Comprehensive Review of Pediatric Dentistry Provided by: American Academy of Pediatric Dentistry
Release Date December 1, 2008
1-800-284-8433 • www.cmeinfo.com 639
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
American Academy of Pediatric Dentistry Comprehensive Review of Pediatric Dentistry
Growth & Development / Orthodontics Andrew L. Sonis, D.M.D. Trauma Constance M. Killian, D.M.D. Dental Materials Steven M. Adair, D.D.S., M.S. Pulp Therapy Steven M. Adair, D.D.S., M.S. Oral Pathology / Oral Medicine / Syndromes Andrew L. Sonis, D.M.D. Oral Pathology / Oral Medicine / Syndromes (cont'd) Andrew L. Sonis, D.M.D. Prevention Steven M. Adair, D.D.S., M.S. Special Needs Patients Constance M. Killian, D.M.D. Dental Development Steven M. Adair, D.D.S., M.S. Hospital Dentistry Constance M. Killian, D.M.D. Special Needs Patients (cont'd) Constance M. Killian, D.M.D. Behavior Management Constance M. Killian, D.M.D.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
PREFACE
ɨF$PNQSFIFOTJWF3FWJFXPG1FEJBUSJD%FOUJTUSZDPOUJOVJOHFEVDBUJPODPVSTFJTQSPEVDFEBOETQPOTPSFECZUIF"NFSJDBO"DBEFNZPG 1FEJBUSJD%FOUJTUSZBTBTFSWJDFUPJUTNFNCFSTɨFDPVSTFJTEFTJHOFEUPQSPWJEFBCSPBESFWJFXBOEVQEBUFPGDMJOJDBMUPQJDTBOELOPXMFEHF CBTFBSFBTJOUIFTQFDJBMUZ*OEJWJEVBMTXIPBSFQSFQBSJOHUPDIBMMFOHFUIF2VBMJGZJOH&YBNJOBUJPO UIF0SBM$MJOJDBM&YBNJOBUJPO PSUIF 3FDFSUJmDBUJPO&YBNJOBUJPOPGUIF"NFSJDBO#PBSEPG1FEJBUSJD%FOUJTUSZNBZmOEUIFDPVSTFIFMQGVMɨPTFJOEJWJEVBMT IPXFWFS TIPVME OPUWJFXUIJTDPVSTFBTUIFJSTPMFQSFQBSBUJPOGPSFJUIFSFYBNJOBUJPO CVUTIPVMEVTFPUIFSSFWJFXBOETUVEZNBUFSJBMTɨFDPVSTFQSFTFOUFST EPOPUQSFQBSFRVFTUJPOTGPSUIF#PBSEFYBNJOBUJPOT OPSEPUIFZTFSWFBTFYBNJOFSTGPS"#1% ɨFDPVSTFNBOVBMJTVQEBUFEBOOVBMMZFBDITVNNFSUPSFnFDUOFXTDJFOUJmDMJUFSBUVSFBOEDMJOJDBMQSBDUJDFTɨFGBDVMUZXFMDPNFTBOE FODPVSBHFTGFFECBDLGSPNUIFBUUFOEFFT$PVSTFFWBMVBUJPOTXJMMCFDPOEVDUFEPWFSUIF8FCTIPSUMZBGUFSUIFDPVSTF1MFBTFFOTVSFUIBUUIF ""1%TUBĊSFQSFTFOUBUJWFBUUIFDPVSTFIBTZPVSDPSSFDUFNBJMBEESFTT ɨFGBDVMUZXJTIFTUPBDLOPXMFEHFUIFIFMQPGWFSZUBMFOUFEBOEEFEJDBUFEJOEJWJEVBMTBUUIF""1%)FBERVBSUFST0ċDFGPSUIFJS BTTJTUBODFJOQMBOOJOHUIJTDPVSTF8FUIBOL,SJTUJO0MTPOGPSIFSBENJOJTUSBUJWFTVQQPSUBOEPOTJUFDPPSEJOBUJPO*OBEEJUJPO XFBSF HSBUFGVMUP$JOEZ)BOTFOGPSIFSFYQFSUJTFJOQSFQBSJOHUIJTDPVSTFNBOVBM 4UFWF"EBJS "OEZ4POJT $POOJF,JMMJBO
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Comprehensive Review of Pediatric Dentistry Provided by: American Academy of Pediatric Dentistry
DVD #1
WARNING: The copyright proprietor has licensed the picture contained on this recording for personal use only and prohibits any other use, copying, reproduction, or performance in public, in whole or in part (Title 17 USC Section 501 506). © 2008
4
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
is not responsible in any way for the accuracy, medical and dental or legal content of this recording. You should be aware that substantive developments in the medical and dental fields covered by this recording may have occurred since the date of original release. Date of Original Release: December 1, 2008
This educational activity is a DVD format. The activity provides a comprehensive review of pediatric dentistry and is organized to assist American Academy of Pediatric Dentistry (AAPD) members in their preparation for the American Board of Pediatric Dentistry (ABPD) examinations. It is estimated that it should take the average learner 22 hours, including completion of the post-test and evaluation form, to complete this activity.
5
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
The American Academy of Pediatric Dentistry is recognized (May 2007 – June 2010) by the ADA Continuing Education Recognition Program (ADA CERP) to provide continuing education opportunities for dentists. Continuing education credit awarded for this activity may not apply toward license renewal in all states or meet
the requirements of other governing bodies. It is the responsibility of each practitioner or resident to verify the requirements of his or her state or governmental licensing board.
6
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
DESIGNATION The American Academy of Pediatric Dentistry designates this educational activity for a maximum of 22 hours of continuing education credits.
OBJECTIVES After viewing this program, the participant should have a better understanding of the following:
1. The major clinical and knowledge base areas of pediatric dentistry. 2. Select clinical cases. 3. The American Board of Pediatric Dentistry testing process.
7
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f,_D3",0,)%5'A#"'2"%*#)%34' W##%&';#-,0,)% ! S)%,"-,)3)U'I3#(4%3-,'5#A%'%355D, " @,"3#*#)%(.'.3U(0,)%
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82
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
RAA,4%'#A'%&,'.3U&%'A#"4,'#)'%&,'@+7 !
Light, continuous forces " Osteoclasts
formed " Removing lamina dura " Tooth movement begins " This process is called “FRONTAL RESORPTION”
Frontal resorption occurs on the osseous margin adjacent to the PDL
83
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
73U&%'A#"4,'.,(*3)U'%#'A"#)%(.' ",5#"/%3#)
Tooth movement (mm)
! Phase 1 – Mechanical compression and tension of the periodontium ! Phase 2 --- Mechanically induced cellular and genetic responses; no tooth movement ! Phase 3 --- Accelerated tooth movement due to frontal bone resorption
Phase 3 Phase 2 Phase 1
FYN
NGYQG
Days
RAA,4%5'#A'&,(-<'A#"4,'#)'%&,' @+7 !Heavy, continuous forces "Blood supply to PDL occluded "Aseptic necrosis "PDL becomes “hyalinized” – “HYALINIZATION” "This process is called “UNDERMINING RESORPTION”.
84
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Undermining resorption results loss of vitality of localized areas of PDL resulting in removal of alveolar bone in area of pressure
>,(-<'A#"4,'.,(*3)U'%#'D)*,"03)3)U'",5#"/%3#)
Tooth movement (mm)
! Phase 1 – Mechanical compression and tension of the periodontium ! Phase 2 --- Continuing mechanical compression; little cellular and genetic responses; no tooth movement ! Phase 3 --- Cells recruited from the undermining side of lamina dura, not within the PDL, to induce undermining bone resorption
Phase 1
85
Phase 2
Phase 3
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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86
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Direction of Force Application !
!
Center of Rotation --- The point around which rotation occurs when an object is being moved. Center of Resistance --- A point on the tooth around which the tooth shall move. For most teeth, COR is 2/5 way between the apex and the crest of the alveolar bone.
Center of resistance
in space
in oral cavity
87
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Center of Rotation
CR
Force on the crown
CR
^
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Force
^
A force (F) is a load applied to an object that tends to move the object.
^
+3",4%3#) ()*'+,U",, #A'' ^#"4,
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89
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
+3",4%3#)'()*'+,U",, #A'%&,' A#"4, ?#*3.<'0#-,0,)% 100gm needed to produce bodily movement, which is double the force needed to produce a tipping movement
Orthodontic Forces and Tooth Movement !
Optimal force levels "
“High enough to stimulate cellular activity without completely occluding blood vessels in the PDL” (Proffit et al. 2000).
90
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Degree of Force Summary
! ! !
!
In the range of 10 to 200 grams. Varies with the type of tooth movement. Light, continuous forces are currently considered to be most effective in inducing tooth movement. Heavy forces cause damage and may fail to move the teeth.
Distribution Nb'U Nb'U Nb'U Nb'U
^'L'FGG'U
91
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Distribution Nb'U Nb'U bG'U
^'L'FGG'U
Duration Force
Intermittent
Time
92
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Duration Force
Continuous and decreasing
Time
Duration Force
Continuous and Constant
Time
93
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
+D"(%3#) • Key to producing tooth movement: •application of sustained force •force must be present for a considerable percentage of time to stimulate cell differentiation .
+D"(%3#) $Relationship of duration to tooth movement $t duration- t tooth movement
94
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Slide 183 als1
photos of dental open bite and skeletal oopen bite asonis, 5/25/2008
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Slide 197 als2
missing laterals bilateral versus unilateral consideration of peg lateral
asonis, 5/25/2008
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198
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Constance M. Killian, D.M.D.
3
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Prevention of Trauma Who is at high risk for trauma?
Prevention of Trauma Trauma is a part of Anticipatory Guidance
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Prevention of Trauma Custom mouthguards
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Injury Assessment
General Considerations 1. “Primum non nocere”
Do no harm 2. Never treat a stranger
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Injury Assessment
General Considerations Be prepared… • • • • • •
Be calm & reassuring Address behavior Communicate Know the Guidelines Have supplies ready Standardized trauma form
Diagnostic Evaluation • Medical condition of patient • • • • • • •
General health Cardiac conditions Bleeding disorders Allergies Medications Chronic conditions Name of physician
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Diagnostic Evaluation
History of Current Injury • • • • • •
Identify adult bringing the child What When Where How Any treatment done elsewhere for this injury
Diagnostic Evaluation
Emergency Assessment • Dental trauma is a subset of head
trauma • Assess awareness/orientation • Assure a patent airway • Observe for rhinorrhea or otorrhea
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Diagnostic Evaluation
Emergency Assessment • Bruising behind ear -
“Battle’s sign” • Abnormal vital signs
Diagnostic Evaluation
Emergency Assessment Rapid Neurologic Exam: Cranial Nerves III – Oculomotor • Penlight • PERRLA • Abnormalities
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Diagnostic Evaluation
Emergency Assessment Rapid Neurologic Exam: Cranial Nerves III, IV, VI: Oculomotor, Trochlear, and Abducens • •
Track movements Extraocular movements intact
Diagnostic Evaluation
Emergency Assessment Rapid Neurologic Exam: Cranial Nerves VII: Facial Ask patient to close eyes, smile, frown • No asymmetry of movement •
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Diagnostic Evaluation
Emergency Assessment • Glasgow Coma Scale – see
Appendix • • • •
Eyes Best Motor Response Best Verbal Response Maximum score 15, minimum 3
Glasgow Coma Scale Finding A. Eyes
Rating
Open spontaneously Open to verbal command Open to pain No response B. Best Motor Response Obeys verbal command Realizes pain Withdraws from pain Flexion to pain (decorticate) Extension to pain (decerebrate) No response C. Best Verbal Response Oriented and converses Confused Inappropriate words Incomprehensible sounds No response Minimal score = 3 Maximum score = 15
4 3 2 1
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6 5 4 3 2 1 5 4 3 2 1
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Diagnostic Evaluation
Intra Cranial Injury Symptoms from clinical history • Post-traumatic seizure • Severe headache • Loss of consciousness • Vomiting • Nausea • Clinical evidence of skull fracture
Diagnostic Evaluation What else should make you think ICI? • Persistent drowsiness • Amnesia • Focal neurological signs – “seeing stars”
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Diagnostic Evaluation What overrides the dental injury? • Cervical spine injury – rare in children • Intracranial injury • Neurological injury • Bleeding that cannot be controlled
If no evidence of head trauma, proceed with dental treatment
Diagnostic Evaluation After dental treatment, follow through…. Give post-op instructions for observation • • • •
Patient is persistently sleepy Vomiting Severe headache Abnormal behavior
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Evaluation and Treatment of Orofacial Trauma
Facial Bones Extraoral: Hard Tissue - Facial bones Classification of fractures Simple Compound Comminuted Favorable Unfavorable
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Evaluation and Treatment of Orofacial Trauma
Craniofacial Trauma Causes Falls – 64% Traffic – 22% Sports – 9% Violence – 5%
Distribution Skull vault – 54% Upper/middle facial third – 37%
Concommitant injuries – 33%
Evaluation and Treatment of Orofacial Trauma
Facial Bones Forces of facial fractures High impact – requires more than 50G Low impact – requires less than 50G What facial bones are most likely to fracture?
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Evaluation and Treatment of Orofacial Trauma
Facial Bones Midface fractures • Rare in children • Skull fractures more common • Causes • Treatment – nonsurgical best
Evaluation and Treatment of Orofacial Trauma
Facial Bones Nasal Fracture: most common midface fracture in children Signs • • • • •
Ecchymosis Laceration Swelling Epistaxis Bony irregularities
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Evaluation and Treatment of Orofacial Trauma
Facial Bones Signs of Zygomatic Fracture • • • • • •
Periorbital swelling Ecchymosis and hematoma Conjunctival hemorrhage Palpable step deformity Paresthesia Limited upward gaze
Frontal view
Submentovertex view
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Evaluation and Treatment of Orofacial Trauma
Facial Bones • LeFort Fractures • • • •
Least common midface fracture in children Many fractures are combinations LeFort I treatment – no fixation Caution in fixation for LeFort II and III
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Evaluation and Treatment of Orofacial Trauma
Facial Bones Diagnostic Aids • Computerized Tomography (CT) • Radiographs • AP and Lateral skull • Waters • Submental vertex
Management - OMS
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Evaluation and Treatment of Orofacial Trauma
Mandible Mandibular Fracture is the most common facial skeletal injury in hospitalized pediatric trauma patients • Boys affected twice as often as girls • Younger patients: condylar/subcondylar
fractures • Adolescents: fracture of angle of mandible • Causes: bicycles, steps, swings
Evaluation and Treatment of Orofacial Trauma
Management of Mandibular Fracture Management – OMS • Timing: can defer 24-36 hrs • Stabilize mandible if deferring treatment
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Evaluation and Treatment of Orofacial Trauma
Mandibular Fracture Diagnosis: Subcondylar/Condylar fracture • Blunt injury to chin • Bite is “off” or deviated • Unilateral vs. Bilateral • Palpate external auditory meatus
Evaluation and Treatment of Orofacial Trauma
Clinical Exam for Possible Subcondylar Fracture
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Evaluation and Treatment of Orofacial Trauma
Management of Mandibular Fracture Condylar fractures carry the greatest risk of growth disturbance
• Goals of treatment
• Preserve function • Maintain ramus height
•
Treatment is usually nonsurgical
•
Complications
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Evaluation and Treatment of Orofacial Trauma
Management of Mandibular Fracture Intracapsular fracture of condyle •
•
Ankylosis risk in children less than 3 yrs. Treatment: mandibular exercises and jaw stretching
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Evaluation and Treatment of Orofacial Trauma
Management of Mandibular Fracture Fracture of body of mandible Signs/Symptoms • • • •
Ecchymosis of floor of mouth Hematoma in buccal vestibule Mobility along fracture site on palpation Possible paresthesia
Evaluation and Treatment of Orofacial Trauma
Fracture of Body of Mandible • Radiographs • Management: OMS • No benefits to prolonged post-operative
antibiotics
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Evaluation and Treatment of Orofacial Trauma
Fracture of Body of Mandible
Evaluation and Treatment of Orofacial Trauma
Types of Soft Tissue Injuries
Laceration
Contusions & Abrasion
Burn Puncture
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Evaluation and Treatment of Orofacial Trauma
Soft Tissue Injuries Soft Tissue Lacerations Identify foreign bodies • ¼ usual exposure for intraoral
xray • ½ usual exposure for extraoral xray
Evaluation and Treatment of Orofacial Trauma
Soft Tissue Injuries Goals of wound management Avoid infection Functional and esthetic scar Repair or Refer Location of injury Patient’s ability to heal
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Evaluation and Treatment of Orofacial Trauma
Soft Tissue Injuries • Timing of closure • Wound preparation • Primary wound closure
Evaluation and Treatment of Orofacial Trauma
Soft Tissue Injuries Suture technique • Trim nonvital tissue • Use reverse cutting needle • Suture inside to outside • Insert through more mobile tissue first • Use interrupted sutures • Synthetic sutures: avoid silk or cotton
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Evaluation and Treatment of Orofacial Trauma
Suturing of Soft Tissue Injuries
Evaluation and Treatment of Orofacial Trauma
Soft Tissue Lacerations Tongue Laceration • May not require sutures • Use heavy thread • Deep bites with needle • Assure good
approximation • Bury knots
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Evaluation and Treatment of Orofacial Trauma
Extraora/Intraoral Soft Tissue
Electrical Burns
Evaluation and Treatment of Orofacial Trauma
Electrical Burn: long-term scarring
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Evaluation and Treatment of Orofacial Trauma
Electrical Burn: Commisural Splint
Evaluation!and!Treatment!of!Orofacial Trauma
Extraora/Intraoral Soft!Tissue
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Evaluation and Treatment of Orofacial Trauma
Intraoral Soft Tissue • Inspect buccal vestibule • Inspect floor of mouth • Evaluate palate for any puncture wounds
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Evaluation and Treatment of Orofacial Trauma
Intraoral Hard Tissue • Note maxillary displacement • Note any changes in occlusion • Note any alveolar displacement • Note any tooth mobility • Note any dental crazing • Dental trauma – see classifications
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Intraoral Trauma
Evaluation and Classification of Dental Injuries WHO Classification of Dental Trauma • Includes primary and permanent dentition • Based on type of tissue injury • 1. Injury to hard dental structures and pulp • 2. Injury to hard dental structures, pulp, and alveolar process • 3. Injury to periodontal tissues
Primary Dentition Trauma
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Primary Dentition Trauma
General Considerations • May be first contact with dentist • Precooperative child • Long-term concerns for permanent
dentition
Primary Dentition Trauma
Epidemiology •
Maxillary primary incisors
•
2-4 years of age
•
Luxation
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Primary Dentition Trauma
Causes • Falls • Automobile accidents • Child abuse • Secondary factors
Primary Dentition Trauma
Emergencies When can treatment be deferred?
What injuries should be seen ASAP?
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Primary Dentition Trauma
Clinical Examination • Address behavior • Assessment of clinical signs in young
children: objective vs. subjective signs
Primary Dentition Trauma
Clinical Examination
Remember to look past the obvious……
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Primary Dentition Trauma
Clinical Examination And get the big picture….
