura. which are large bruises consisting of blood extravasated into the tissues. Bruises are bluish-purple in color. hrulent: Containing pus. P1lstule: A well-circumscribed. pus-containing lesion. usu· ally less than I cm in diameter. QuaJitati,'e: Of or pertaining to quality: descriptive information ahoUl what something looks and feels like. Quantitalh'e: Of or pertaining to quantity: descriptive Information ahout how much of something there is or how big something is.
Sarcoma: A malignant growth of cells of embryonic connective tissue origin. This condition is highly capable of infiltration and metastasis. Sarcomatous: Pertaining to sarcoma. which is a malignant tumor of mesenchymal tissue origin. Scar: A mark or cicatrix remaining after the healing of a wound or other morbid process. Sclera: The strong outer tunic of the eye. or whites of the eyes. When the sclera turns blue or yellow. it is a sign of systemic abnormality. Sepsis: A morbid state resulting from the presence of pathogenic microorganisms. usually in the bloodstream. Sepficemia: The presence of pathogenic bacteria in the blood.
Sequestration: Abnormal separation of a pan from the whole. such as when a piece of hone sequestrates from the mandible because of osteomyelitis: the act of isolating a patient. Serpiginous: Chamcterized by a wavy or undulating margin.
Radiation: In dentistry. electromagnetic energy or x-rays transmitted through space. Radiation also means divergence from a common center: one of the properties of xrays is that. like a beam of light. they diverge from their source.
Serum: The watery nuid remaining after coagulation of the blood. If clolled blood is left long enough. the clot shrinks and the fibrinogen is depleted. the remaining fluid is the serum.
Ibdiolherapy: Radiation therapy: the use of radiation from "arious sources to lreal or cure malignant disorders.
Sessile: Auached to a surface on a broad base: does not have a stalk.
RecrudeS4:ence: Recurrence of signs and symptoms of a disease after temporary abatement.
Sign: An objective finding or observation made by the examiner of which the patient may be unaware or does not complain.
dractory:
01 readily responsive to treatment.
Rtmission: Improvement or abatement of the symptoms of a disease: the period during which symptoms abate.
Sinus: An airspace inside the skull. such as the maxillary sinus: an abnonnal channel. fistula. or tract allowing the escape of pus.
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Appendix V
GLOSSARY Supernumerary: In excess of the regular number.
within the heart or blood vessels from conSlllueDb the circulating blood. Patients prone to the formauc. thrombi are placed on anticoagulant therapy.
Splenic: Of or penaining to the spleen. which is tl struclUre in the upper left abdomen juSt behind and under the stom· ach. TIle spleen contains the largest collection of reticuloendothelial cells in the whole body; its functions include blood fonnation, blood storage, and blood fihr.llion.
Tooth bud: The embryonic tissue of origin of tht tooth buds develop from the more primitive tiss~ at dental lamina.
Sponlaneous: Occurring unaided or without apparent cause; voluntary.
Torus: A bony nodule on the hard palate or on the- 11 .:: aspect of the premolars.
Superficial: Located on or near the surface.
Tourniquet test: When pressure is applied to the vessels of the upper ann. using a blood pressure etdf_ .a bleeding tendency is detected when petechiae de" in the region.
Symptom: A manifestation of disease of which the patient is usually aware and frequently complains. S)'ndrome: A combination of signs and symploms occurring commonly enough to constitute a distinct clinical entity.
Transient: TemporMy: of short duration. Translucent: Somewhat penetrable by rays of light.
Taurodont: A malformed multirooted tOOlh characterized by an allered crown-to-root ratio. the crown being of oonnallenglh, the roots being abnonnally shon. and the pulp chamber being abnormally large. Telangiectasia: The formation of capillaries near the surface of a tissue. Telangiectasia may be a sign of hereditary disorder, alcohol abuse, or malignancy in the region. Template bleeding time: The amount of time necessary for bleeding to stop. following a skin incision of consistent length and depth. Texture: Pertains to the characteristics of Ihe surface of an area or lesion. Some descriptions of texture are as follows: smooth, rough. lumpy. and vegetative. The tiny bumps on the surface of a wan cause it to have a vegetative texture. Therapeutic: Of or penaining to therapy or ttealmCnt; beneficial. Therapy has as its goal the elimination or control of a disease or olher abnormal state.
Trauma: A wound or injury; damage produced external force.
b~
_
Trismus: Tonic contraction of the muscles of maslieatM& commonly referred to as lockjaw. Trismus is cau:.ed oral infections. salivary gland infections. tetanus. u..rna and encephalitis. Trunk: The main pan of the body. to which the limbs ~ attached. The trunk consists of the thorax and abdorne-.. and contains all of the internal organs. This term 1 a.b.; used to describe the main part of a nerve or blood \-essd.. Tumor: A solid. raised mass that is larger than I em .. diameter and has the dimension of depth. This teon describes a mass consisting of neopla~tic cells. Ulcer: Loss of surface tissue due to a sloughing of necroo.: inflammatory tissue; the defect extends into the UJ1dcr. lying lamina propria. Unilateral: Affecting only one side of the body.
Thorax: That part of the body between the neck and abdomen. enclosed by the spine. ribs. and sternum. In the vernacular. the thorax is referred to as the chest. The main contents of the thorax are the hean and lungs. Thrombophlebitis: The development of venous th.rombi in the presence of inflammatory changes in the vessel wall. Thrombosis: Formation of thrombi within the lumen of the hean or a blood vessel. A lumen is the space within a passage: a thrombus is a solid mass that can fonn
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Uremia: A toxic condition caused by the accumulation nitrogenous substances in the blood that are no~ eliminated in the urine. Urticaria: A vascular reaction of the skin charactenzed the appearance of slightly elevated patches that art either more red or paler than the surrounding Unicaria is also known as hives. and may be caused • allergy. excitement. or exercise. These patches ~ sometimes intensely itchy.
\asoconstriction: To diminish the diameter or caliber of a blood vessel.
a feeling of dizziness or that one's surroundings are spinning or moving.
'mlral: Directed toward or situated on the belly surface (opposite of dorsal).
Vesicle: A well-defined lesion of the skin and mucous membranes that resembles a sac. contains fluid. and is less than 1 em in diameter.
'ennilion: That part of the lip which has a naturally pinkish red color and is exposed to the extraoral environment. The vennilion contains neither sweat glands nor 3CCessory salivary glands. \~milion
border: The mucocutaneous margin of the lip.
Visceral: Pertaining to body organs. Viscous: Thick or sticky.
\ermilionectomy: Surgical removal of the vennilion border of the lip.
Wheal: A localized area of edema on the skin. Usually the area is raised. smooth-surfaced and is often very itchy.
\e-rtigo: An unpleasant sensation characterized mainly by
Xerostomia: Dry mouth.
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