Primary Dentition Trauma
Radiographic Examination • Avoid further injury • Parental assistance • Possible immobilization • Usually record size 2 film • Extraoral lateral radiographs not helpful in
intrusion
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Primary Dentition Trauma
Treatment Refer to tables in appendices: p. 32-33 •
www.iadt-dentaltrauma.org Guidelines for the management of traumatic dental injuries Flores, Guidelines III. 2007
Primary Dentition: Tooth and/or Alveolar Fractures Injury
Diagnostic Findings Clinical
Treatment / Follow-up
Radiographic
Enamel fracture or
Take one x-ray
Smooth sharp edges with sandpaper disk
Uncomplicated Crown fracture
Enamel + dentin fracture
Evaluate pulp chamber, stage of root development, root resorption
Smooth smaller fractures, place bandage restoration with glass ionomer or composite Clinical exam at 1 week Clinical and x-ray exam at 3-4 weeks
Complicated Crown fracture
Enamel + dentin fracture with pulp exposure
Take one x-ray Evaluate pulp chamber, stage of root development, root resorption
Pulpotomy, pulpectomy (if possible) or extraction Clinical exam at 1 week Clinical and x-ray exam at 3-4 weeks, 6 months, 1 year
Crown-root fracture
Coronal fragment mobile Minimal to moderate displacement
Take one x-ray - may be able to see gingival extent of fracture
Cautious extraction so as not to disturb developing permanent tooth while trying to retrieve root fragments; if necessary, leave root fragment to resorb
Coronal fragment usually mobile and may be displaced or absent
Take one x-ray – determine location of fracture (coronal, middle, or apical third)
If displaced - extract coronal fragment only. Leave apical fragment to resorb Clinical, x-ray exam annually until successor erupts
Root fracture Coronal fragment may be firm
Alveolar fracture
Patient instructions
Tooth-bearing segment is mobile and may be displaced. Step in arch form may be noted
Take one x-ray
Take one x-ray - determine if teeth are in line of alveolar fracture
If crown firm - monitor only Clinical exam at 1 week Clinical, x-ray exam at 2-3 wks, 6-8 wks, 1 year, then annually until successor erupts Reposition segment Splint to adjacent teeth 3 - 4 weeks Sutures if needed Clinical exam at 1 week Clinical, x-ray exam, splint removal at 3-4 weeks Clinical, x-ray exam at 6-8 weeks, 1 year Xray exam annually until exfoliation
Soft diet for 10 - 14 days Gentle toothbrushing after each meal, Clorhexidine swabbed on gingival twice daily, if splinted Follow-up as indicated based on type of injury
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Primary Dentition: Luxated or Avulsed Teeth Injury
Diagnostic Findings Clinical
Radiographic
Treatment / Follow-up
Concussion
Percussion sensitive No mobility or sulcular bleeding
Take one x-ray No abnormalities expected
Observation Clinical exam at 1 week Clinical and x-ray exam at 6-8 weeks
Subluxation
Tooth mobile but not displaced Sulcular bleeding
Take one x-ray No abnormalities expected Increased PDL space may be noted
If no occlusal interference - observation Clinical and x-ray exam at 6-8 weeks
Lateral luxation
Tooth displaced laterally, usually in a palatal/lingual direction
Take one x-ray May see increased periodontal space at apex of tooth
Treatment depends on degree of displacement/occlusal interference: Observation, extraction Clinical exam at 2-3 wks Clinical, xray exam at 6-8 wks, 1 year
Intrusion
Tooth may not be visible. Check orientation of crown Check for apex through labial bone
Take one or two x-ray{s} If displaced toward labial bone, tooth appears shorter and more opaque If displaced toward permanent successor, tooth appears longer
Observation for re-eruption Clinical exam at 1 week, Clinical, xray exam at 3-4 wks Clinical exam at 6-8 wks Clinical, xray exam at 6 months, 1 year, then annually until successor erupts Extraction x-ray annually until successor erupts
Avulsion
Tooth out of socket
Take one x-ray - confirm avulsion
Do not replant. Suture if needed Clinical exam at 1 week Clinical, x-ray exam at 6 months, 1 year, then annually until successor erupts
Patient instructions
Soft diet for 10 - 14 days Gentle toothbrushing after each meal, Clorhexidine BID if splinted Follow-up as indicated based on type of injury
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Primary Dentition Trauma
Complications in Primary Teeth • Color changes – 53% • Pulp necrosis – 25% • Pulp canal obliteration – 36% • Gingival retraction – 6% • Disturbances in physiologic resorption -4% • Premature tooth loss – 46% • Ankylosis
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Primary Dentition Trauma
Primary Tooth Complications Discolored primary incisors • • • •
>50% dark coronal discoloration fades Yellowish teeth develop less pathology >50% of dark teeth remain asymptomatic Root canal treatment not indicated
When to extract? • • • •
Swelling Sinus tract Increased mobility Sensitivity to percussion
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Primary!Dentition!Trauma
Primary!Tooth!Complications:! Pulp!Canal!Obliteration
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Primary!Dentition!Trauma
Intrusion!Injury
Primary Dentition Trauma
Intrusion Injury Considerations • 80% of intruded teeth pushed labially • Majority re-erupt and survive >36mos • Common findings • Role of systemic antibiotics
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Primary!Dentition!Trauma
Intrusion!Injury!Sequence
Baseline
Baseline
4 weeks
12 weeks
Primary Dentition Trauma
Luxated or Avulsed Teeth: Avulsion
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Age 1
Age 3.5
Primary Dentition Trauma
Complications in Permanent Successors What primary tooth trauma poses the greatest risk to permanent successor ? •Intrusion and avulsion of primary teeth •Age less than 3 years at time of trauma
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Primary!Dentition!Trauma
Complications!in!Permanent!Successors
What are the possible consequences to permanent successors?
Primary!Dentition!Trauma
Complications!in!Permanent!Successors:! Discoloration/Hypoplasia
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3.3 yrs
4.5 yrs
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7 yrs 8.5 yrs
8 yrs of age
9 yrs
8.5 yrs
10 yrs
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12 yrs
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Primary Dentition Trauma
Parental Discussion Topics The parents want to know what will happen as a result of the trauma. How do you respond?
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Permanent Dentition Trauma
Permanent Tooth Trauma
General Considerations • • • • • •
Age of patient Medical status Cooperation Type of trauma Dental development Parental desires/concerns
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Permanent Tooth Trauma
Treatment Timing Should be seen immediately • Avulsion • Alveolar fracture • Extrusive or lateral luxation
Can be deferred several hours • • • • •
Intrusion Concussion Subluxation Root fracture Crown fracture with pulp exposure
Treatment may be deferred • Crown fracture without pulp exposure
Permanent Tooth Trauma
Treatment Refer to tables in appendicies: p. 3438 •
www.iadt-dentaltrauma.org Guidelines for the management of traumatic dental injuries Flores, Guidelines I. 2007 Flores, Guidelines II. 2007
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Permanent Dentition: Tooth and/or Alveolar Fractures Injury Uncomplicated Crown fracture
Diagnostic Findings Clinical Enamel fracture Enamel + dentin fracture
Treatment / Followup
Radiographic Take x-rays from 3 angulations Radiograph of lip or cheek lacerations Evaluate pulp chamber, stage of root development Baseline pulp test
Smooth with sandpaper disk or bond with composite resin as needed Rebond fractured segment if intact. Bandage restoration with glass ionomer or composite Clinical,xray exam at 6-8 weeks, 1 year
Complicated Crown fracture
Enamel + dentin fracture with pulp exposure
Take x-rays from 3 angulations Radiograph of lip or cheek lacerations Evaluate pulp chamber, stage of root development
Partial pulpotomy with Ca(OH)2 Restore with composite Pulpectomy for some mature teeth depending on time pulp exposed and pulp condition Clinical exam, xray at 6-8 weeks, 1 year
Crown-root fracture
Enamel, dentin and root fracture Pulp may or may not be exposed Coronal fragment mobile Minimal to moderate displacement
Take x-rays from more than one angle to detect fracture Pulp test usually positive
Reposition / splint coronal fragment as needed Longterm: Subgingival fracture site may require crown lengthening and/or orthodontic extrusion Clinical exam, xray, splint removal at 3-4 wks Clinical exam, xray at 6-8 wks, 6 mos, 1 year
Root fracture
Coronal segment may be mobile/displaced Transient crown discoloration
Take xray from more than one angle Consider occlusal xray for fractures in cervical 1/3 Pulp test is usually negative initially – monitor over time at clinical exams
Reposition coronal segment, splint 4 weeks with flexible splint; If fracture is in cervical 1/3 splint longer, up to 4 months Clinical exam, xray, splint removal at 4 wks Clinical exam, xray 6-8 wks, 4 mos, 6 mos, 1 year, then annually for 5 years
Alveolar fracture
Tooth containing segment mobile and may be displaced. Step in arch form noted
Take x-ray; panograph is helpful in determining fracture lines Pulp test may or may not be positive
Reposition segment and splint 4 weeks. Sutures if needed Clinical exam, xray, splint removal at 3-4 wks Clinical exam, xray at 6-8 wks, 6 mos, 1 year
Patient instructions
Soft diet for 10 - 14 days Gentle toothbrushing after each meal, Clorhexidine BID if splinted Follow-up as indicated based on type of injury
Permanent Tooth Trauma
Crown Fracture Crown fracture with/without pulp exposure
• Injury to enamel, dentin, pulp • Factors affecting pulpal healing • Management
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Permanent Tooth Trauma
Crown Fracture: Uncomplicated Enamel & Dentin Fracture Crown fracture with/without pulp exposure – what are the likely outcomes?
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Permanent Tooth Trauma
Crown Fracture: Complicated Enamel & Dentin Fracture
Crown fracture with pulp exposure
• Within hours and small exposure • Longer interval and larger exposures
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Permanent Tooth Trauma
Intra-Alveolar Root Fractures • Injury to pulp, PDL, cementum, dentin • Coronal displacement – considered as luxation • Healing depends on bacterial contamination of
pulp • Importance of radiographs at multiple angles • Treatment delay possible
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Permanent Tooth Trauma
Intra-Alveolar Root Fractures To Splint or not to Splint… • • •
Non-displaced teeth with no mobility Fracture in middle third – mobile fragment Fracture in cervical third
Antibiotics?
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Permanent Tooth Trauma
Intra-Alveolar Root Fractures Types of healing • Hard tissue: dentin & cementum form • Connective tissue: cells from pdl form • Non-healing: necrosis in coronal
segment
Permanent Tooth Trauma
Intra-Alveolar Root Fractures Monitor pulpal vitality in coronal segment • Open apex: necrosis rare • Pulp necrosis in coronal segment: treat
as immature permanent tooth • Apical root segment: no treatment
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Permanent Tooth Trauma
Intra-Alveolar Root Fractures • Calcium hydroxide as pulp canal
medicament • Apexification • Disinfection of root canals • Weakens dentin walls
Permanent Tooth Trauma
Intra-Alveolar Root Fractures • Mineral Trioxide Aggregate (MTA)
as pulp canal medicament • Alkaline, like Ca(OH)2 • Grainy texture • Hydrophilic • No thinning of dentinal walls
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Permanent Tooth Trauma
Benefits of MTA • Biocompatible • Stimulates interleukin regulation • Calcium from MTA diffuses through dentin to
resorptive lesions • May help stop inflammatory root resorption • Does not thin dentinal walls • Better fracture resistance over time than Ca(OH)2
Permanent Tooth Trauma
Fracture resistance: MTA vs. Ca(OH)2
Hatibovic-Kofman et al, 2008
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Permanent Tooth Trauma
Luxation Injuries: Concussion Concussion • Sensitive to percussion • No mobility • No sulcular bleeding
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Permanent Tooth Trauma
Luxation Injuries: Subluxation • Subluxation • Sensitive to percussion • Mobile • No displacement
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Permanent!Tooth!Trauma
Luxation Injuries:!Subluxation
Permanent!Tooth!Trauma
Luxation Injuries:!Subluxation
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Permanent!Tooth!Trauma
Luxation Injuries:!Subluxation As time goes by …
Injury
6 mos
3.5 yrs
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1yr 9 mos
4.5 yrs
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Permanent Tooth Trauma
Luxation Injuries: Lateral Luxation • Lateral luxation - displacement in a
direction other than axial • Pulp supply is ruptured • PDL becomes compressed • Sequelae
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Age 8 yrs.
Age 20 years
Permanent Tooth Trauma
Luxation Injuries: Intrusive Luxation Factors in Intrusive Luxation • Age of patient: <12-fewer complications • Concurrent gingival laceration: more
necrosis • Root development: immature = necrosis • Multiple intrusions – more bone loss
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Permanent Tooth Trauma
Luxation Injuries: Intrusive Luxation Permanent Intrusion Injuries • Rare injury • More common in boys • Maxillary central and lateral incisors • Multiple intrusions occur often • Intrusions >7mm –more complications • Intrusions 1-3mm – less root resorption
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Permanent Tooth Trauma
Avulsion Factors affecting Prognosis • • • •
•
Extraoral time Loss of PDL vitality Storage media Handling of tooth before replantation Patient immune response
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Permanent Tooth Trauma
Avulsion Effect of storage media on PDL cell apoptosis • Apoptosis: programmed cell death (differs from necrosis) • In vitro study comparing milk, HBSS, Gatorade, and
contact lens solution as storage media • At 24 & 72 hours, Gatorade and contact lens solution displayed greatest % apoptotic cells • Cells treated in the solutions on ice showed less apoptosis than those at room temperature Chamorro, Regan et al, 2008
•
Permanent Tooth Trauma
Avulsion Contraindications to replantation • • • • •
Severe cardiac disease Seizure disorder Severe mental disability Compromised healing Poor alveolar support
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Permanent Tooth Trauma
Avulsion Tooth cannot be found •
Verify avulsion
•
Assess labial plate of bone
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After bone grafting
Permanent Tooth Trauma
Avulsion Replantation Basics Extraoral period <60 min • On-site replantation is best • Meet patient/parent at office • Place tooth in reconstituting media (HBSS) • Take clinical photo, radiograph as indicated • Review procedure and likely outcomes
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Permanent Tooth Trauma
Avulsion Replantation Basics • Obtain informed consent • Provide local anesthesia • Curette socket, remove clot • Replace tooth • Place flexible splint
Permanent Tooth Trauma
Avulsion Replantation Basics • Systemic antibiotics • •
> 12 years: Doxycycline < 12 years: Penicillin V
• Post-op instructions
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Permanent Tooth Trauma
Avulsion How does root development affect pulp therapy in avulsed teeth? • Closed apex • Open apex
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1 year
2 years
3 years
6 months
4 years
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5 years
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3 years
Permanent Tooth Trauma
Avulsion Delayed Replantation Extraoral period >60 minutes • Emphasize poor prognosis • Remove necrotic tissue from root • Root canal treatment • Tooth in 2% sodium fluoride - 20 minutes • Replant tooth and stabilize
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Permanent Tooth Trauma
Avulsion Healing mechanism in avulsion • 4 days: pulp revascularization begins • 1 week: gingival attachment re-established • 2 weeks: PDL at original state
Permanent Tooth Trauma
Avulsion How can PDL and Pulp Problems affect outcome for avulsed teeth? Replacement vs. Inflammatory Resorption
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Permanent Tooth Trauma
Avulsion Closed Apex Outcomes • Favorable • Unfavorable
Permanent Tooth Trauma
Avulsion Open Apex Outcomes • Favorable • Unfavorable
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Permanent Tooth Trauma
Avulsion Inflammatory Resorption • Begins as early as 2-3 weeks • Radiolucencies: bone and/or cementum • Endodontic treatment necessary • Enamel matrix protein derivative
Permanent Tooth Trauma
Avulsion Replacement Resorption • Begins within 2 weeks • Tooth gradually replaced by bone • Transient or permanent • Enamel protein matrix derivative
(Emdogain) not beneficial
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8 yrs post avulsion (age 15)
Permanent Tooth Trauma
Avulsion • Decoronation: conservative therapy • Indications • Technique • Timing • 7-10 years: within 2 yrs. • 10-12 years: decide each case individually • >12 years: as soon as detected • Further procedures: ridge augmentation
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Permanent Tooth Trauma
Avulsion Plan for future restoration • Interdisciplinary approach • Alveolar development near completion • Extraction of tooth – plan for bone graft • Orthodontic closure of space
Splinting for luxations, avulsions and root fractures: a review • Reviewed 12 clinical studies and 9 animal studies • Assessed splinting’s biological processes that affect healing • Prognosis is determined by type of injury rather than factors associated with splinting • Problems with some studies – did not simulate injury • Current protocols by IADT & AAE: Best Practice Kahler & Heithersay, 2008
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Child Abuse
Child Abuse
Reporting Requirements • Failure to report suspected child abuse is a misdemeanor • Know state guidelines • Organizations for support: • Childhelp National Child Abuse Hotline • Prevent Abuse and Neglect through Dental
Awareness
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Child Abuse
Statistics National Pediatric Trauma Registry (NPTR): • Physical abuse: 11% of all blunt trauma ages 0• • • •
4 Premature birth: high risk factor Intracranial injury more common with abuse Injuries to thorax and abdomen more common Increased hospital stays for abused children
Child Abuse
Orofacial Injuries Injuries to head, face, mouth and neck are present in over 50% of physically abused children
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Child Abuse
Child Characteristics Which children are at higher risk? • Low birth weight • Physical disability • Mental disability • Hyperactivity or aggressivity • One of many (4 or more) siblings • Age 2-4 years
Child Abuse
Neighborhood Characteristics Where is child abuse more likely? In neighborhoods with: • • • • • • • •
Increased number of one-parent families Increased unemployment Many children younger than 6 years Many families at poverty level Families living at current address <1 year Many vacant houses Many families isolated from kin Low number of single family dwellings
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Child Abuse
Characteristics of Abuser • • • • • • • • •
Young maternal age Single marital status Low level of education Low level of employment Poverty level income Low self esteem Substance abuse Mother not living with her mother at age 14 Presence of surrogate in home
Child Abuse
Other Characteristics Perpetrator, location and mechanism of injury • 27% mother • 26% father • 13% mother’s partner • 53% in home • 23% punched or slapped around head, neck, or face • 17% struck by object
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Child Abuse
Forms of Child Abuse • Physical abuse • • • •
•
Non-accidental injuries Parent punishing child Parental frustration and lack of self-control Physical presentation not consistent with history Bruises, welts, fractures, burns, lacerations
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Child Abuse
Forms of Child Abuse Sexual abuse • •
Trauma to mouth Various infections
Child Abuse
Forms of Child Abuse Neglect Emotional or verbal
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Child Abuse
Physical Indicators Injury and explanation don’t match • • • •
Handprint on face is not from a fall Accounts that change over time Conflicting accounts Unwitnessed injury
Child Abuse
Physical Indicators What injuries are seen in abused children? • • •
<1 year 2-5 yrs 6-12 years
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Child Abuse
Behavioral Indicators • Child • Adult
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Child Abuse
In the Medical Setting Munchausen syndrome by proxy • Parent
fabricates pediatric illness • Child subjected to unnecessary tests/procedures
Child Abuse
Role of the Dentist Role of dentist who suspects child abuse • • • •
Dental and general physical exam History from child and parent Ask questions If suspicious of abuse, contact protective agency
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Trauma: A Case Presentation This 14-year-old boy fell and struck his mouth on the edge of a fence. How do you proceed?
Discuss the components of your examination of this patient. • Medical history review, identifying the adult
with the patient • History of the injury • •
What, When, Where, How Any care sought elsewhere?
• Physical assessment for head trauma • • •
Orientation Rapid neurological exam Physical examination of head/neck
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The medical history is noncontributory, and your physical assessment is within normal limits. The parents say the accident happened about 3 hours ago and he broke off part of his front tooth. It hurts when he breaths in. What other information do you need to complete your diagnosis? • Continue with dental/soft tissue examination – extraoral, intraoral • It looks like he also has a lip laceration – that may need suturing after I treat his dental injury • I would examine his mouth intraorally to examine the traumatized area, and then I would probably record some radiographs.
The following images represent the condition of the patient at your office:
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You mentioned that you would record radiographs; what radiographs would you record? Based on my clinical findings – assuming no problems with any other teeth, I would record a few periapical radiographs of the injured tooth, taken from different angles.
The following radiographs were recorded:
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What is your diagnosis? This is a complicated enamel and dentin fracture of tooth #10, involving the mesial, distal, labial, lingual, and incisal surfaces. There is also a lip laceration, just coming up to the vermillion border on the left maxillary lip.
Describe in detail your management of this patient.
• I would anesthetize the tooth with local anesthesia • Since it had been 3 hours since the trauma, I would likely do a Cvek pulpotomy – maybe a pulp cap, if the injury were still fresh. • Then, I would restore the tooth with composite resin, or reattach the segment if the parents had it.
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Describe the Cvek Pulpotomy procedure. • The coronal pulp is removed (1-2 mm), making sure that the tissue is fresh and vital • Cover the pulp stump with calcium hydroxide, then restore the tooth. • The goal is for the pulp further down in the canal to retain its vitality.
What are your post-operative instructions to the patient and his parents? When do you want to see the patient again, and what will you do at that appointment? • I would tell them to seek medical care regarding the lip laceration, and I would tell them to watch for any signs of head trauma (vomiting, sleepiness, etc.). If these occur, they should head to the ED • I would tell them to give him acetaminophen or ibuprofen for any pain, and to try to keep his diet soft for the next several days. Additionally, I would encourage him to be thorough with his oral hygiene. • I would want to see him in about 4 weeks; at that time, I would check the pulp vitality of #10, and assess for any color change, mobility, etc. I would also record a follow-up radiograph.
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The parents ask you about the long-term consequences of the injury. What do you tell them? • I would tell them that there is always a possiblity that the tooth could undergo necrosis (the nerve dying), and that it may require endodontic therapy. • I would also tell them that it would at some time likely need a full coronal restoration. • We won’t know about the long-term survival of the tooth for a while, but we’ll monitor it for about 5 years.
If the injury had occurred 2 days ago, would your treatment recommendations be the same? If it occurred two days ago, there would be more bacteria entering the pulp, and if I were to attempt a Cvek pulpotomy, I’d have to go further into the chamber, and possibly into the canal to get to vital tissue. Most likely, though, the tooth would need endodontic therapy, if I wasn’t able to get to a bleeding pulp in the chamber or canal
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If the patient were 8 years old, with incomplete root formation, would your immediate treatment be the same? Yes, my immediate treatment would be the same (assuming that we’re now talking about the accident happening 3 hours ago); the goal of treatment is continued vascularity of the pulp so that the apex of the tooth can continue to develop normally. I would hope that in an 8-year-old, the pulp would be able to retain its vascularity and provide the healthy tissue needed for the apex to develop. Still, I would need to make the parents aware of the challenges we face with this type of injury.
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307
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308
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Steven M. Adair, DDS, MS Medical College of Georgia
•
75% of direct restorations placed in last 50 years
•
Most widely used restorative material for permanent teeth in past
•
Ratio of amalgams to composites has fallen below 50:50
310
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Study
Number
Results
Braff
150 Cl. II
11.3% success over 33.5 months
Holland et al
1139
3y survival: Ds 38%; Es 48%
Qvist et al
1715
50% failed by 2y
Levering and Messer
1177 Cl. II
76% success
Roberts and Sheriff
706 Cl. II
5y survival 67%
Study Holland
Patient Age at Placement 3 years
11 months
Holland
7-8 years
44 months
Levering/Messer
<4 years
5 years (51%)
Levering/Messer
>4 years
5 years (70%)
Roberts/Sherriff
4-5 years
>7.5 years
Welbury et al.
5-11 years
41.4 months
311
MST
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Wide range of failure rates reported (058%)
•
Failure rates in context of controlled clinical environment: 0-22%
•
Concluded that amalgam remains appropriate choice for restoration of primary teeth
Kilpatrick!&!Neumann!2007
•
Children 6-10 randomized to receive • amalgams only (N=267), or • compomers in primary teeth, and • composites in permanent teeth (N=267)
•
Follow-up scheduled q6mo for 5 y
Soncini et!al!2007
312
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Primary teeth: overall: 6% compomers, 4% amalgams ! NS
2ry caries: 3% compomers, 0.5% amalgams ! statistically significant
Permanent teeth: overall: 15% composites, 11% amalgams ! NS
repairs: 3% composites, 0.4% amalgams ! statistically significant (7X difference)
•
472 children ages 8-12
•
Randomly assigned to receive posterior restorations with • amalgam (N=856) • composite s (N=892)
•
Followed for up to to 7 years Bernardo!et!al!2007
313
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Overall failure rate: 10% Survival rates amalgam: 95% composite: 86%
Annual failure rates amalgam: 0.16-3% composite: 1-9%
Primary failure reason: 2ry caries 3.5X higher for composites
•
ADA Council on Scientific Affairs (1998): “no justification for discontinuing the use of dental amalgam”
•
Supported by USPHS (“no solid evidence of any harm”) and NIH (“no scientific evidence… (of) significant side effects (from dental restoratives)”
•
Amalgam disposal issue
314
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•
Dalen et al J Dent 2003 • No correlation was detected between
memory variables and exposure to amalgam
•
Hujoel et a Am J Epidemiol 2005 • No evidence that mercury-containing dental
fillings placed during pregnancy increased low-birth-weight risk
•
Bellinger et al 2007 • no evidence that exposure from dental
amalgam is associated with any adverse neuropsychological effects over 5 years •
Lauterbach et al 2008 • exposure to Hg from amalgams does not
advesely affect neurological status of chilren
315
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•
Roberts et al 2008 • no measurable change in level of resistance to
Hg or antibiotic resistance in children with / without amalgam restorations •
DeRouen et al 2006 • no statistically significant differences in
neurobehavioral assessments or nerve conduction velocity over 7 years in children with amalgam vs. composite restorations
•
2006: review called for more studies on amalgam safety • did not ban amalgam
•
2008: set deadline (7/28/09) to complete reclassification process for amalgam
•
Beazoglou et al 2007 • economic impact of amalgam ban estimated to
be $8.2 billion first year (2005) and >$98 billion in US 2015-2020 • reductions in access to care
316
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•
Restoration longevity is no longer the primary factor
•
Restoration esthetics is more important
•
Parents may be concerned about mercury “issue”
•
Parents are generally not aware of the estrogenicity “issue” with resin composites
Introduced in 1950 Chrome-steel (18-8) and nickel-chrome alloys (older; not in use)
Chrome-steel properties
heating does not increase strength work hardens high chromium reduces corrosion soldering w/ flux reduces corrosion resistance
317
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Age of patient at SSC placement Years of Service
<4 years
>4 years
1
92%
97%
5
76%
80%
10
64%
61% Messer!and!Levering!1988
•
Data collected from 10 studies
•
Failure rates of SSCs: 1.9 to 30.3%
•
Failure rates of amalgams: 11.6 to 88.7%
•
1.5 - 9 failed amalgams for every failed SSC
•
Odds ratio 0.23 (95% CI 0.19, 0.28) Randall!et!al!JADA!2000
318
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•
No studies met inclusion criteria • no randomized prospective studies
Evidence to support SSCs over other types of fillings for primary molars (but low quality) • Strong need for prospective RCTs • Lower levels of evidence consistently favor SSCs • Should not be misinterpreted as lack of evidence for SSC efficacy •
Materials Continuum
Glass ionomer cements – evolved from search for replacement for silicate cement
Resin modified glass ionomers – “glass ionomer hybrids”
Polyacid modified resin composites “compomers”
319
Resin composites
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Historical development • acrylic and other resins, early composites
•
Composition filler particles; various; hydrophilic resin matrix; dimethacrylate resin; hydrophobic silane coupling agent pigments, stabilizers, polymerization inhibitor, photoinitiator, radiopaquing agents
• • • •
•
Filler - range of materials, sizes
Category
Particle size (microns)
w/w% Filler
Filler Type
Characteristics
Traditional
8-12
>80
quartz
rough
Small particle
1-5
60-78
quartz/glass
better stress resistance
Microfilled
0.04-0.4
50-60
silica/ppc
esthetic
Hybrid
0.4, 1-5 blend
50-75
silica/glass
esthetic
Nanofilled
5-25 nm 75-80 75-100 nm clusters
320
nanosilica, highly esthetic zrconium/silica
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Particle size 0.005 – 0.01 "m though 40 nm particles present in microfills
Comparisons: hydrogen atom: 0.1 – 0.2 nm small bacterium: 1000 nm (1 "m)
Reduced interstitial spacing of filler particles Increased filler loading Better properties (?) Longer retention of surface polish
•
“Finishability” • nanofilled > microfilled > hybrid > small particle >
traditional •
Tensile strength • small particle = hybrid = nanofilled > traditional >
microfilled •
Compressive strength • small particle > hybrid = nanofilled > microfilled =
traditional
321
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
•
Reduce polymerization shrinkage
•
Decrease coefficient of thermal expansion
•
Increase hardness
Composite resin polymerization shrinkage: 2 – 3.5% • leads to gap formation/microleakage, and cusp
deflection
•
Necessitates incremental filling technique
Layering technique
Gap formation
From Ruiz & Mitra 2006
322
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Bonding agent strength must be >17 MPa to overcome shrinkage stress (1MPa=150 psi) • Less shrinkage if cured in contact with a set RMGI liner (“stress breaker”) • Composite shrinks toward strongest area of bond •
•
Not truly condensable
•
SureFil, ALERT, Filtek P60
•
Fillers • fibrous, porous, or irregularly-shaped
particles • different sizes of particles •
Wear rates similar to amalgam (?)
•
Must place incrementally (polymerization shrinkage)
323
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•
•
• • •
Lower filler volumes (45-70 w/w%), same particle size as hybrids, decreased viscosity/stiffness Increased polymerization shrinkage, decreased wear resistance, decreased strength, bond strength 8-10 MPa Most contain fluoride Designed as sealants, but used as restorative agents Radiopacity important if used beneath resin composites
Materials Continuum
Glass ionomer cements – evolved from search for replacement for silicate cement
Resin modified glass ionomers – “glass ionomer hybrids”
Polyacid modified resin composites “compomers”
324
Resin composites
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Type I: luting cements
•
Type II: restorative materials • II.1 esthetic • II.2 reinforced
•
Type III: lining materials and fissure sealants
Sealant Luting cement Crown cementation Orthodontic band cementation Orthodontic bracket adhesive
Cavity liner Dentinal adhesive Sandwich technique or dentin “replacement” Tooth restoration, including ITR (ART)
325
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Chelation bond to dentin and enamel
•
Leaches fluoride (how long? “burst” effect? rechargeable? antimicrobial effects?)
•
Biologically compatible with connective tissue
•
Thermal expansion similar to enamel and dentin
•
Low setting shrinkage
•
Bond strength 0.5-4.0 MPa to dentin
Technique sensitive - moisture imbibition and dessication Bond strength less than composite/dentin Brittle Porosity Surface finish not as smooth as composite Surface wear greater than composite
326
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•
Clean surface required for good chelation
•
10% polyacrylic acid, water rinse
•
Removes smear layer, tubules plugged
•
Must cover GIC with varnish or unfilled resin immediately after placement
•
Initial finishing delayed ~3-5 minutes
•
Finish using standard techs (hand instruments?)
327
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•
Cover again with varnish or sealant
•
No pressure for 1 hour
•
Cracks caused by dehydration can be closed by rehydration
•
Effect was greater for RMGIs than conventional GICs Sidhu et al 2004
•
Proper dentin conditioning
•
Proper manipulation of material
•
Protection during setting or whenever dessication might occur
328
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Materials Continuum
Glass ionomer cements – evolved from search for replacement for silicate cement
Polyacid modified resin composites “compomers”
Resin modified glass ionomers – “glass ionomer hybrids”
•
Resin modified with hydrophilic monomers that contain no water
•
Specialized fillers, dehydrated polyalkenoic acid
•
LC plus auxiliary acid-base reaction with uptake of water (insufficient in dark)
•
Require use of primers and adhesives; acid etching recommended
329
Resin composites
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Low fluoride release with water uptake (20% of GIC); limited reservoir effect Weaker, more likely to wear than RCs and RMGIs Excellent handling characteristics Water uptake degrades some physical characteristics, buffers acidic environment, affects color stabiliby
Advantages no mixing easy to place and polish; excellent handling good esthetics less susceptible to dehydration radiopaque stronger than GICs higher bond strengths than RMGIs clinical success rates similar to amalgam, GI, RMGI, resin composites
330
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•
Disadvantages • bonding agent required • more leakage than RMGIs • expand from water sorption over time • wear more readily than resin composites • fluoride release into tooth structure inhibited by
resin bonding agent • limited fluoride uptake (recharge) • no major advantages over resin composites
Materials Continuum
Glass ionomer cements – evolved from search for replacement for silicate cement
Resin modified glass ionomers – “glass ionomer hybrids”
Polyacid modified resin composites “compomers”
331
Resin composites
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
80% GIC + 20% LC composite resin
•
Powder similar to conventional GIC
•
Liquid is HEMA, water, and a polyacid; significant acid-base reaction
Fuji II LC
Setting reactions:
acid-base reaction (self-cure) photoinitiated (light cure) chemically-activated polymerization (resin cure)
Fluoride release similar to/less than GICs: initially high, decreases rapidly; can be “recharged” F in filler particles, radiopaquing agent, resin matrix
332
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Strength and solubility intermediate to GIC and composites Less prone to hydration problems than GIC F release equal to GIC; can be recharged Ease of use intermediate to GIC and composites; requires mixing
•
• • •
Vitrebond Plus
•
Esthetics intermediate to GIC and composites
•
Bond to tooth structure > GIC
•
Less microleakage than GIC
•
Coefficient of thermal expansion lower than GIC
333
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In comparison to flowable composites RMGIs have: lower adhesion to dentin fluoride release coefficient of thermal expansion closer that that of natural tooth lower (better) modulus of elasticity – can act as stress-absorbing buffer for polymerization contraction forces
•
RMGI + composite resin performs better than flowable + composite resin
RMGI absorbs contraction stress, counterbalances cusp deformation
334
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•
15-60 sec etch with 37% phosphoric acid
•
Resin tag formation - 1075 "m
•
Hydrophobic bis-GMA or urethane dimethacrylate resins
•
Bond strengths >20 MPa
•
Type I – rod cores
•
Type II – peripheries of rods
•
Type III – delineation of rods not evident
335
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Dentin histology is major factor in bonding success
Factors smear layer dentinal tubule density, size, length dentin sclerosis (caries-affected)
1 - 5" thick; dentin chips, debris Partly porous, but reduces fluid flow from tubules Weak attachment to dentin - ~6 MPa Biological “band-aid” Permeability increased by primers
336
Courtesy of Dr. Jorge Perdigao
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Tubule diameter increases with depth toward pulp Superficial dentin fewer tubules per surface area less area for lateral diffusion of bonding agent
Bond strength decreases with progressive depth from DEJ water in dentinal fluid competes with collagen for hydrophilic monomers fluid dilutes concentration of monomer less intertubular dentin available for creation of hybrid layer
337
Courtesy of Dr. Jorge Perdigao
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Sclerotic dentin denser in mineral content
•
Reduces penetration of bonding agent
•
Additional/extended etching on cariesaffected dentin increases tensile bond strength (Arrais et al 2004)
•
Removes or modifies smear layer, increases permeability
•
Demineralizes underlying dentin
•
Chemistry • • • • •
EDTA phosphoric acid maleic acid phosphoric/nitric acid/Al oxalate others
338
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Current systems use hydrophilic wetting agents
•
Provides micro-mechanical retention to modified dentin
•
Wets/penetrates collagen meshwork, creates “hybrid layer,” increases wetability of dentin
Unfilled resin Bonds with composite restorative material Bonds with primer in hybrid layer Courtesy of Dr. Jorge Perdigao
339
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Two-bottle etch and rinse system (total etch/complex)
One-bottle etch and rinse system (total etch/simplified)
Two-bottle self-etch system (self-etch/complex)
One-step self-etch system (self-etch/simplified) De Munck et al 2005
•
Etch-rinse-prime-bond (two bottle) system: • gold standard for bonding agents
•
Any simplification in the procedure results in loss of bonding effectiveness
•
Only two-step self-etch primer + adhesive approaches the gold standard
340
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Self-etch systems modify but do not remove the smear layer
•
May result in less postoperative sensitivity
•
Not as good as total etch systems for enamel bonding
•
“Total etch technique”
•
Dentin is left slightly wet - “glistening”
•
Enamel and dentin bond strengths 21-30 MPa for permanent, 10-18 primary
341
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Smear layer removed more easily than in permanent teeth 25-30% thicker hybrid layer Greater reactivity of primary dentin to conditioner; deeper demineralized zone; precludes complete penetration of primer and adhesive? Recommended less time for conditioning primary teeth (7 vs. 15 sec) Nor et al 1996, Torres et al 2007
•
Microtensile bond strength of adhesive systems similar with permanent and primary dentin (Soares et al 2005)
Shorter etch times may not be necessary with self-etch products
342
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•
Osseointegrated (endosseous) implants • titanium or titanium alloy • surface treatments to enhance
osseointegration
• acid etching • grit blasting / acid etching
• surface treatment with hydroxyapatite
leads to biointegration
• direct biochemical bond of bone to implant surface independent of mechanical interlocking
•
Implants behave as ankylosed teeth
•
Can interfere with position of adjacent tooth germs, eruption of adjacent teeth
•
May become dislocated or lost as result of jaw growth
343
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Cannot participate in drift and displacement mechanisms of growth in maxilla
Fixed!implants!that cross!the!midline!will restrict!maxillary!growth
•
In mandible, however, increases in width are generally related to posterior growth at rami Transverse!growth!in anterior!region!ends!in early!childhood
344
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Most risky areas for implant placement in growing child are: • anterior and posterior maxilla • posterior mandible
•
Best site: • anterior mandible (but not for single tooth
replacement)
•
Mandibular rotation and resorption of anterior alveolar ridge may lead to displacement / loss of implants
345
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Prior to placing implants, use a conventional prosthesis to: gain information on function and esthetics allow for as much growth as possible
Problem with prosthetic approach: retention Examples of implants in children with ectodermal dysplasia: see Kramer et al 2007, Guckes et al 1997
346
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6-year-old white male with ectodermal dysplasia
Rockman RA, Hall KB, Fiebiger M. JADA 2007
Rexillium alloy copings cemented to maxillary and mandibular primaryteeth; copings used to hold “keeper” magnets
347
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Cast metal frameworks
Magnets were attached with cold cure resin Some dental anatomy placed in maxillary posterior acrylic Mandibular acrylic left as monoplane
348
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349
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
16-15)&3"1:*/13*."3: "/% :06/(1&3."/&/55&&5) 4UFWFO."EBJS %%4 .4 5PQJD0VUMJOF
350
* 1SJNBSZ1VMQ)JTUPMPHZBOE$PNQBSBUJWF.PSQIPMPHZ ** "TTFTTNFOUPG1VMQBM4UBUVT ***7JUBM1VMQɨFSBQZ *7/POWJUBM1VMQɨFSBQZ
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pulp Therapy in Primary and Young Permanent Teeth Steven M. Adair, DDS, MS Medical College of Georgia
Histologic Components of Primary Pulp •
Lymph vessels
•
Blood vessels
•
Nerve tissue
•
Collagenous fibers
•
Fibroblasts
•
Defense cells •
•
Lymphocytes
•
Odontoblasts
•
Odonto-/osteoclasts
•
macrophages, neutrophils
351
Histologically similar to young permanent pulp – cell rich, vascular
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Comparative Morphology •
Increased number of accessory canals
•
Curved roots
•
Ribbon-like radicular pulp
•
Relatively longer roots in molars
•
Coronal pulp position
•
Apical resorption
•
Position/proximity of premolars
•
Larger pulp relative to crown size
•
Mesial pulp horns closer to DEJ than distal
Clinical Assessment of Pulp Status •
Problem: making histologic assessment from clinical signs and symptoms In general, the correlation between the clinical findings and the histologic condition is weak.
352
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Assessment of Pain Types of Pain
Pulp Status
Spontaneous Nocturnal
Irreversible: Non-vital treatment
Constant Thermal Reversible: Vital treatment
Chemical Intermittent
Further Clinical Assessment •
Extent of lesion •
•
location, color
Mobility •
•
R/O root resorption
•
Soft tissue swelling
•
Lymphadenopathy
Sensitivity to percussion •
•
Pulp exposure •
•
hemorrhagic v necrotic
Pulp testing • • •
353
reliable in primary teeth
electrical thermal percussion
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Reliability of Pulp Testing Teeth:
Primary
Young permanent
Mature permanent
Electrical
---
+
+
Thermal
+
+
++
Percussion
++
+
+
No single diagnostic test is reliable
Radiographic Criteria for Healthy Pulp •
Adequate periodontal support
•
No decalcified lesions or root fractures
•
No internal/external resorption or radiolucency
•
Integrity of lamina dura
•
See manual for more
354
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Radiographic vs. Histologic Assessment Moss et al 1965: accessory canals in furcation area no vital pulp tissue with interradicular bone loss increased porosity of pulpal floor when infected
Wrbas et al 1997: 77.5% of mandibular primary molars had accessory canals in floor of chamber
Vital Pulp Therapy •
Protective base/liner
•
Indirect pulp treatment (IPT)
•
Direct pulp capping (DPC)
•
Pulpotomy • •
•
pharmacotherapeutic non-pharmacotherapeutic
Partial pulpotomy (permanent teeth)
355
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Protective Base/Liner Indications (AAPD):
•
• • • • •
normal pulp dentin tubules exposed by cavity prep all caries removed minimize injury to pulp minimize post-op sensitivity
Objectives
•
• • • •
preserve pulpal vitality promote pulpal healing promote tertiary dentin formation minimize microleakage/sensitivity
Indirect Pulp Treatment •
Indications • • • • •
•
deep carious lesion no/reversible pulpitis incomplete caries removal no pulp exposure pulp vital
Objectives •
complete seal, preserve vitality, no post-tx signs or symptoms, no harm to succedaneous teeth, continued root development in permanent teeth
356
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
IPT Technique •
Apply medicament/material over carious or sound dentin [Ca(OH)2 most commonly used]
•
Vitality should be preserved
•
If planning to re-enter, wait 6-8 weeks for tertiary dentin; remove remaining caries, restore; eliminate microleakage
IPT Technique •
Need to re-enter controversial
•
Radiolucency beneath IPT decreased in size or did not increase under Dycal/ZOE in majority of cases (Maltz et al 2007)
•
Success rate up to ~90%
•
Stepwise excavation leads to fewer pulp exposures in young permanent teeth
357
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
IPT in Primary Teeth •
Recent data: •
•
•
•
IPT (GIC) had higher success rate than FMC pulpotomies Farooq et al 2000; Vij et al 2004 total etch technique more successful in primary molars than IPT (Ca[OH]2) Falster et al 2002 IPT (Ca[OH]2) success rate in primary molars was 95% in retrospective study Al-Zayer et al 2003 Carious dentin undergoes mineral gain when sealed in IPT Oliveira et al 2006
Indirect Pulp Treatment •
Vij et al 2004 0-1 year
1-2 years
2-3 years
>3 years
FMC success
95%
84%
76%
70%
IPT success
98%
96%
94%
94%
Treatment of deep dentinal lesions with caries control procedures prior to FMC or IPT improved the success of both.
358
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Direct Pulp Cap •
Indications •
•
•
Small mechanical or traumatic exposure in primary teeth with normal pulp Small carious or mechanical exposure in permanent teeth with normal pulp
Contraindicated for carious exposure in primary teeth
Direct Pulp Cap: Objectives (AAPD) •
Preserve vitality
•
No post-treatment signs or symptoms
•
Pulp healing
•
Tertiary dentin
•
No pathologic changes
•
No harm to successors
•
Continued apexogenesis for permanent teeth
359
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pulp Capping Agents •
Ca(OH)2 still widely used and taught
•
ZOE - chronic inflammation
•
•
Mineral trioxide aggregate (MTA; permanent teeth) Total etch technique
Direct Pulp Cap - Bleeding • •
•
•
Success inversely related to bleeding at site Debris at exposure site: clean out with saline or anesthetic to prevent inflammation caused by dentinal chips; keep pulp moist Clot will prevent contact of material with the pulp; clot may release products that attract bacteria Success rate up to 80-90%; 50% if pulp inflamed
360
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Biocompatibility of Materials with Dental Pulp •
Pulpal response to contact with a variety of materials is severe inflammation when bacterial microleakage occurs
•
Biocompatibility with dental materials allows pulpal healing in absence of microleakage
•
Dentin bridge formation possible even in contact with sterile food in germ-free environment
•
Biocompatibility is a function of microleakage
Partial Pulpotomy - Criteria •
No/recent pain of short duration
•
No swelling, mobility, rxn to percussion
•
No internal/external resorption, changes in PDL, radiographic abnormalities
•
Pulp exposure 1-2 mm, bleeding stops <1-2 min
•
Inflammation, infection superficial only
•
Only superficial pulp removed Mass et al 1995
361
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Partial Pulpotomy Technique •
Enlarge exposure
•
Partial extirpation
•
Place capping material
•
Place leak-proof seal •
ZOE covered with GIC or CH if resin composite is to be used
Partial Pulpotomy – Objectives (AAPD) •
Remaining pulp stays vital
•
No adverse clinical signs/symptoms
•
Continued apexogenesis in immature teeth
362
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Partial Pulpotomy •
Advantages • • • • • • • • •
removes inflamed, infected portion of pulp preserves cell-rich coronal pulp facilitates washing away carious debris allows better contact with more material increases healing potential physiologic apposition of cervical dentin no need for RCT natural color/translucency preserved maintenance of vitalometer response
Pulpotomy for Primary Teeth •
Indications •
• • •
•
deep lesion adjacent to pulp that is normal or reversibly inflamed, or pulp exposed by trauma coronal tissue can be amputated remaining radicular tissue vital (clinically and radiographically)
Objectives • • • •
preserve vitality of radicular pulp no adverse signs or symptoms no radiographic changes no harm to succedaneous teeth
363
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Technique •
Prepare tooth for restoration (typically SSC)
•
Excavate carious dentin, unroof pulp chamber
•
Amputate coronal pulp
•
Hemostasis (diagnostic value)
•
Treat remaining pulp (medicament/energy)
•
Seal and restore
Pulpotomy: Clinical Indications •
Mechanical/carious exposure, trauma
•
Inflammation limited to coronal pulp
•
Absence of spontaneous pain (?)
•
•
Absence of swelling or alveolar abscess formation Restorable tooth
364
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pulpotomy Contraindications •
•
•
•
History of unprovoked pain (?)
•
Presence of fistula or swelling
•
Evidence of necrotic pulp
•
Uncontrolled pulpal hemorrhage
•
Periapical or bifurcation radiolucency Pathologic resorption Dystrophic calcification More than 1/3 root resorption
Pulp Treatment Medicaments 1883 At a meeting of the American Dental Association in St. Louis in 1883, Dr. F.A. Hunter claimed a 98% success rate using a pulp capping agent made from one pint of sorghum molasses and one pound of the droppings from the English sparrow.
365
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Categories of Medicaments •
Fixatives •
•
•
Ca(OH)2
Palliative sealers •
•
FMC, glutaraldehyde
Mineralizing and/or bacteriostatic agents •
•
•
erythromycin, others
Tissue healing agents
•
•
mineral trioxide aggregate
epi, ferric sulfate, aluminum chloride
Antibiotics/Antimicrobials
•
ZOE
Obturators •
Coagulants
•
collagen, BMP
Glucocorticoids
•
•
corticosteroids
Medicament Combinations •
Vitapex •
•
Maisto’s paste •
•
iodoform, Ca(OH)2 iodoform, parachlorophenol, camphor/menthol
Ledermix • •
dimethylchlorotetracycline triamcinolone
366
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Formocresol Pulpotomy Success Rates Range of success rates in literature: 62-100% depending on study and criteria used Clinical>Radiographic>Histological
Formocresol pulpotomies may be empirical clinical successes, but histologically they are failures to one degree or another.
Actions of Formocresol •
Composition (open to interpretation) •
•
19% formaldehyde, 35% cresol in vehicle of 15% glycerin and water
Fixation with progressive fibrosis • • •
acidophilic zone: fixation pale staining zone: atrophy broad zone of inflammatory cells
•
Bactericidal - biggest benefit?
•
No dentin bridging
367
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Fixation Preserves cellular detail Minimizes alteration from tissue in living state Inhibits autolytic changes and bacterial growth Coagulates protoplasm rendering it insoluble Increases affinity for particular stains
Dr. Suzi Seale
Histology Glutaraldehyde pulpotomy in monkey incisor
One week
Three weeks
368
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Effects on Succedaneous Teeth Pruhs et al (1977)
Rolling and Poulsen (1978)
It is possible that enamel defects in premolars were caused by inflammation prior to the pulpotomy
Dilution of Formocresol •
1:5 dilution •
1 part FMC, 4 parts vehicle (3 parts glycerin, 1 part distilled water)
•
Histology and clinical success comparable to full strength
•
Neither produces ideal histology
•
Long-term clinical success of 1:5 still questioned by some
369
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Glutaraldehyde •
Powerful fixing agent
•
Antibacterial
•
Large molecule
•
Minimal systemic distribution
•
Low antigenicity
•
Treatment concentration 2-5%
Ferric Sulfate •
FS forms protein complex, occludes capillaries; no antibacterial action
•
Must assume healthy radicular pulp (?)
370
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Systematic Review of Ferric Sulfate •
Loh et al. 2004; 3 RCTs, 10 CTs analyzed
•
Clinically, FS significantly more successful than formocresol: OR 1.95
•
Radiographically, no difference between medicaments: OR 0.90
•
Conclusion: Pulpotomies performed with either material are likely to have similar clinical/radiographic success.
Meta-analysis of Ferric Sulfate vs FMC •
6 prospective controlled trials
•
Both treatments similar in clinical outcomes, radiographic success, other findings
•
Overall clinical success of FS: 78—100%
•
Overall radiographic success of FS: 42-97%
371
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Mineral Trioxide Aggregate •
Gray: tricalcium silicate, tricalcium phosphate, tricalcium oxide, Fe, Al
•
Broadly similar to Portland cement
•
White: more esthetic
•
Hydrophilic particles set in presence of moisture 3-4 hours; compressive strength similar to IRM
•
Better seal than amalgam
•
Pricey (~$325/box of 5 1g packets)
MTA vs FMC Controlled Trials •
Aeinehchi et al 2007 •
•
•
significantly more teeth with root resorption in FMC group no root resorption in MTA group
Noorollahian 2004 •
no significant difference in radiographic success rates between FMC and MTA
372
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Sodium Hypochlorite •
Vargas et al 2006
•
Compared NaOCl (N=32) and FS (N=28)
•
12 months: •
NaOCl: 100% clinical, 79% radiographic success
•
FS: 85% clinical, 62% radiographic success
Non-pharmacotherapeutic Pulpotomy •
Basic principles: • •
amputate infected coronal pulp treat remaining radicular pulp by controlled energy
•
neutralize residual infectious process
•
avoid dystrophic pulpal changes
•
avoid breakdown of periradicular supporting tissues
373
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Electrosurgical Pulpotomy
Disadvantages Advantages heat leads to tissue destruction quick persistent inflammation self-limiting energy cannot be isolated to surface hemostasis root resorption good visibility pulp inflammation no systemic effect
RCT of Primary Pulpotomy Techniques •
Huth et al 2005
•
Prospective randomized controlled trial
•
200 primary molars, 107 patients
•
Treatments: • • • •
50 dilute FMC (control group) 50 Er:Yag laser 50 calcium hydroxide 50 ferric sulfate
374
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Huth et al 2005 •
Pulp hemostatis was an inclusion criterion
•
All treatment followed by ZOE, GIC
•
Final restoration: SSC or composite resin, based on amount of tooth destruction
•
Clinical and radiographic follow-up at 6, 12, 18, and 24 months •
•
2 blinded examiners (neither was an operator)
Some teeth lost to follow-up (exfoliation, patient drop-out): final sample – 175
Huth et al 2005 Total success rate %
12 months
24 months
FMC
96
85
Laser
93
78
Ca(OH)2
86
53*
Ferric sulfate
86
86
Clinical success rates were higher in all cases; *statistically significantly different
375
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Huth et al 2005 •
Only calcium hydroxide performed significantly worse than FMC (p<.001) at 24 months
•
Larger sample size, more statistical power, needed to determine whether the nonsignificant differences between FMC, laser, and ferric sulfate are, in fact, truly not different
Pulpotomy in Permanent Teeth Indications: can remove infected or affected tissue; time/money constraints prevent RTC (closed apices)
376
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Agents for Permanent Tooth Pulpotomy •
Ca(OH)2 most widely used
•
Formocresol • •
•
Glutaraldehyde •
•
limited circumstances short-term preservation of permanent molar not well tested in permanent teeth
MTA
Apexogenesis •
Encourage continued root formation
•
Promote tertiary dentin formation
•
No evidence of inflammatory resorption
•
No evidence of root and periradicular pathosis
•
Immediately obturate canal or observe?
377
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MTA vs Ca(OH)2 Pulpotomy •
El Meligy & Avery 2006
•
Immature permanent teeth 15 received MTA 15 received Ca(OH)2
• •
2 Ca(OH)2 failures at 6 & 12 months
•
pain, swelling
•
•
No MTA failures
•
MTA judged to be suitable alternative to Ca(OH)2
Non-vital Pulp Therapy •
Indications for primary teeth •
irreversible pulpitis
•
pulpal necrosis
•
•
excessive hemorrhage from radicular pulp in tooth planned for pulpotomy minimal/no root resorption
378
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Non-vital Pulp Therapy for Primary Teeth •
Pulpectomy •
•
necrotic pulp/irreversible inflammation abscessed (in very limited instances - strategic importance of tooth is major consideration)
Primary Tooth Pulpectomy Other indications: tooth of strategic/esthetic importance restorable poor chance of success with vital therapy adequate root remaining cooperative patient
Reserve for incisors, 2nd molars
379
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Primary Pulpectomy Technique Remove coronal pulp Remove radicular pulp remnants up to size 35 file Irrigate repeatedly; dry; treat with medicament?; one-visit, two-visit? Obturate with resorbable paste
Criteria for Ideal Obturant •
Antiseptic
•
Resorbable
•
Harmless to adjacent tooth germ
•
Radiopaque
•
Non-impinging on erupting permanent tooth
•
Easily inserted and removed
•
Biocompatible
380
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Zinc Oxide and Eugenol Most widely used to date Biocompatibility is questionable; effects are related to concentration of free eugenol Resorbability is questionable
Calcium Hydroxide in Pulpectomies •
Good biocompatibility
•
Longevity of material and action is questionable - too resorbable
•
Other materials • • •
•
Kri-1 paste Vitapex (iodoform, calcium hydroxide) Ciprofloxacin/metronidazole/minocycline (Takushige et al 2004) Endoflas (Moskovitz et al 2005)
381
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ZOE vs. Vitapex •
Mortazavi & Mesbahi 2004
•
29 ZOE, 26 Vitapex; randomly assigned
•
3- and 10-16 mo follow-ups
•
More short fills with ZOE; more overfills with Vitapex
•
Overall success at 10-16 months • • •
Vitapex 100% ZOE 78% statistically significant
Pulpectomy Success Rates •
Success rates in molars & incisors comparable
•
Predictors of success: • •
•
• •
minimal root resorption ZOE fill to or slightly short of apex
Enamel defects in succedaneous teeth (19%) related to pre-tx root resorption Extraction of molars required about 20% of time 20% chance of altering eruption path of succedaneous tooth
382
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FS Pulpotomy vs. Pulpectomy •
Casas et al 2004
•
Compared FS pulpotomies (n=15) and ZOE pulpectomies (n=14)
•
3-year survival probabilities: • • •
•
0.62 for FS pulpotomies 0.92 for ZOE pulpectomies statistically significant difference
Pulpectomies demonstrated significantly greater survival than FS pulpotomies after 3 years
Systematic Review of Pulp Therapies •
Nadin et al, Cochrane Database, 2004
•
82 studies identified: FMC, FS pulpotomies; electrosurg; ZOE pulpectomy
•
Conclusion: no reliable evidence to support superiority of one type of pulp treatment for primary molars
383
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Non-vital Tx: Young Permanent Teeth •
Objectives: • •
•
promote continued apical development achieve apical closure (Frank technique)
Technique: apexification • •
•
necrotic tissue removal short of apex place agent (calcium hydroxide) to achieve closure or apical stop MTA being used in place of calcium hydroxide
MTA vs Ca(OH)2 Apexification •
El Meligy & Avery 2006
•
Necrotic permanent teeth requiring root-end closure • •
15 received MTA 15 received Ca(OH)2
•
Recalled at 3, 6, and 12 months
•
2 Ca(OH)2 failures at 6 & 12 months •
•
persistent periradicular inflammation
No MTA failures
384
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MTA Apexification Case Series •
57 permanent teeth, open apices
•
Single appointment MTA tx followed by gutta percha obturation
•
Blinded evaluation of films with >2 yrs f/u
•
95% of apical lesions demonstrated complete or progressive healing
•
Apical closure seen in 26% Simon et al 2007
•
Pulpal Revascularization of Immature Necrotic Permanent Teeth Assumption: •
•
Goal: •
•
apical portion of pulp may still be vital encourage this vital tissue to migrate coronally
Procedure: • •
disinfect root canal place triple antibiotic paste (ciprofloxacin, metronidazole, cefaclor)
385
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Pulpal Revascularization of Immature Necrotic Permanent Teeth •
Procedure, cont’d • • • •
•
remove paste after several weeks induce bleeding by stimulating tissue beyond apex allow clot to reach CEJ cover with MTA, restore
Resulting clot acts as scaffold to aid growth of new tissue in canal
Pulpal Revascularization of Immature Necrotic Permanent Teeth
386
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Pulpal Revascularization of Immature Necrotic Permanent Teeth
Expect continued root lengthening and thickening Pulp responsive to cold stimulus
387
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388
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Oral Pathology and Oral Medicine Andrew L. Sonis, D.M.D. Senior Associate in Dentistry Children’s Hospital, Boston Clinical Professor Harvard University School of Dental Medicine Private Practice Newton, Massachusetts
Correction in manual: p. 73 & Alveolar bone: & Should be Intramembranous bone formation, not Endochondral bone formation
389
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Developmental variations of normal oral structures
Epstein’s Pearls
&Epithelial inclusion cyst &Palatal midline
390
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Bohn’s Nodules
&Buccal and lingual aspect of alveolus &Ectopic mucous glands
Dental Lamina Cysts
&Crest of the alveolus &Remnants of dental lamina
391
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Hyperplastic foliate papillae &Lateral border of tongue &Easily traumatized &Normal lymphoid tissue
Fordyce granules & Ectopic sebaceous glands in oral mucosa & Elevated yellowish nodules & Maybe discrete or confluent & Common sites: buccal mucosa, upper lip
392
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Median rhomboid glossitis & ? Result of anomalous vascularity vs. persistence of tuberculum impar & Usually asymptomatic, but may cause soreness/burning & Surface flat or slightly raised & Color varies from pale pink or whitish to bright red & Candidial infection present ~ 40%
Fissured tongue & Rarely seen before age 4 years & ? Genetic (A.D.) & 3-5% frequency, but higher in mentally retarded population & Maybe associated with Melkersson-Rosenthal syndrome
393
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Leukoedema & Most commonly seen in blacks & Grayish-white thickening of buccal mucosa & Usually bilateral & Extensive intracellular edema of epithelium
Idiopathic osteosclerosis & Well-defined radiopacity in the toothbearing area of jaw & No surrounding radiolucent space & Not typical of any other condition & Mandibular premolar/molar area most common & Maybe related to root apex, but normal PDL
394
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Stafne bone defect &Cyst-like radiolucent area near angle of mandible &Indentation of bone containing extension of submandibular gland
Bifid tongue & Developmental malformation & May coexist with orofaciodigital syndrome & Complete form requires surgical reconstruction
395
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Bifid Uvula
&Minor expression of cleft palate &Must r/o sub mucous cleft &May require surgical correction
Macroglossia
396
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Discrete Swellings or Lumps/Bumps &Congenital &Inflammatory &Traumatic &Neoplastic &Others
Lingual thyroid & Redundant thyroid tissue in tongue & Hypothyroidism~20 % & ~70% lack normal thyroid tissue in neck
397
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Lingual thyroid & Redundant thyroid tissue in tongue & Hypothyroidism~20 % & ~70% lack normal thyroid tissue in neck
Vascular Malformations &Present at birth &Become clinically evident in late infancy/early childhood &May increase in size following trauma, infection, or endocrine changes &~35% associated with skeletal changes
398
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Lymphangioma &Diffuse vs. discrete &Tongue most common site &Surface often papillary or vesicular &Tx: surgical excision
Hemangioma & Common vascular tumor of infancy & Usually appear early in infancy, grow rapidly until age 6-8 mos., then slowly involutes & Blanch on pressure & Generally do not involve the adjacent skeletal tissue & Tx: watch and wait
399
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Hemangioma: Indications for Treatment &Kasabach-Merritt syndrome with severe thrombocytopenia (<40,000) &Lesions interfering with function &Recurrent bleeding, ulceration, infection &Rapidly growing lesion that causes facial distortion
Infection/abscess & Uncommon, but may follow traumatic injury & May represent secondary infection of neoplasm/cyst & Tx: remove source of infection/antibiotics
400
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Tongue pyogenic granuloma & Common reactive lesion & Painless, nodule, red lesion & Typically pedunculated with ulcerated surface & Tx: surgical excision
Tongue trauma due to neurocomatose chewing
401
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Tongue trauma: Riga-Fede syndrome &Chronic trauma from primary incisors &Typically ulcerated lesion on tip of tongue &Tx: smooth incisal edges
Fibroma & Most common tumor of oral mucosa & Often the result of chronic trauma & Typically painless, firm, sessile or pedunculated & Tx: surgical excision
402
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Papilloma & Human papilloma virus & Exophytic, well circumscribed & Usually pedunculated with either finger-like projections or cauliflower surface & R/O condyloma acuminatum & Tx: surgical removal
Neurofibroma & Rare in childhood & Tongue and buccal mucosa commonly affected & Maybe solitary or multiple (neurofibromatosis) & Tx: surgical excision
403
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Neurofibroma & Rare in childhood & Tongue and buccal mucosa commonly affected & Maybe solitary or multiple (neurofibromatosis) & Tx: surgical excision
Neurofibromatosis & A.D. ( ~50% spontaneous mutations) & Peripheral form most common ~90% & ~70% have oral involvement & Café-au-lait spots, subcutaneous neurofibromas, Lisch nodules
404
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Neurofibromatosis & A.D. ( ~50% spontaneous mutations) & Peripheral form most common ~90% & ~70% have oral involvement & Café-au-lait spots, subcutaneous neurofibromas, Lisch nodules
John Merrick: The Elephant Man
405
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Granular-cell Tumor & Uncommon benign lesion & Tongue most common site (25%) & Typically solitary, asymptomatic, welldefined, sessile lesion & Tx: surgical excision
Tongue Foreign Body
Fractured palatal cusp
406
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Exophytic Lesions in BMT
Diffuse Swelling of the Tongue
&Congenital &Inflammatory &Traumatic &Others
407
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Just a “BIG” Tongue
Positive Gorlin sign
Ehlers Danlos Syndrome & Collagen defect (procollagen) & Classic form: & & & &
Loose jointedness Fragile, bruisable skin Laxity of skin “cigarette paper” scars
& Dental: oral bleeding, periodontal disease, delayed healing
408
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Ehlers Danlos Syndrome
bruisability
Loose jointedness
Down syndrome & Chromosomal disorder: trisomy 21 & 1:800 births average & Commonest identifiable cause of intellectual disability & Risk increases with maternal age
409
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Maternal Age and Risk of Down Syndrome
Medical Conditions Associated With Down Syndrome
& Congenital heart disease ~50% & ECD, VSD, TOF
& Gastrointestinal anomalies ~15% & & & &
Tracheoeosophageal fistula Pyloric stenosis Duodenal atresia Celiac disease
& Increased incidence of ALL (20X non-DS) & Mental retardation
410
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Dental conditions associated with Down syndrome
& Relative macroglossia & Microdontia & Oligodontia & Class III malocclusion & Open-mouth posture & Fissured tongue & Decreased caries rate (historical)
& Increased periodontal disease & Delayed eruption and over-retained teeth & Atypical root morphology & Abnormal palate & Enamel hypoplasia
Hypothyroidism (Cretinism) & Short stature & Mental retardation & Delayed eruption & Enamel hypoplasia & Generalized edema & Tx: replacement therapy
411
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Hypothyroidism (Cretinism) & Short stature & Mental retardation & Delayed eruption & Enamel hypoplasia & Generalized edema & Tx: replacement therapy
Mucopolysaccharidoses & Hurler’s syndrome(prototype) & Progressive infiltration of tissues by mucopolysaccharides & Coarse facies, large head & Spacing of teeth & Tx: bone marrow transplantation
412
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Cystic Hygroma & Large diffuse lymphangioma & Extends from tongue into neck & May cause dysphagia or respiratory embarrassment & Tx: plastic surgery
Cystic Hygroma
413
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Cystic Hygroma
Cystic Hygroma
414
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Cystic Hygroma
Inflammatory Causes of Diffuse Tongue Swelling & Infection & Allergic reaction/irritation & Ludwig’s angina (rare in children)
415
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Multiple Endocrine Neoplasm, type 2B &Oral mucosal neuromas &Medullary cell carcinoma of the thyroid &Pheochromocytoma
Multiple Endocrine Neoplasm
416
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Angioedema & Allergic form maybe precipitated by drugs, foods, etc. & Hereditary form A.D. & Most are idiopathic & Tx: & Allergic formantihistamines & Hereditary form: androgens
Beckwith-Wiedeman syndrome & Macroglossia & Omphalocele or umbilical hernia & Cytomegaly of adrenal cortex & Post-natal somatic gigantism & Severe hypoglycemia & Neoplasms (nephroblastoma most common) & Very prone to OSA
417
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Indications for Tongue Reduction &Airway difficulty &Speech difficulty &Dentoalveolar protrusion &Esthetics &Drooling &Recurrence of openbite/bimaxillary protrusion/spacing
Surgical tongue reduction
418
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Common Causes of a Sore Tongue &Ulceration &Geographic tongue &Median rhomboid glossitis &Foliate papillitis
Common Causes of a Sore Tongue &Ulceration &Geographic tongue &Median rhomboid glossitis &Foliate papillitis
419
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Common Causes of a Sore Tongue &Ulceration &Geographic tongue &Median rhomboid glossitis &Foliate papillitis
Glossitis & Generalized erythema and depapillation & Anemia & Candidiasis & Vitamin B deficiency & Radiotherapy & Depression & Diabetes & Hypothyroidism
420
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Sublingual Swelling/Mass of the Tongue & Trauma & Ranula & Abscess & Hemorrhage & Salivary gland infection & Dermoid cyst & Salivary gland tumor & Other
Ranula & Mucous retention & Typically painless & Dome-shaped, soft swelling of normal or blue color & Involves submaxillary or sublingual gland & Tx: excision or marsupialization
421
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Sublingual Dermoid Cyst
Sublingual Dermoid Cyst
422
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Sublingual Dermoid Cyst
Cheeks/Buccal Mucosa
423
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Trauma &Acute or chronic mechanical injury &Dx based on history and clinical findings &Generally heals in 7-10 days &Tx: symptomatic
Candidiasis & Several forms:
& Acute pseudomembranous & Hyperplastic & Erythematous & Common oral organism & Newborns may acquire infection from mother & Increased susceptibility with long-term antibiotics, corticosteroids, immunosuppression & Tx: nystatin, chlortrimazole, fluconazole, amphotericin B
424
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Candidiasis (Erythematous form)
Candidiasis (hyperplastic form)
425
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Nystatin (topical) & Neonate: 100,000 U PO qid & Continue 48h after resolution
& Infant: 200,000 U PO qid & Continue 48h after resolution
Fluconazole (systemic) &Loading dose: 6mg/kg PO x 1 &3mg/kg qd x 14 days &Be aware of drug interactions & Budesonide & Theophylline & Erythromycin
426
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White Sponge Nevus & A.D. & Buccal mucosa, tongue, floor of mouth & Symmetrical, bilateral white thickened plaques & Lesions maybe present at birth
Frictional Keratosis/Cheek Biting & Hyperkeratosis secondary to irritation & Smokeless tobacco products & White hyperkeratotic lesions & Early changes erythematous & Snuff > chewing
427
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Lupus Erythematosus & Immunologically-mediated disorders involving connective tissue & Discoid form (rare): & Skin disorder & ~20% have oral involvement & Systemic form (more common in children): & Arthralgia and rashes common & Affects many organ systems & Stomatitis common (3040%) & Tx: steroids
Systemic form
Lupus Erythematous
428
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Lupus Erythematous
“Moon Facies”
Contact Dermatitis: Two Major Types & Irritant & I.e. harsh soaps, chemicals: direct toxic effect upon contact with mucosa/skin & Allergic contact dermatitis: T-cell mediated immune reaction requiring sensitization to specific antigen
429
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Burns (thermal, chemical) & Common & White appearance due to necrotic tissue & Associated with a number of chemicals, i.e., ASA, formocresol, phosphoric acid, phenol, etc.
Chemical Burn
Thermal Burn
“Pizza Palate”
430
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Lip Lesions
Causes of Angular Stomatitis & Candidiasis & Common finding in HIV infection
& Staphylococcal, streptococcal, or mixed infections & Nutritional deficiencies & Crohn’s disease & Anemia
431
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Crohn’s Disease & Chronic inflammatory granulomatous disease & Affects entire G.I. tract (mouth to anus) & Etiology unknown, likely autoimmune & Oral lesions ~30% & Facial swelling & Ulcerations & Mucosal tags & Tx: antibiotics; 5-ASA; corticosteroids
Crohn’s Disease: mucosal tags
Cobblestone appearance
432
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Oral concerns in patients with inflammatory bowel disease & Increased risk of aphthous ulcers & Increased risk of periodontal disease & Steroid therapy & Patient maybe immunosuppressed & Drug therapy may cause gingival hyperplasia (cyclosporin)
When does adrenal-pituitary axis suppression occur in prolonged steroid treatment?
& Pharmacological doses of steroids used for < 10 days & Relatively small risk of permanent adrenal insufficiency & Typically full recovery in 6-12 months
& Daily use > 30 days & High risk of transient or permanent adrenal suppression
& Alternative day & Very low risk
& Inhaled steroids & Essentially no risk
433
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Who Needs Steroid Bump/Supplement? &Patients under stress &Fever > 101º &Surgery, I.e. third molar extractions &General anesthesia &Fractures &Prolonged fasting/vomiting
Causes of Lip Ulcerations/Vesicles/Blisters & Herpes simplex & Burns & Herpes zoster & Erythema multiforme & Epidermolysis bullosa & Impetigo & Allergic cheilitis
434
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Herpes simplex &Herpes labialis & Reactivation of HSV & Recurrent & Antiviral agents of limited value
Herpes labialis
1 week f/u
435
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Penciclovir (Denavir)
Denavir Promo
436
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Burns & Maybe electric, thermal, chemical & Treatment directed at preventing contraction of orafice
Varicella/Zoster & Varicella zoster virus (chicken pox) & Crops of pruritic vesicles on skin and mucous membranes & Vesicles may precede fever & Begins on trunk and spreads to limbs/face
& Infectious 24 hrs. before to 6-7 days after vesicles appear & Incubation period may last up to 20 days & Resolves in 7-10 days & Tx: palliative and supportive
437
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Herpes Zoster
Erythema Multiforme & Erythematous macules, papules, bullae, and erosions & Possible allergic etiology (drug reaction) & Target lesions & May have ocular, genital lesions (Stevens-Johnson syndrome) & Tx: palliation; steroids
438
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Erythema Multiforme (StevensJohnson syndrome)
Epidermolysis Bullosa &Hereditary vesiculobullous disease of skin and mucous membranes &E.B. simplex: most common form & A.D.
&Junctional E.B.: several subtypes & A.R.
&Dystrophic E.B. & Dominant form & Recessive form
439
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Epidermolysis Bullosa
Dystrophic EB-dominant form
Epidermolysis Bullosa
Dystrophic EB- dominant form
440
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Epidermolysis Bullosa
Dystrophic EB-recessive form
Impetigo &Most commonly caused by: & staphylococcus aureus & beta hemolytic strep
&Tx: & Localized: topical antibiotics & Widespread: systemic antibiotics
441
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Allergic cheilitis & Maybe due to contact irritation or true allergy & Tx: remove irritant or allergen
Causes of Diffuse Swelling of Lips & Edema secondary to trauma & Angioedema & Crohn’s disease & Cheilitis granulomatosis & MelkerssonRosenthal syndrome & Lymphangioma & Hemangioma
442
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Hemangioma
7 months
12 years
5 years
Vascular malformation
S/p laser surgery
443
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Causes of Localized Swellings of the Lips & Mucoceles & Tumors & Neuroma & Neurofibroma
& Cysts & Abscesses & Insect bites & Hematomas
Causes of Lip Crusting/Desquamation & Dehydration & Febrile illness & Chemical/allergic cheilitis & Mouth-breathing & Actinic cheilitis & Erythema multiforme & Psychogenic & Drugs
444
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Soft Tissue Lesions in the Newborn/Infant
Vascular Malformations &Lymphangioma &Capillary malformation & Port wine stain
&Sturge Weber syndrome &Venous malformation & “cavernous hemangioma”
&Arterial malformation &Combined
445
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Capillary Malformation:Port Wine Stain
Capillary Malformation:Port Wine Stain
446
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Sturge Weber Syndrome & Venous angiomatosis of leptomeniges & Ipsilateral facial angiomatosis & Ipsilateral gyriform calcifications of cerebral cortex & MR & Seizures & Hemiplegia & Ocular defects & Telangiectasias
Sturge Weber Syndrome
447
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Vascular Tumors &Hemangioma &Treatment modalities: & Steroids & Interferon & Pulsed dye laser & Chemotherapeutic agents & Embolization & Surgery
Congenital Epulis & Firm pedunculated mass arising from alveolus at birth & Maxillary lateral and canine region most common & Females>males & Maxilla>mandible & Tx: surgical excission
448
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Congenital Epulis
Congenital Epulis
449
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Melanotic Neuroectodermal Tumor of Infancy & Maxilla>mandible & Destructive lesion & Submucosal pigmentation (may appear blue clinically) & # urinary VMA & 15% may recur & Tx: radical excision
Melanotic Neuroectodermal Tumor of Infancy
450
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Hemifacial Hypertrophy & Unilateral oral and facial enlargement & Usually evident at birth & Involves hard and soft tissues & Teeth may exfoliate prematurely & MR: 25% & Increased incidence of embryonal tumors & Tx: cosmetic surgery
Hemifacial Microsomia & Etiology unknown & Unilateral microtia, macrostomia, and failure of formation of mandibular ramus and condyle & 50% have cardiac pathology (PDA, VSD) & Tx: orthognathic surgery
451
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452
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453
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Dwarfism
454
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Seven major cateogories of causes of short stature 1. 2. 3. 4. 5. 6. 7.
Genetic Constitutional delay Chronic disease Chromosomal/syndromic Endocrine Psychosocial Intrauterine
Achondroplasia & 80% sporatic mutations, A.D. & 1/20,000 live births & Short limbed dwarfism & Enlarged head, depressed nasal bridge & Short, stubby, trident hands & Lordotic lumbar spine & Prominent buttocks & Protuberant abdomen
455
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Hypopituitarism & Well proportioned body & Fine, silky hair, wrinkled atrophic skin & Hypogonadism & Delayed eruption /exfoliation & Malocclusion common due to small dental arches & Panhypopituitarism may lead to other systemic problems
Causes of Hypopituitarism & Tumors & Pituitary & Parasellar & Suprasellar (hypothalamic) & Radiation & Pituitary apoplexy
& Infiltrative diseases & Granulomatous diseases & Infection & Miscellaneous
456
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Mucopolysaccharidoses
Nutritional
457
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Chrondroectodermal Dysplasia (Ellis van Crevald syndrome) &Dwarfism &Polydactaly &Ectodermal dysplasia(hidrotic) affecting nails and teeth &Multiple frenae &Cardiac defects: 50%
Chondroectodermal Dysplasia
Nail dystrophy/ Spade-shaped hand
polydactaly
458
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Chondroectodermal Dysplasia
Hallerman-Streiff syndrome (Oculo-mandibulo-dyscephaly) & Dyscephaly & Hypotrichosis & Microphthalmia & Cataracts & Beaked nose & Micrognathia & Short stature & May have supernumerary teeth/natal teeth
459
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Syndromes Characterized by Senile-like Appearance &Progeria &Werner syndrome &Cockayne syndrome &RothmundThomson syndrome
Hypothyroidism & Large posterior fontanel & Macroglossia & Hypothermia & Lethargy & Hypotonia & Bradycardia & Delayed growth and skeletal maturation
460
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Turner’s syndrome & 45X karyotype & 1/8000 & Females only & Near normal IQ & Sterile & Coarctation of aorta most common cardiac defect & Webbed neck & Enamel hypoplasia
Osteogenesis Imperfecta & Type I: mildest form & Associated with blue sclera; type IBdentinogenesis imperfecta
& Type II: perinatally lethal; severe fragility of connective tissues; multiple in utero fractures & Type III: progressive deforming; severe fragility; usually associated with in utero fractures & Type IV: similar to type I but more severe & Type IVB-dentinogenesis imperfecta
461
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Osteogenesis Imperfecta
Osteogenesis Imperfecta Blue Sclera
462
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Osteogenesis Imperfecta
Dentinogenesis Imperfecta
Self-Mutilation &Common in children with MR/psychological problems/autism &Usually due to repeated trauma
463
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Autism &Profound withdrawal &Obsessive desire for preservation of sameness &Skillful relation to inanimate objects &Retention of intelligent, pensive physiognomy &Language development not understandable &Often self-abusive, self-stimulating
Congenital Indifference to Pain &Autosomal recessive &Frequent scarring of face with mutilations of lips, tongue, arms, legs &Mild mental retardation
464
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Congenital Indifference to Pain
Lesch Nyhan syndrome & X-linked recessive & MR & Spastic CP & Choreoathetosis & Bizarre self-mutilating behavior & Absence of hypoxanthineguaninephosphoribosyltransferase
465
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Erythematous Gingiva
&Gingivitis &Periodontitis
Characteristics of Gingivitis in Children & Most common periodontal infection in children and adolescents & Generally increases with age, eruption, puberty & Rounded gingival margins accentuate inflammatory changes; tissues may become fibrotic & Generally reversible with improved oral hygiene & Does not occur to same degree as in adults with comparable plaque
466
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Systemic Factors influencing Gingivitis - Endocrine System & Puberty-associated, menstrual cycleassociated, pregnancy-associated & Presence of steroid hormones (esp. estrogen, progesterone) may amplify inflammatory changes in gingiva & Plaque is generally non-specific
Periodontitis & Prevalence of destructive disease in children & Age 5-11 years: 1-9% & Age 12-15 years: 1-46%
& Clinical attachment loss precedes radiographic bone loss & Disease threshold CEJ-ABC > 2 mm in primary dentition & Loss of lamina dura
467
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Types and characteristics of periodontal disease in children & Aggressive periodontitis & Common characteristics of localized and generalized forms: & Primary findings: $ Rapid bone loss $ Familial aggregation: (?) genetic predisposition
& Secondary findings: $ Phagocyte abnormalities $ Hyper-responsive macrophage phenotype $ Reports of disease being self-limiting
Localized Aggressive Periodontitis &Prevalence in U.S. & Overall: 0.3% &African Americans: 10% &Hispanics: 5.5%
468
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Localized Aggressive Periodontitis & Interproximal attachment loss on at least 2 permanent molars and incisors with attachment loss on no more than two additional teeth & No evidence of systemic disease
Localized Aggressive Periodontitis & Radiographic signs & vertical bone loss around molars & horizontal bone loss around incisors & rate of progression 3-5x times adult periodontitis (5 microns/day)
469
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Localized Aggressive Periodontitis & Etiology & genetic basis?; familial distribution & Actinobacillus actinomycetemcomitans and bacteroides –like species & depressed neutrophil chemotaxis in ~70% & possible defect in phagocytosis
LAP Diagnosis & History and clinical findings & & & &
Medical history Familial pattern Ethinicity Loss of attachment pattern
& Radiographic findings & Pattern of bone loss
& Microbiologic findings & DNA probing
470
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LAP Diagnosis & History and clinical findings & & & &
Medical history Familial pattern Ethinicity Loss of attachment pattern
& Radiographic findings & Pattern of bone loss
& Microbiologic findings & DNA probing
LAP Diagnosis & History and clinical findings & & & &
Medical history Familial pattern Ethinicity Loss of attachment pattern
& Radiographic findings & Pattern of bone loss
& Microbiologic findings & DNA probing
471
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LAP Diagnosis & History and clinical findings & & & &
Medical history Familial pattern Ethinicity Loss of attachment pattern
& Radiographic findings & Pattern of bone loss
& Microbiologic findings & DNA probing
Treatment: Surgical and nonsurgical root debridement with antimicrobial therapy & Scaling, curettage, root planing & Antibiotic therapy & & & &
tetracycline, doxycycline amoxicillin metranidazole metranidazole + Augmentin
& Periodontal surgery & Regenerative techniques & root conditioning, composite graft, ePTFE membranes
472
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Generalized Aggressive Periodontitis & Prevalence in U.S. & Overall: 0.15% & Higher in males and African Americans
& Generalized attachment loss including at least 3 teeth that are not 1st molars
GAP & Considered a disease of adolescents and young adults & Marked periodontal inflammation with heavy plaque and calculus & Subgingival bacterial cultures typically nonmotile, facultative, anaerobic gram (-) rods & Suppressed neutrophil chemotaxis
473
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GAP - Radiographic Signs
Generalized Aggressive Periodontitis & Treatment & surgery & scaling, root planing, curettage & Antibiotics & Does not always respond to conventional mechanical and antibiotic therapy & Culture and sensitivity maybe helpful in refractive cases
474
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c.c.: premature loss of primary incisors & 3 y.o Caucasian male is referred by pediatrician for consultation with c.c. of premature loss of primary incisors & This is the patient’s first dental visit
History of Present Illness & Mother noticed teeth becoming loose several months ago & 5 days ago teeth spontaneously exfoliated & Mother denies any history of trauma & Mother presents primary incisor which appears grossly normal with age appropriate root length
475
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Past Medical History & Prenatal history: unremarkable & Family history: unremarkabale & Hospitalizations: Patient sustained broken leg at age 30 months following a “minor fall” & Meds: none & ROS: wnl & NKA & Childhood illnesses: 2 bouts of O.M.
Clinical findings: & Extra-oral soft tissues WNL & Intra-oral soft tissues WNL & Missing primary incisors & 2+/3 mobility of remaining incisors & No mobility of remaining primary teeth
476
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Potential causes of premature loss of primary teeth & Trauma & Genetic/ hereditary & Neoplasms & Infectious & Miscellaneous
Trauma & Accidental & Psychiatric/self-abuse & Iatrogenic & Radiotherapy & Intubation
& Child abuse
477
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Genetic & Acatalasia & Chediak-Higashi syndrome & Chronic neutropenia & Dentin dysplasia & Down syndrome & Hypophosphatasia & Hypophosphatasia vitamin D resistant rickets & Lesch-Nyhan syndrome & Papillon-Lefévre syndrome
Neoplasms & Lymphoma & Leukemia & Langerhans’ cell histiocytosis & Soft and hard tissue neoplasms (benign and malignant)
478
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Infectious & Dental abscess & Osteomyelitis & Periodontitis
Miscellaneous & Acrodynia & Odontodysplasia & Vitamin C deficiency & Leukocyte adhesion deficiency-1
479
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Differential Diagnosis & Hypophosphatasia & TNSALP & Urinary phosphoethanolamine
& Papillon-LeFévre syndrome & Examine palmar/plantar surfaces for hyperkeratosis
& Periodontitis & DNA probing
Congenital Causes of Erythematous Gingiva & Hereditary hemorrhagic telangiectasia & AD & Mucosal and cutaneous telangiectases & May result in repeated bleeding episodes
& Sturge Weber syndrome
480
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Hereditary Hemorrhagic Telangiectasia
Palatal telangiectases
Acquired Causes of Erythematous Gingiva & Trauma & Physical, chemical, radiation, thermal
& Drugs: chlorhexidene, cinnamonaldehyde & Infectious: candidiasis & Desquamative gingivitis & Leukemia
481
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Causes of Gingival Bleeding & Localized disease & & & & & &
& Systemic disease & & & & & &
Periodontal disease Chronic gingivitis Chronic periodontitis ANUG HIV gingivitis HIV periodontitis
& & & &
Clotting defects Hepatobiliary disease Hemophilias Von Willebrand’s disease Vitamin K deficiency Lymphoproliferative disorders ITP Hereditary hemorrhagic telangiectasia Ehlers-Danlos syndrome Scurvy
Causes of Gingival Bleeding (cont.) &Drugs & Anticoagulants & NSAID &ASA &Non-ASA & Cytotoxics & Sodium valproate
482
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Generalized Gingival Enlargement: Congenital &Gingival fibromatosis &Mucopolysaccharidoses
Generalized Gingival Enlargement: Acquired & AML & Aplastic anemia & Drugs & Phenytoin & Cyclosporin & Calcium-channel blockers & Sodium valproate (rare) & Tranexamic acid (rare)
& Scurvy
483
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Acute Myelogenous Leukemia
Pre-chemotherapy
Post-chemotherapy
Localized Gingival Enlargement: Congenital & Fabry’s disease & Cowden’s disease & Tuberous sclerosis & Focal dermal hypoplasia & Sturge-Weber syndrome & Congenital granular cell tumor
Cowden’s Disease
484
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Tuberous Sclerosis & A.D. & Seizures (90%) & MR (60%) & Angiofibromas of face (70%) & May involve oral mucosa
& Enamel defects
Localized Gingival Enlargement: Acquired & Heck’s disease & Lymphoma & Histiocytosis & Peripheral giant cell epulis & Pyogenic granuloma & Peripheral ossifying fibroma & Papilloma & Crohn’s disease & Neoplasms
Pyogenic granuloma Peripheral Giant Cell Epulis
485
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Peripheral Ossifying Fibroma
Initial presentation
Relapse 2y later
Fibro-osseous lesions
486
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Fibro-osseous lesions
Facial Swelling/Enlargement-Hard Tissue: Congenital &Albright’s syndrome &Cherubism &Hemihypertrophy
487
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Albright’s Syndrome & Polyostotic fibrous dysplasia & Abnormal skin pigmentation & “coast of Maine” café-au-lait spots
Kennebunkport
& Endocrine dysfunction & Precocious puberty
& X-ray: ground glass
Albright’s syndrome
Ground glass
“Chinese characters”
488
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Cherubism & A.D. & Bilateral fullness of cheeks & Hypertelorism & Irregularly spaced 1º dentition & Giant cell histology & X-ray: multilocular radioluncencies
Cherubism
Multilocular radioluncencies
Giant cell histology
489
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Facial Swelling/Enlargement-Hard tissue : Acquired/Inherited
&Fibrous Dysplasia &Sickle cell anemia &Thalassemia &Neoplasms
Monostotic Fibrous Dysplasia
Sickle Cell Anemia
Hair on end
490
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Neoplasm: Neuroblastoma
“racoon eyes” Periorbital ecchymosis
Obstruction of palpebral vessels
Facial Swelling: Inflammatory &Oral infections &Cutaneous infections &Insect bites Poison Ivy
491
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Facial Swelling: Inflammatory
Odontogenic Infection
Facial Swelling: Traumatic &P/O edema/hematoma &Traumatic edema/hematoma &Surgical emphysema
492
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Facial Swelling: Immunologic
&Allergic angioedema &HANE
Facial Swelling: Immunologic
&Allergic angioedema &HANE
493
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Facial Swelling: Endocrine/Metabolic & Systemic corticosteroids & Cushing’s disease/syndrome & Myxedema & Acromegaly & Obesity & Nephrotic syndrome
Facial Swelling: Others & Cysts
Most common cause of lumps in children
& Nasolabial cyst & Soft tissue cyst & Forms deep to nasolabial fold & May cause obliteration of nasolabial fold & Tx: surgical excision
& Vascular malformations & Vascular tumors & Melkersson-Rosenthal syndrome & Crohn’s disease
494
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Nasolabial Cyst
Nasolabial Cyst
495
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Facial Swelling: Major Salivary Glands: Inflammatory & Mumps & Recurrent parotitis & Sjögren’s syndrome & Ascending sialadenitis & Recurrent sialadenitis & Sarcoidosis & Actinomycosis
Facial Swelling: Major Salivary Glands: Neoplasm
Pleomorphic adenoma
496
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Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease
Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease
497
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease
Facial Swelling: Major Salivary Glands: Others & Duct obstruction & Sialosis & Parotid & Submandibular & Mikulicz disease & Amyloidosis & HIV disease
498
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HIV Disease
&Bilateral parotid enlargement
Facial Swelling: Major Salivary Glands: Drug associated & Chlorhexidene & Phenylbutazone & Iodine compounds & Thiouracil & Catecholamines & Sulphonamides & Phenothiazines & Methyldopa
499
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Intraoral Ulcerations
Traumatic & Very common & Usually caused by accidental biting, hard foods, appliances, etc. & Less common causes: child abuse, recurrent bouts of severe coughing, oral sex
500
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Neoplastic &Carcinoma &Histiocytosis &Other malignancies Lymphoma
Recurrent Aphthous Stomatitis & Isolated & Behçet’s syndrome & MAGIC syndrome & Mouth, genital lesions/inflamed cartilage
& Sweet’s syndrome & Acute febrile neutrophilic dermatosis
& PFAPA & Periodic Fever/Aphthous ulcers/Pharyngitis/Adenitis
501
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Recurrent Aphthous Ulcers &Etiology unknown &Predisposing factors, I.e. stress &Involves “unbound” mucosa &Tx: palliative
& Minor: most common & Shallow, round ulcer & Erythematous halo & 7-10 day duration
& Major: less common & Deep, large ulcers & 3-6 week duration
& Herpetiform: rare & Clusters of small ulcers & 1-2 week duration
Apthous Ulcers: treatment modalities
502
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behçet’s Syndrome & Etiology unknown & Rare in children < 5 y & Males > females (5:1) & Oral, genital, ocular, and skin lesions & Mucosal lesions similar to aphthous ulcers & Tx: steroids
Behçet’s Syndrome
503
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Systemic Disease: Cutaneous & Erosive lichen planus & Pemphigus vulgaris & Mucous membrane/bullous pemphigoid & Erythema multiforme & Dermatitis herpetiformis & Epidermolysis bullosa
Pemphigus Vulgaris
Systemic Disease: Gastrointestinal &Crohn’s disease &Chronic inflammatory granulomatous disease &Affects entire GI tract &Etiology unknown, likely autoimmune &Oral lesions (~30%) &Tx: antibiotics, 5-ASA, corticlsteroids
504
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Systemic Disease: Connective Tissue Disease &Lupus erythematosus &Reiter’s syndrome &Mixed connective tissue disease &Felty’s syndrome Systemic Lupus Erythematosus
Oral infectious disease &Herpetic gingivostomatitis &Hand, foot, and mouth disease &Herpangina &Acute necrotizing ulcerative gingivitis
505
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Herpetic gingivostomatitis & HSV type1 typically & Oral ulcers, gingivitis, fever, lymphadenopathy & Painful & Tx: palliative and supportive
Hand, Foot, and Mouth Disease & Cocksackie virus & Epidemic & Fever, malaise, lymphadenopathy & Vesicles and ulcerations intraorally and on hands, arms, feet, legs & Duration 7-10 days & Tx: supportive and palliative
506
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Hand, Foot, and Mouth Disease
Herpangiana & Cocksackie virus & Multiple vesicular lesions involving tonsillar pillars, uvula, soft palate & Vesicles rupture leaving ulceration & Malaise, fever & Most common in summer months & Tx: supportive and palliative
507
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Acute Necrotizing Ulcerative Gingivitis & Fusospirochetes & Rare in children & Necrosis, ulceration, punched out papillae & Sore, bleeding gingiva & Foul breath & Tx: oral hygiene, topical and/or systemic antibiotics
Systemic Disease: Infective (cont.) & Histoplasmosis & Coccididioidomycosis & Blastomycosis & HIV & Gram-negative infection
& Atypical mycobacterium infection & Syphilis & Aspergillosis & Cryptocococcosis & Leishmaniasis & Tularemia & Lepromatous leprosy & Paracoccidiodomycosis
508
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Systemic Disease: Drugs
&Cytotoxics &Methotrexate &5-FU
Systemic Disease: Others & Wegener’s granulomatosis & Midline lethal granuloma & Histiocytosis & Noma Noma
509
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Histiocytosis (Langerhans Cell Histiocytosis) & Variety of disorders of mononuclear phagocytes & Acute disseminated & Infants
& Chronic & Skull lesions & Diabetes insipitus & Exopthalamus
& Acute localized & Limited to bone
Histiocytosis
510
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Generalized Pigmentation Vitiligo
Racial &No direct correlation between skin color and oral pigmentation &Typically seen only on gingiva
511
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Food/Drugs &Carotenemia &Antimalerial drugs &Minocycline &Doxorubicin Carotenemia
Food/Drugs &Carotenemia &Antimalerial drugs &Minocycline &Doxorubicin Minocycline
512
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Endocrinopathies &Addison’s disease &Nelson’s syndrome &Ectopic ACTH production Addison’s Disease
Others & Pigmentary incontinence & Albright’s syndrome & Hemochromatosis & $-thalassemia & ACTH therapy & Biliary atresia & Heavy metals
Biliary Atresia
513
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Localized Pigmentation & Ecchymoses & Ephelis & Melanoma & Melanoacanthoma & Melanotic macule & Nevus & Peutz-Jeghers syndrome & Kaposi’s sarcoma
& Neurofibromatosis & Neuroectodermal tumor & Tattoos & Epithelioid angiomatosis & Smoker’s melanosis & Acanthosis nigricans
Localized Pigmentation & Ecchymoses & Ephelis & Melanoma & Melanoacanthoma & Melanotic macule & Nevus & Peutz-Jeghers syndrome & Kaposi’s sarcoma
& Neurofibromatosis & Neuroectodermal tumor & Tattoos & Epithelioid angiomatosis & Smoker’s melanosis & Acanthosis nigricans
514
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Peutz-Jeghers Syndrome &A.D. &Perioral and intraoral pigmentation &Intestinal polyposis &Tx: intestinal polyps may occasionally require surgical intervention
Peutz-Jeghers Syndrome
515
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Soft Tissue Neck Mass/Swelling
Cervical Lymph Nodes: Inflammatory &Lymphadenitis &Glandular fever syndromes &Mycotic infections &Other infections
516
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
When to consider biopsy of lymph node: &? of malignancy, i.e. fixed node &Suspected atypical mycobacterium &Failure to respond to antimicrobials &After 3 months of observation with either no change or increase in size
Cervical Lymph Nodes: Neoplasms &Primary malignancy & Hodgkin’s disease & Leukemia & Lymphoma
&Secondary malignancy
Hodgkin’s Disease
517
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Cervical Lymph Nodes: Others &Connective tissue disease &Drugs &Mucocutaneous lymph node syndrome
Mucocutaneous lymph node syndrome (Kawasaki’s disease)
Salivary Glands &Mumps &Tumors &HIV &Sjögren’s syndrome &Sarcoidosis &Sialadenitis &Sialosis
518
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Side of Neck Swelling/Mass &Actinomycosis &Branchial cleft cyst &Parapharygeal cellulitis &Pharyngeal pouch &Cystic hygroma &Carotid body tumor
Middle of Neck Swelling/Mass & Submental lymphadenopathy & Thyroglossal duct cyst & Ectopic thyroid & Thyroid tumor & Plunging ranula & Ludwig’s angina & Dermoid cyst
Thyroglossal Duct Cyst
519
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Palatal Lesions/Malformations
Cleft Palate & Isolated (with and without cleft lip) & Associations (reported with > 100 syndromes) & Pierre-Robin sequence & Cleidocranial dysplasia & Down syndrome & Mandibulofacial dysplasia & Orofaciodigital syndrome & Apert’s syndrome & Crouzon’s syndrome
520
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cleft Palate
Pierre-Robin Sequence &Glossoptosis &Micrognathia &Cleft palate &15-25% cardiac defect
521
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cleidocranial Dysplasia & Brachycephaly & Frontal and parietal bossing & Depressed nasal bridge & Delayed closure of sutures and fontanels & Wormian bones
& Supernumerary teeth
& Clavicular defect & Delayed or failure of exfoliation of 1º teeth & Delayed eruption of 2º teeth & Highly arched palate often with submucous or complete cleft & Roots lack layer of cellular cementum
Cleidocranial Dysplasia
522
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cleidocranial Dysplasia
Wormian bones
Multiple unerupted teeth
Mandibulofacial Dysostosis (Treacher Collins Syndrome) & Defect of 1st branchial arch/pouch/groove & Microtia/malformed ears & Hypoplastic midface & Downward sloping palpebral fissures & Coloboma & Hypoplastic mandible
& 30% cleft palate
523
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
524
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Orofaciodigital Syndrome & Type 1 most common form & X-linked dominant trait & MR
& Oral findings: & Multiple hyperplastic frenae & Bifid/multilobed tongue & Hypodontia (mandibular lateral incisors) & Supernumerary teeth & Cleft palate
525
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Orofaciodigital Syndrome
“Copper-beaten Skull” &Craniosynostosis & Apert’s syndrome & Crouzon’s syndrome & Pfeiffer’s syndrome
526
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Apert’s Syndrome & Syndactaly & Shallow orbits, ocular hypertelorism & Parrot nose & 30% cleft palate & Mental retardation & Crowded dentition & V-shaped maxilla & Class III with openbite
Apert’s Syndrome
Syndactaly
527
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Crouzon’s Syndrome & Brachycephaly & Maxillary hypoplasia & Ocular hypertelorism & Parrot nose & Crowded dentition & V-shaped maxillary arch & Exopthalamus
528
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
529
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Palatal Swelling/Lump: Developmental &Unerupted tooth &Torus palatinus &Cysts
Palatal Swelling/Lump: Inflammatory &Abscess &Cyst &Papillary hyperplasia &Sarcoidosis
530
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Palatal Swelling/Lump: Neoplasm & Minor salivary gland tumor & Fibroma & Kaposi’s sarcoma & Papilloma & Neuroma & Neurofibroma
Kaposi’s sarcoma
Halitosis & Oral sepsis & Food impaction & Chronic dental/periodontal sepsis & ANUG & Dry socket & Pericoronitis & Xerostomia & Oral ulceration
531
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Halitosis: Nasopharyngeal Disease
& Foreign body & Sinusitis & Tonsillitis & Neoplasm
Halitosis: Nasopharyngeal Disease
& Foreign body & Sinusitis & Tonsillitis & Neoplasm
532
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Volatile Foodstuffs
&Garlic &Onions &Highly spiced foods
Drugs & & & & & & & & & & &
Solvent abuse Alcohol Smoking Choral hydrate Nitrates/nitrites Dimethyl sulphoxide Disulphiram Cytotoxic drugs Phenothiazines Amphetamines Paraldehyde
533
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Radiographic Key Concepts
See what’s under the surface…
Radiographic Description and Interpetation 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Shape Size Anatomic location Degree of lucency or opacity Recognizable structure(s) Single or multiple Unilocular or multilocular Quality of border Cortical involvement Lamina dura PDL Root resorption VCU School of Dentistry, Dept. of Oral Pathology
534
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Differential Diagnosis of Radiographic Lesions 1. Benign and Neoplastic Lesions 2. Inflammatory Lesions 3. Aggressive and Malignant Lesions
Benign Cystic and Neoplastic Lesions & Uncommon occurance & Non-tender to palpation & Slow growing (months to years) & Localized expansion & Surrounding mucosa normal & Usually etiology unknown & No systemic involvement & May interfere with tooth eruption & Subtle facial asymmetry
535
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Radiolucent lesions & Pericoronal location & Unilocular & Eruption cyst & Dentigerous cyst & Unicystic ameloblastoma
& Multilocular & Odontogenic keratocyst $ Basal cell nevus syndrome
& Ameloblastic fibroma
Eruption Cyst & Follicular cyst involving soft tissue & Most frequently involves 1º dentition/permanent molars & Bluish, painless swelling over erupting tooth & Tx: typically none necessary as cysts spontaneously rupture & Typically don’t interfere with eruption
536
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Dentigerous Cyst & Surrounds crown/attached to neck of unerupted tooth & Cystic enlargement of dental follicle & Usually asymptomatic & Tx: surgical enucleation
Ameloblastoma (Unicystic) & Most common primary tumor of jaws & 80% in molar/ramus area of mandible & Frequently contain tooth & May mimic dentigerous cyst & 10% recurrance rate & Tx: surgical excession
537
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
538
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
539
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
540
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Odontogenic Keratocyst & Most often found in mandible & Bone expansion uncommon & Pain, discharge, or paresthesia uncommon & Tx: “vigorous” enucleation & Recurrence not uncommon
541
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Common Findings in Basal Cell Nevus Syndrome & & & & & & & & & &
Enlarged occipitofrontal circumference Mild ocular hypertelorism Multiple basal cell carcinomas Odontogenic keratocysts of the jaws Epidermal cysts of skin Palmar and/or plantar pits Calcified falx cerebri Rib anomalies Spina bifida occulta of cervical or thoracic vertebrae Hyperpneumatization of paranasal sinuses
Basal Cell Nevus Syndrome
542
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Ameloblastic Fibroma & Slow growing benign tumor & Usually asymptomatic & Posterior mandible most common site & Tx: conservative excision & Note: ameloblastic fibrosarcomas have arisen in ameloblastic fibromas
Peripheral or central location & Unilocular & & & &
Traumatic bone cyst Nasopalatine duct cyst Globulomaxillary cyst Median palatal cyst
543
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Traumatic Bone Cyst & Mandible most common site & Usually asymptomatic w/o expansion & Teeth are vital & Tx: surgical intervention
Traumatic Bone Cyst pretreatment
Post-treatment
544
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
• 16yo M • Incidental finding of radiolucent lesion in posterior mandible • Healthy
545
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
546
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
547
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Traumatic bone cyst •First described by Lucas in 1929 •Hemorrhagic bone cyst, solitary bone cyst, unicameral bone cyst, extravasation cyst, idiopathic bone cavity •Pathogenesis not understood – Trauma • Intraosseous hematoma'enzymatic clot liquification leads to bone resorption… • subperiosteal hematoma compromises blood supply'osteoclastic bone resorption Xanthanaki AA, Konstantinos CI, et al. Traumatic bone cyst of possible iatrogenic origin: Case report and review of the literature. Head and Face Medicine. 2006; 40:1-5.
Nasopalatine Duct Cyst &Derived from epithelium of nasopalatine duct &May perforate labial plate &Teeth are vital
548
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Nasopalatine Duct Cyst
Globulomaxillary Cyst & Originally thought to occur due to epithelial entrapment & Most likely radicular cyst & May cause displacement of teeth & Tx: surgical enucleation
549
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Globulomaxillary Cyst
Median Palatal Cyst & Fissural cyst & Epithelial entrapment & Maybe confused for posteriorly positioned nasopalatine duct cyst & Firm of flucuant swelling of midline of hard palate & Tx: surgical excision
550
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Median Palatal Cyst
Unilocular when small/multilocular when large & Central giant cell granuloma & Aneurysmal bone cyst & Central hemangioma & Odontogenic myxoma & Cherubism
551
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Central Giant Cell Granuloma & Painless swelling sometimes causing displacement of teeth & Posterior mandible most common site & Tx: curettage & R/O other jaw lesions with giant cell histology
J.L. & 4 yo male & Otherwise healthy & Left mandibular swelling & No pain or paresthesia
552
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
553
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
554
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
555
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
556
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Aneurysmal bone cyst & Eccentric ballooning of mandible & 50% associated with pain & Associated with concurrent lesion
Aneurysmal bone cyst & Eccentric ballooning of mandible & 50% associated with pain & Associated with concurrent lesion
557
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HS 6 yo female
558
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
559
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Central hemangioma & Vague margins & Gingival bleeding, bruit, pulsation & Tooth mobility & Potentially life threatening
560
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Odontogenic myxoma & Faint radiopaque striations & Posterior mandible & Moderate recurrance rate
A.L.
561
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
562
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
563
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
564
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cherubism & Bilateral & “Burns out” over time
565
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
A.B. & Painless midface swelling & 4yo F & Healthy
2005
2005
566
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
567
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
2005
2007
2005
2007
568
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Mixed radiolucent-radiopaque & Pericoronal location & Calcifying odontogenic cyst & Adenomatoid odontogenic tumor & Ameloblastic fibro-odontoma
& Periapical or central location & Central ossifying fibroma & Juvenile ossifying fibroma
Calcifying Odontogenic Cyst & Affects both maxilla and mandible & Painless swelling/ may expand & Radiographic: may contain scattered radiopacities & 25% associated with odontoma & Tx: surgical excision
569
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Adenomatoid Odontogenic Tumor & 90% appear before 30 y & 60% form in anterior maxilla & 75% associated with unerupted tooth (canine) & Radiographic: may contain faint radiopaque foci & Tx: surgical excision
Adenomatoid Odontogenic Tumor & 90% appear before 30 y & 60% form in anterior maxilla & 75% associated with unerupted tooth (canine) & Radiographic: may contain faint radiopaque foci & Tx: surgical excision
570
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Ameloblastic Fibro-odontoma & Most often found in children & Typically asymptomatic and discovered radiographically & Most frequently associated woth unerupted tooth
571
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
572
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Periapical or Central Location & Central ossifying fibroma & Juvenile ossifying fibroma
573
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Central ossifying fibroma & Maybe unilocular or multilocular & Progresses from radiolucent to radiopaque
Juvenile ossifying fibroma & Multilocular & Maxilla>mandible & Aggressive
574
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
DR 8yo male
575
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
576
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
577
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Radiopaque & Pericoronal location & Odontoma
& Periapical or central location & Fibrous dysplasia & Cementoblastoma & Osteoblastoma
& Peripheral location & Torus/exostosis & Osteoma
578
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Radiopaque: pericoronal location Odontoma & Compound & Small separate denticles (tooth-like) & Anterior maxilla
& Complex & irregular mass of hard and soft dental tissues & Morphology grossly distorted
& May interfere with tooth eruption & Tx: surgical enucleation
Complex odontoma
Radiopaque: periapical or central location Fibrous dysplasia & Non-neoplastic condition & Maybe multifocal & Maxillary premolar/ molar region & Progresses from radiolucent to radiopaque & “Ground glass” appearance
& Poorly defined margins & Expansile, but “burns out” with time
579
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Radiopaque: periapical or central location Fibrous dysplasia & Non-neoplastic condition & Maybe multifocal & Maxillary premolar/ molar region & Progresses from radiolucent to radiopaque & “Ground glass” appearance
& Poorly defined margins & Expansile, but “burns out” with time
Radiopaque: periapical or central location Fibrous dysplasia & Non-neoplastic condition & Maybe multifocal & Maxillary premolar/ molar region & Progresses from radiolucent to radiopaque & “Ground glass” appearance
& Poorly defined margins & Expansile, but “burns out” with time
580
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
C.B. & 6 yof & 1 yr s/p dental extraction LUQ, ? Mesial drift of molar & Painless swelling in palate, expanding rapidly & PMH: s/p laser ablation of L temporal hemangioma & Alls: Latex, tape & FH: Brother with von Willebrand
581
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
582
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
583
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
584
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cementoblastoma & Cementum-like tissue resorbs/fuses with root & 50% patients > 20 yrs & 75% form in mandible & Usually molar or premolar & Expansion/pain common
& Tx: extraction/removal of tooth and mass
585
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Osteoblastoma & Posterior mandible & Progresses from radiolucent to radiopaque & Pain common & Vital tooth & May demonstrate “sunburst” appearance
Radiopaque: peripheral location Torus/exostosis & Non-neoplastic & Rare before age 10 y & May interfere with appliance therapy
586
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Radiopaque: peripheral location Torus/exostosis & Non-neoplastic & Rare before age 10 y & May interfere with appliance therapy
Osteoma/Gardner’s syndrome & A.D. & Multiple osteomas & Epidermoid/dermoid cysts (50-60%) & Multiple polyposis of large intestines with high malignant potential & Multiple supernumerary/impacted teeth
587
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Gardner’s Syndrome
Inflammatory lesions & Common & Tender or painful to palpation & Rapid enlargement (days to weeks) & Diffuse or localized enlargement & Red, tender, swollen mucosa & Fluctuates in size
& Drainage, sinus tract formation & Cause is often apparent & Mobile, non-vital tooth & Systemic involvement occurs with advanced infection & Trismus, occasional paresthesia & Regression with treatment of source
588
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Localized lesions & Periapical location & Radiopaque & Focal sclerosing osteomyelitis
& Radiolucent & Periapical abscess & Periapical granuloma & Periapical cyst
Focal sclerosing osteomyelitis & Chronic pulpal disease & Non-expansile & Posterior mandible & Well-defined margins
589
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Periapical abscesses associated with Dentin Dysplasia, type I & Amber colored crowns & Obliteration of pulp chamber & Poor root formation & Periapical radiolucencies around malformed roots
Periapical Granuloma & Chronic infection & Flare-ups common & Unilocular, distinct margins & Non-vital tooth
590
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Periapical Cyst & Tender? & Well-defined margin & Non-vital tooth & Granuloma develops into cyst
& Maybe expansile & May cause displacement of unerupted tooth & Variation: lateral radicular cyst
Lateral Radicular Cyst
&Forms at side of necrotic tooth as result of lateral canal
591
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pericoronal location: Paradental Cyst & Inflammatory cyst & Most frequently associated with partially erupted third molars & Mandibular buccal infected cysts & Buccal aspect of 1st molars in children & Pain/swelling & Tx: enucleation
Peripheral cortex location: Traumatic osteoma & Radiopaque & History of facial trauma & Inferior border of mandible & Maybe associated with jaw fracture & Irregular or sunburst appearance
592
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diffuse lesions & Radiolucent/infectious etiology & Acute osteomyelitis
& Mixed radiolucent/radiopaque/infectious etiology & Chronic diffuse sclerosing osteomyelitis & Chronic osteomyelitis with prolerative periostitis (Garre’s osteomyelitis)
& Mixed radiolucent/radiopaque/idiopathic & Infantile cortical hyperostosis
Mixed radiolucent/radiopaque/infectious etiology: Chronic diffuse sclerosing osteomyelitis & Chronic dental infection & Indistinct borders & Mottled bone pattern & Sequestrum common & May result in ankylosis & Posterior mandible
593
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Chronic osteomyelitis with proliferative perostitis & Chronic dental infection & Diffuse, expansile & Indistinct margins & Mottled bone pattern & “Onion skin” appearance & Posterior mandible
Proliferative periostitis
Mixed Radiolucent/radiopaque/idiopathic: Infantile cortical hyperostosis Inherited disease (A.D.) Onset prior to 6 m of age Tender, soft tissue swelling Febrile Lymphadenopathy Bilateral mandibular involvement & “Onion skin” appearance & Spontaneous resolution & & & & & &
594
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Aggressive and Malignant Lesions & Uncommon or rare & Maybe tender or painful & Moderate to rapid growth (days to weeks to years) & Diffuse enlargement & May have multifocal distribution & Mucosa red, ulcerated & Lymph nodes firm and fixed
Vital, mobile teeth Extrusion of teeth Progressive increase in size No apparent cause or source & Systemic involvement common & Frequent paresthesia/anesthesia & Trismus with advanced disease & & & &
Unifocal and radiolucent & Benign & Neuroectodermal tumor of infancy & Desmoplastic fibroma of bone & Localized histiocytosis (Eosinophilic granuloma)
& Malignant & Central sarcoma of bone & Primary soft tissue malignancies adjacent to bone
595
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Neuroectodermal tumor of infancy & Anterior maxilla & Poorly defined margins & Expansile & May displace developing teeth/tooth buds & Pigmented surface & Recurrence moderate to high
Desmoplastic fibroma of bone & Maybe multilocular & Poorly defined margins & Expansile & “Floating” toothbuds & Soft tissue extension & High recurrence rate
596
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Localized histiocytosis (eosinophilic granuloma) & Maybe multifocal & Punched radiolucencies & Usually non-expansile
& “Floating” teeth & Often soft tissue involvement
Central sarcomas of bone & Body of mandible & Paresthesia & Unilocular or multilocular & Cortical perforation
597
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Primary soft tissue malignancies adjacent to bone & Well to poorly defined margins & “Cupped” out appearance & Fine “ground glass” appearance
Primary soft tissue malignancies adjacent to bone & Well to poorly defined margins & “Cupped” out appearance & Fine “ground glass” appearance
598
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Unifocal and mixed radiolucent-radiopaque & Ewing’s sarcoma & Osteosarcoma & Mesenchymal chondrosarcoma
Ewing’s sarcoma & Posterior mandible and ramus & Painful expansion & Febrile & Leukocytosis & “Moth-eaten” appearance & Periosteal proliferation
599
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Multifocal and radiolucent & Disseminated histiocytosis & Burkitt’s lymphoma & Leukemia (AML) & Metastic disease
Disseminated histiocytosis & Multiple organ involvement & Pain & Lymphadenopathy & Gingival involvement & Premature exfoliation of teeth & “Floating” teeth appearance
600
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Disseminated histiocytosis & Multiple organ involvement & Pain & Lymphadenopathy & Gingival involvement & Premature exfoliation of teeth & “Floating” teeth appearance
E.D. •PMH: normal development •E/O: •Slight mand asymmetry •Palpable, nontender mass left preauricular area •I/O: •palpable mass left ramus •normal dentition
601
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
602
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Burkitt’s lymphoma & Posterior maxilla and mandible & Single or multiple quadrants & Painful swelling & First signs often tooth mobility & “Moth eaten” or multilocular radiocency & Periosteal bone formation
603
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Leukemia (AML) & Widespread involvement & Occasional gingival enlargement due to leukemic infiltrates & Loss of lamina dura & Diffuse, poorly defined radiolucency & Occasional periosteal bone formation
604
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
605
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Differential Diagnosis & Leukemic infiltrate & Ewing’s Sarcoma & Primary malignancy (NH Lymphoma) & Langerhans Cell Histiocytosis (E.G.) & Giant Cell Granuloma/Tumor
606
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Metastic disease & Posterior mandible & Poorly defined radiolucency & Soft tissue extention common & paresthesia
607
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Metastic disease & Posterior mandible & Poorly defined radiolucency & Soft tissue extention common & paresthesia
608
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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609
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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612
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Etiology, Epidemiology, and Prevention of Dental Disease in Children Current Concepts and Recent Evidence Dr. Steve Adair Medical College of Georgia
Definition Dental caries is a dietary carbohydratemodified bacterial infectious disease with saliva as a critical regulator.
It is the most common chronic infectious disease of childhood. Caries is a disease process, as is “diabetes.”
613
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Non-specific Plaque Hypothesis •
Microorganisms in dental caries first observed by van Leeuwenhoek in 1683
•
W.D. Miller – University of Berlin 1890 – considered all bacteria in mouth were potentially cariogenic – hence, non-specific plaque theory
•
Acid production by bacteria considered responsible for breakdown of tooth
“Miller time”
Specific Plaque Hypothesis •
1924 – Clarke isolated a streptococcus species from a cavity in a child
•
The bacteria were more oval than round – Clarke named it Streptococcus mutans for “mutation”
614
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Mutans streptococci •
1960 – Keyes “rediscovered” S. mutans
•
He demonstrated that: • specific microorganisms were responsible for caries • caries was transmissible
•
Responsible bacteria were found to comprise seven distinct species – only mutans and sobrinus are associated with caries in humans
Characteristics of MS •
Ecological niche: human oral cavity
•
Cariogenic properties • ability to produce acid (acidogenicity) • ability to withstand acid conditions (aciduricity) • adherence to teeth
615
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Characteristics of MS •
Metabolism yields: • acids, primarily lactic, from a variety of sugars • extracellular polyglucose, called glucan
•
MS is responsible for initiation of caries
•
MS is a necessary, but not solely sufficient, factor for dental caries
Acquisition of MS - “Classic” Data •
MS colonize oral cavity after eruption of teeth – require hard, nondesquamating surface
•
Window of infectivity relies on virgin tooth surfaces for initial colonization
•
Second window may open when permanent dentition erupts
616
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Acquisition of MS by Infants •
MS is poor competitor for colonization – once stable biofilm is in place, ability for MS to colonize is reduced
Birth S mitis 1
S sanguis 8
11
25%
S mutans
19
26
75%
33 m
Infants who acquire S sanguis early may acquire less MS. Those who acquire MS early may be at higher risk for caries.
Transmission of MS Transmission may be direct or indirect • Source is usually mother • Vertical transmission • Fidelity >70% •
617
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More Recent Data •
Transmission may occur at birth
•
Fissures of tongue may be ecological niche
•
Early MS acquisition associated with Bohn’s nodules and high maternal levels
•
Horizontal transmission may occur within or outside of the family
Acquisition of MS •
50% of infants are infected by 6 months
•
By 24 mo, 84% harbor MS
•
Mean age of MS colonization - 15.7 mo in dentate infants Wan et al 2003
618
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Acquisition of MS •
Factors associated with colonization • sweetened fluids taken to bed • frequent sugar exposure • snacking • sharing of foods with adults • maternal MS levels > 105 cfu/mL saliva
Wan et al 2003
Acquisition of MS •
Factors associated with non-colonization • toothbrushing • multiple courses of antibiotics
Wan et al 2003
619
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More Evidence of Early Transmission
•
Li et al 2005 156 primigravid women
•
127 vaginal deliveries; 29 C-sections
•
Followed for 4 years for S mutans colonization
More Evidence of Early Transmission •
S mutans detected in 35% of children
•
Mean age of acquisition 22.3 mos
•
C-section infants acquired S mutans at earlier age: 17 vs 29 mos
•
100% fidelity for C-section group
•
Earlier colonization by competing strains in vaginally-delivered infants?
620
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Prevention of Transmission •
Söderling et al 2000
•
169 mothers with high MS levels during pregnancy
•
Three groups: • xylitol gum (65% w/w) 2-3 x/day starting at 3 mo • chlorhexidine varnish at 6, 12, 18 months • fluoride varnish at 6, 12, 18 months
Percent of Children Infected Age (years)
Mothers treated with Xyl
CHX
F Varnish
2
10%
28%
48%
3
28%
37%
65%
6
52%
87%
84%
Söderling et al 2001
621
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Other Microorganisms !
Lactobacilli sp. ! found in large numbers in some children ! considered opportunistic, not initiators ! numbers in cavity increase after DEJ invaded ! lactobacilli are good indicators of total carbohydrate intake
Other Microorganisms •
Li et al 2007 • children with S-ECC have less microbial diversity/complexity in biofilm compared to caries-free children
•
de Carvalho et al 2006 • frequency of C albicans higher in children with ECC than in children with non-ECC caries, or those who were caries-free
622
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Etiology - Diet !
Hopewood House (Australia) 1947 - 52
!
Vipeholm (Sweden) 1945 – 52
! diets devoid of sugar and white flour ! extremely low dental caries prevalence
! effects of frequency of sugar consumption ! effects of consistency (retentiveness) of sugar ! sugar at meals vs. in between meals
Lessons from Vipeholm •
Sugar consumption at meals – slight increase in caries
•
Sugar between meals – marked increase in caries
•
Sugar in sticky candies – greatest caries activity
•
Increased caries risk from increased frequency of ingestion
•
Caries activity differs among individuals
•
Caries activity declines with withdrawal of sugar-rich foods
623
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Sucrose •
Glucose + fructose
biofilm bacteria
metabolized by
fructan
+
glucan
Glucan From sucrose only
•
Water soluble
•
Extracellular “glue”
•
Enables adhesion to tooth • reduced susceptibility to mechanical disruption
•
Inhibits diffusion properties of biofilm • reduces buffering capacity of saliva • inhibits transport of acid away from tooth
624
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Fructan •
Produced extracellularly
•
Water soluble
•
May be used by MS as energy source
From fructose only
Biofilm •
Dental plaque now viewed as dynamic biofilm • maintains its own microenvironment
•
Influences oral health • negatively: acid attack, periodontal disease • positively: fluoride reservoir, protects against colonization by more pathogenic bacteria
625
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Role of Other Sugars •
Fructose and glucose are as effective as sucrose in vitro in their ability to cause a pH drop
•
In animal studies, fructose is nearly equal to sucrose in cariogenicity
•
Raw starch causes only a small drop in biofilm pH
Role of Refined Starch •
Soluble starch and refined starch can be broken down by salivary amylase into sugars
•
These refined carbohydrates cause a variable pH drop that may be as large as that caused by sucrose
626
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Biofilm pH after Sucrose Ingestion Stephan curve
7.0
Remineralization 6.0 pH
Demineralization 5.0
4.0
1
10
30
45
60
Minutes
Stephan Curves 7
6.5 Caries Resistant
6
Caries Susceptible
5.5
5 0
5
10
15
20
627
25
30
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Other Dietary Factors 7.0
Frequency of ingestion
6.0 pH 5.0
Refined CHO ingestions
4.0
1
10
30
45
60
Minutes
Other Dietary Factors !
Retentiveness/clearance
!
pH
!
Salivary stimulation
!
Fat content - protective
!
Inability of MS to metabolize (sugar alcohols)
!
Difficult (futile?) to categorize “good” vs. “bad” foods
628
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Protective Food Factors
Ca, PO4, casein, proteose peptones
similar to milk, fat salivary stimulation, CPP-ACP
gustatory stimulus, fat
flavonoids, antibacterial actions
masticatory stimulus
Carbonated Beverages •
Two studies using data from NHANES III
•
Heller et al 2001: found no relationship between soft drink consumption and DMFS in persons <25 years old, or dfs in those <12
629
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Carbonated Beverages •
Sohn et al 2006
•
Children identified as “high carbonated soft drink” users had significantly higher dental caries experience in primary dentition than did those in “high milk,” “high water,” and “high juice” groups
Sugar Consumption and Caries Risk •
Relationship between sugar consumption and caries (number of papers) • strong: 2 • moderate: 16 • weak: 18
•
Relationship is much weaker in modern age of fluoride exposure
•
Controlling sugar intake justifiable part of caries prevention, but maybe not always most important part of prevention program Burt and Pai 2001
630
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Etiology – Host Factors !
Tooth factors
!
Saliva
! ! ! ! ! ! ! ! !
quality of enamel presence/depth of pits and fissures hypoplasia fluoride exposure mineral content pH flow rate buffering capacity (carbonate, phosphate) antimicrobial components, fluoride
Antimicrobial Components •
Lysozyme: Gram-pos bacteria
•
Lactoferrin: Gram-pos and Gram-neg
•
Peroxidase: antimicrobial activity
•
Agglutinins: agglutination/aggregation
•
Secretory IgA: inhibition of adhesion
•
IgG: enhancement of phagocytosis
•
IgM: enhancement of phagocytosis?
631
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Saliva !
Flow rate reduced by:
!
Increased by:
! medications (antihistamines, antiasthmatics, antidepressants, others) ! disease (degenerative, metaplastic) ! dehydration ! radiation ! age ! gustatory stimulants (sugar-free candy) ! masticatory stimulants (s-f chewing gum)
Caries Factors Dietary intake of refined CHO
Oral flora – principally MS Caries
Host factors
632
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The Caries Balance Protective Factors • Saliva flow and components • Fluoride - remineralization • Antibacterials:chlorhexidine, xylitol, new?
Pathological Factors Acid-producing bacteria • Frequent eating/drinking of fermentable carbohydrates •Sub-normal saliva flow and function
No Caries
Caries
Courtesy of Dr. John Featherstone, UCSF
Modifying Effects Stress Genetics
Diet
Oral flora Culture
Caries
General health Host factors
Race / ethnicity
Healthcare delivery system
Behavior/education Socioeconomic status
633
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Shifts in Caries Presentation •
19th vs 20th/21st centuries • 19th century - disease of affluence • 20th/21st century - disease of poverty
•
1900-1950 - pandemic • presumption of caries inevitability • dental disease was among highest causes of time lost at work/school • could not target preventive efforts
Shifts in Caries Presentation •
1950-1970s - era of fluoridation • 50% reductions in caries • ~70% of US population on naturally- or artificially-fluoridated water supplies • preventive efforts could be targeted to non-fluoridated communities - still a broad target (population strategy)
634
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Epidemiology of Caries •
1970s - present • NIDR documented decline in caries prevalence Mean DMFT
Age
1963-70
1971-74
6-11 12-17
1.4 6.2
1.7 6.2
1979-80 1986-87 1.1 4.6
0.71 3.35
Shifts in Ethnic/SES Distribution !
80% of caries is in 20-25% of the population
!
Disproportionately more caries found in lower SES groups
!
Disproportionately more caries in minority groups - native Americans, African-Americans, Hispanics
!
Access to care is a problem for many of these children
635
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Recent Data - NCHS •
Prevalence of dental caries in primary teeth increased from ~40% during 1988-94 to 42% during 1999-2004
•
Among children 2-5, prevalence of primary tooth caries increased from ~24% to 28%
•
Caries rates in children 2-11 still greater for lower SES groups Dye et al 2007
The Caries Process •
Epidemiology
if one tooth erupted every year of life
dmf/DMF
Birth
age Caries is “steady-state” disease
636
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
The Caries Process •
root surfaces
Epidemiology
permanent crowns dmfs/ DMFS
Birth
primary
age Expression is variable over time
Histopathology of Caries •
Demineralization - remineralization dynamic process, constant, not on/off
637
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Histopathology of Caries Zones of early lesion surface (5-10% mineral loss) body – 60% loss translucent zone – 5-10% loss normal enamel
Histopathology of Caries
White spot lesion Radiographic
638
Histologic
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Histopathology of Caries Remineralization is possible as long as enamel surface is intact
Remineralization is accelerated if there is sufficient ambient fluoride; remineralization of deep lesions in enamel and dentin is experimentally possible (ten Cate 2001)
Primary Tooth Considerations More rapid caries progression (less mineral) • Thinner enamel and dentin •
•
Relatively larger pulp
•
Flat contacts
•
Caries sequence • lower molars, upper molars, anteriors
•
2nd molars more susceptible than 1st
639
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Medical Approach to Caries Management !
Characteristics of caries that enable a medical approach ! diet-dependent infectious disease ! biphasic (demin-remin) ! threshold for expression ! external interface disease ! site specific and symmetric ! steady state phenomenon with variable expression over time (eruption)
Medical Approach to Caries Management •
Principles • reorient management from treatment of cavities (disease) to management of caries (process) • surgical approach problematic when applied to dynamic process • better to treat cause rather than manifestation of disease
640
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Medical Approach to Caries Management •
Strategy • determine child’s current caries experience • estimate risk for future caries • develop plan to address current problem and prevent future disease
•
Goal • minimize lifelong caries experience while using least intervention consistent with level of risk
Medical Approach to Caries Management Historical approach: Diagnosis No cavities
Cavities Treatment
Maintenance (“Recall”) Health
641
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Medical Approach to Caries Management Diagnosis Caries-
Caries+
Cavity+ Cavity-
Cavity+ Cavity-
Treat Caries Treat Cavity Maintenance Health
Medical Approach to Caries Management Classification: Findings
Status Group
Caries+ Cavity+
Manifest disease
Caries+ Cavity-
Premanifest disease
Caries- Cavity+
Postmanifest/arrested
Caries- Cavity-
Inactive disease
642
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Management of Status Groups •
Manifest disease: arrest and restore; caries removal; sequential cultures; anticipatory guidance; restoration
•
Premanifest disease: arrest process
•
Postmanifest disease: maintain suppression of process; restore lesions
•
Inactive disease: anticipatory guidance
Interim Therapeutic Restorations
Lesions in young patient
643
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Interim Therapeutic Restorations Caries removal – no local anesthesia
Lesions in young patient
Interim Therapeutic Restorations Caries removal – no local anesthesia
Lesions in young patient
Lesions restored
644
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Rationale for Earlier Initial Visits !
Health supervision, not disease treatment
!
Old model: caries inevitable; treat effects of disease, then institute preventive (suppressive) care; OK to start at age 3 (can’t manage behavior any earlier)
!
New model: examine early; risk assessment; anticipatory guidance; true prevention
!
Early identification/intervention are cost effective (Savage et al 2003)
Rationale for Earlier Initial Visits •
Further support: • acquisition of MS as early as birth • recognition of ECC - BBTD, nursing caries, rampant caries • feeding management • risk assessment for fluorosis • non-nutritive sucking • trauma prevention; early ID of abuse/neglect • anticipatory guidance for growth and development
645
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Initial Evaluation •
ADA, AAPD, AAP, AGD, others support initial evaluation by 1 year of age
Knee-to-Knee Exam
Positive reinforcement for caregiver; use toothbrush to facilitate exam
646
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Anticipatory Guidance •
Developmentally paced information
•
Provides practical, developmentallyappropriate health info to parents
•
Alerts parents to impending changes
•
Teaches parents their role in maximizing child’s developmental potential, identifies special needs
Dental Home !
Modeled after AAP’s medical home
!
Accessible, family-centered, continuous, comprehensive, coordinated, compassionate, culturally competent
!
Early prevention; emergency care
!
Coordinates specialty care
!
Individualized recall programs
647
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Early Childhood Caries (ECC) Defined as presence of >1 dmf surfaces in any primary tooth in a child <71 months old
Early Childhood Caries (ECC) !
Distinguishing characteristics of ECC:
! ! ! !
distinctive pattern of decay many teeth may be affected caries develops rapidly caries develops in tooth surfaces normally at low caries risk
648
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Early Childhood Caries •
Prevalence: • no accurate data on national prevalence • 1-70% reported, depending on criteria/definition, sample characteristics • probably ~3-6% in US, and costly to manage
Implications of ECC !
Higher risk for caries in permanent dentition
!
Expensive to treat ! >$1000/child ! may require GA or deep sedation
!
Associated with malnutrition, retardation of growth (Acs et al 1992; Clarke et al 2006)
!
Dental care under GA significantly improves: o o
OHRQoL impact of the disease on the family (Malden et al 2007)
649
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Caries Risk Assessment •
A systematic evaluation of the presence and intensity of etiologic and contributory disease factors
•
The assessment is designed to provide an estimation of disease susceptibility, and an aid to targeting preventive and treatment strategies
Salivary Assays •
CRT system assays LB and MS
MS in biofilm/saliva of young caries-free children appears to be associated with a considerably increased caries risk. Thenish et al 2006
650
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cariostat Caries Activity Test •
Predicts caries risk of 3½ year olds based on test results at 18 months and 2 years
•
Changes that were effective in reducing caries risk: • lower sucrose intake • toothbrushing by parents
•
Cariostat not yet available in US Nishimura et al 2008
Demographic Data !
Age ! MS transmission? ! expected dental development
!
Race/ethnicity
!
Socioeconomic status
!
Maternal education level - strong caries predictive value in 1-year-olds (Grindeford et al 1993)
651
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Other Clinical Data •
Maternal age
•
Maternal DMF
•
Maternal gingivitis
•
Parental smoking
•
Consumption of candy
•
Sweetened beverages
•
Visible biofilm on maxillary anterior teeth
Medical History !
Prenatal/perinatal history ! low birth weight/hypoplastic defects
!
General health ! growth lags: children with ECC were in lowest 10th percentile for weight (Acs et al 1992)
! asthma (?) ! medications
652
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Overweight / Obesity •
Not significantly associated with increased caries risk in all studies
•
NHANES III and NHANES 1999-2002 • no evidence that overweight children are an increased risk for caries
•
Significant association between high weight and caries frequency found in primary and permanent dentitions of German schoolchildren
Behavioral Factors •
Oral hygiene • gingivitis - marker for home care • biofilm accumulation rates
•
Infant feeding patterns/diet • breast/bottle patterns • amount/frequency of fermentable carbohydrates • adhesiveness, pH, protective factors
653
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Nursing Caries - Bottle Use •
Distinct patterns of cavities
•
Relationship with bottle contents not certain in all studies
•
Nursing bottle used by 95% in U.S. 6 mo to 5 years
•
Almost 20% have been put to bed with bottle
•
>8% ages 2-5 years continue to use bottle
Nursing Caries - Bottle Use Many children continue to use bottle at ages 2-3 • Working mothers tend to bottle feed longer • Working parents may engage in more bottle use •
654
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Nursing Caries - Role of Milk •
Recent animal and in vitro studies suggest that milk/components are not cariogenic
•
Does not cause appreciable drop in pH
•
May aid in remineralization
•
May support/promote growth of cariogenic bacteria
Nursing Caries - Role of Formula !
Some common formulas are as cariogenic as sucrose (Erickson et al 1998)
!
Sucrose is an ingredient in some infant formulas; also lactose, glucose
!
Rinsing with formula reduces biofilm pH significantly (Sheikh and Erickson 1996)
!
Others have found that formulas cause less caries than sucrose in lab animals
655
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Role of Breast Milk !
Case reports suggest ECC related to prolonged, ad lib breastfeeding
!
Erickson et al (1999): does not cause pH drop, supports bacterial growth, deposits Ca and P, poor buffer, does not cause demineralization alone; but with 10% sucrose causes dentinal caries
Role of Breast Milk •
Exclusive breastfeeding is associated with: • older mothers • urban residence • higher education level • higher income
656
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Systematic Review – Valaitis et al 2000 •
Quality of studies • • • •
0 strong 3 moderately strong 9 weak 16 very weak
•
Lack of methodological consistency
•
Moderately strong studies suggest that breastfeeding >1 yr and at night after eruption of teeth may be associated with ECC
Secondary Data Analysis •
NHANES 1999-2002 data • 1576 children ages 2-5
Those breastfed >1 year more likely to have ECC (33%) than those breastfed 1 year (22%) • After adjusting for confounding variables, no association seen between breastfeeding or bf duration and risk for ECC •
Iida et al 2007
657
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Randomized Trial – Kramer et al 2007 13,889 Belarusian mother/child dyads • No evidence of beneficial or harmful effects of •
• prolonged breastfeeding • exclusive breastfeeding
on dental caries in early school age children • Prolonged/frequent breastfeeding may be associated with other factors that increase caries risk
Nursing Caries - Bottle Use •
Fruit juices • low pH • fermentable carbohydrates • enhance demineralization by oral bacteria • use of sweetened beverages in bottle may lead on increased mutans strep colonization (Mohan et al 1998)
658
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
AAPD Caries-Risk Assessment Tool (CAT) - Caveats •
“Snapshot” – should be used periodically
•
Can be used by dental and non-dental personnel – does not render a diagnosis
•
Treatment decisions are to be made by dentist
•
Radiographic and microbiologic testing are not essential for use of CAT
659
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Shifts in Preventive Strategies •
Old paradigm: • primary - suppression of disease • secondary - reparative procedures • tertiary - prosthetic procedures
•
New paradigm: • primary - truly preventive/pre-emptive • secondary - suppression of process below threshold • tertiary - limit extent of lesion prior to restoring
Prevention Pharmacotherapeutics •
Fluoride
•
Xylitol
•
Chlorhexidine
•
Other Antimicrobials
•
Remineralizing Agent
660
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Fluoride: Mechanisms of Action !
Topical (most important) ! inhibits demineralization ! promotes remineralization
!
Antibacterial (somewhat important)
! disrupts enzyme systems (enolase) ! reduces acidogenesis, extracellular polysaccharide
!
Systemic (not very important/no effect)
! improves enamel crystallinity, reduces acid solubility ! improves tooth morphology (?) ! recirculates through saliva
Dietary Fluoride Supplements •
Rationale: • to provide a systemic dose of F equivalent to that ingested by children who consume optimally-fluoridated water
•
Questions: • How much F is ingested by children in OF communities? • How effective is a single daily dose? High dose-low frequency vs. low dose-high frequency
661
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Effectiveness of F Supplements •
Primary teeth: • 22-80% reduction in defs • 40-93% reduction in deft
•
Permanent teeth: • 20-80% reduction in DMFS • 16-36% reduction in DEFT
•
Level of evidence is poor for some studies
Supplementation Goals •
Determine the proper dosage
•
Select proper supplement
•
Write the prescription
•
Educate parent and patient
662
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Current Supplementation Schedule Drinking Water F Level (ppm) Age
0<0.3 0.3 - 0.6
>0.6
6 mo<3 yr
0.25*
0
0
3 < 6 yr
0.50
0.25
0
6 to at least 16 yr
1.00
0.50
0
*mg F ion per day Safety tip: Prescribe <120 mg F ion at one time for a family
Supplemental Fluoride Issues •
Fluorosis
•
Prenatal fluoride
•
Breastfeeding
•
Bottled water
•
Water filtration systems
•
Water analysis
•
Inappropriate prescriptions
663
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Fluoride Dentifrices
Fluoride Dentifrices •
High dose - low frequency regimen
•
Best vehicle for topical F application
•
Current formulations: • NaF and MFP: 1000, 1500 ppm F • 1 g of 1000 ppm F = 1 mg F ion
664
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Systematic Reviews !
Pooled prevented fraction – 24% (Cochrane); 25% (Twetman)
!
Effect was increased with ! ! ! !
!
higher baseline caries rates higher fluoride concentration higher frequency of use supervised brushing
Little information concerning primary dentition
Issue: Retention of Dentifrice % dentifrice retained
60
(Data compiled from several studies)
50 40 30 20 10 2
4
Age
665
7
10
13
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Dentifrice Recommendations !
Use fluoridated toothpaste beginning at ~1-2 yr based on risk assessment
!
Use “smear” or “pea-sized” amount
!
Parents should supervise loading of brush and brushing
!
Avoid highly abrasive dentifrices
NaF Mouthrinses •
OTC preparations • 0.05% (~225 ppm) - daily
•
Rx preparations: • 0.05% NaF/APF (~225 ppm) - daily • 0.2% (~900 ppm) – weekly
Omni CaviRinse
666
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
SnF2 Mouthrinses 0.044% (~100 ppm F) in acidulated phosphate solution • 0.63% diluted to 0.1% (~250 ppm F) •
Fluoride Mouthrinses !
Indications ! orthodontics (?) ! radiation therapy ! prosthetics
!
No proven additional efficacy in healthy children demonstrated when fluoridated dentifrice is used
667
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Effectiveness – F Mouthrinses •
Cochrane Review meta-analysis • DMFS pooled prevented fraction: 26%
•
No association with: • higher baseline DMFS, background F exposure, rinsing frequency, F concentration
Effectiveness – F Mouthrinses •
Twetman et al 2004 • limited evidence (PF=29%) for individuals with limited fluoride exposure • inconclusive for individuals exposed to other sources of fluoride (eg, toothpaste)
•
Long-term use of F mouthrinse associated with reduced salivary levels of MS (Kaneko et al 2006)
668
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
F Retention from F Mouthrinse Age Volume of Rinse (years)
Rinse Time (s)
Mg F Retained
3
5 mL 5 mL
30 60
0.38 0.41
4
5 mL 5 mL
30 60
0.25 0.35
5
7 mL 10 mL
30 60
0.27 0.32
Self-Applied Fluoride Gels •
High dose - variable regimen
•
Designed for custom tray use • rampant caries • orthodontic patients • special-needs patients • post-radiation • impaired salivary flow • high susceptibility to caries
•
Now used in brush-on technique
669
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Effectiveness of Self-Applied Gels Community
Preparation
Application Frequency
% DMFs Reduction
Optimally fluoridated
APF
3x/week (total 225) 3x/week (total 162)
19% 15% (dfs)
Fluoride deficient
APF NaF
5x/week (total 245) 5x/week (total 245)
75% 80%
No controlled trials with SnF2
Professionally-Applied Fluoride •
Gels • NaF 2% - 9000 ppm F • APF 1.23% - 12,300 ppm F
•
Foam • APF 1.23%
•
Varnish • 2.26 % F = 22,600 ppm F
670
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Fluoride Foam and Varnish !
Fluoride varnish (22,600 ppm)
! Duraflor, Duraphat, Cavity Shield ! approved for use in US as cavity varnish (liner) or desensitizing agent ! used since early 1960s in Europe ! typical use 0.2 - 0.5 mL = 5 - 11 mg F ! topical use is “off-label,” but legal
Effectiveness –Gels/Foam •
Cochrane Reviews meta-analysis • DMFS pooled prevented fraction: 28%
•
Marinho et al 2003 • DMFS prevented fraction: 21%
671
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Effectiveness - Varnish Prevented fraction in meta-analyses:
•
• Cochrane: 46% • Petersson: 30%
No significant association with
•
• baseline caries • background exposure to F
Inconclusive evidence for effect in primary dentition
•
Effectiveness Against ECC •
Weintraub et al JDR 2006
•
Randomized controlled trial
•
3 study groups, ages 6-44 months at start • counseling only – control • counseling with FV 1x/year (2 intended applications • counseling with FV 2x/year (4 intended applications
672
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Effectiveness Against ECC •
Caries incidence of counseling-only group compared to: • FV 1x/year: OR 2.2 • FV 2x/year: OR 3.77
•
Significant protective effect of FV vs. early childhood caries
•
No adverse events reported
Fluoride Prophylaxis Pastes •
Caries reductions probably 0%
•
Will remove F-rich enamel - should replace with topical F treatment
•
Not necessary for topical F deposition from F gel/foam/varnish, but use as necessary to remove biofilm and stain
•
Use low abrasive, light pressure
673
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
White Spot Lesion Avoid use of prophy paste on white spot lesions
ADA Recommendations for Professionally-Applied Topical Fluoride (2006) •
Under age 6 • low caries risk: possibly no benefit from topical F • moderate risk: F varnish q 6 mo • high risk: F varnish q 3-6 mo
674
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADA Recommendations for Professionally-Applied Topical Fluoride (2006) •
Ages 6-18 • low caries risk: possibly no benefit • moderate risk: F varnish or gel q 6 mo • high risk: F varnish or gel q 6 mo • F varnish or gel q 3 mo may provide additional protection
Acute Fluoride Toxicity •
Mechanisms of toxicity • corrosive action on stomach lining • affinity for calcium - tetany • enzyme inhibition
•
Toxic doses • “certainly lethal dose” - 32-64 mg F/kg • lethal pediatric dose - 15 mg F/kg • “probably toxic dose” - 5-8 mg F/kg
675
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Treatment of Fluoride Ingestion •
<8 mg F/kg: give milk; observe > 6 hours; refer if symptoms develop
•
>8 mg F/kg: induce vomiting (if recent ingestion), followed by milk; refer immediately
•
Unknown ingestion: if asymptomatic, give milk, observe >6 hours, refer if symptoms develop; if symptomatic, give milk and refer immediately
Xylitol !
5-carbon sugar alcohol (also sorbitol, mannitol, erythritol)
!
Looks/tastes/relative sweetness same as sucrose (40% fewer calories)
!
Found in plants, esp. birch trees, grasses, fruits, vegetables
!
Oral intake shown to be safe in long term human studies
676
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Xylitol Properties • • • • •
Reduced acid production in biofilm Reduction in amount of biofilm Reduced adherence of biofilm Reduced numbers of MS No accommodation by MS to xylitol
Xylitol Properties •
Accumulates intracellularly in MS, inhibits growth
•
Long-term intake has selective effect for MS that are less adherent to teeth
•
Osmotic diarrhea at high doses (>200 g/day)
677
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Stephan Curves
Fugleman et al 1977
Milgrom et al JDC 2006 •
MS dose response to xylitol chewing gum
•
4 study groups based on daily xylitol dose • placebo - 9.8 g sorbitol and 0.7 g maltitol • 3.44, 6.88, or 10.32 g xylitol
•
Each group chewed 3 gum pellets 4x/day
•
Randomized controlled trial
678
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Log MS CFU/mL
Milgrom et al 6-Month Data
placebo 10.32 g/d 3.44 g/d 6.88 g/d
Xylitol Dose (g/day)
Over the Counter Xylitol, mannitol, aspartame $.10-.15/piece 1.5g xylitol/piece Cost per 7g dose: $.50-.75 For xylitol content & cost of other products, see Ly et al Pediatr Dent 2006;28:154-63.
679
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Other Xylitol Gums
Percentage of xylitol is proprietary information; percentage may vary; No data to support the caries-inhibitory potential of OTC U.S. chewing gums
Use of Xylitol Gums •
Chew 20-30 minutes 2-3 times/day (a total of >7g/day)
•
Chewing immediately after meals especially helpful – salivary buffering
•
Use with mothers of infants to reduce MS transmission?
680
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Chlorhexidine •
Available in U.S. as chlorhexidine gluconate oral rinse 0.12% • Peridex (Omni) • PerioGard (Colgate) • GUM (Butler) alcohol-free
•
Available in Europe as 0.2% rinse, 1% gel, 3% varnish
Chlorhexidine •
More effective against MS than lactobacilli or S. sanguis - thus selective for anticaries effect
•
Can reduce biofilm and salivary MS concentrations to low/nondetectable levels
•
Shown to be effective in high-risk subjects
•
Professionally-applied gel and varnish more effective than mouthrinse use at home
681
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Chlorhexidine Meta-analyses •
Prevented fraction: 46% (van Rijkom et al 1996)
•
No significant influence for variables: • application method, application frequency • caries risk, fluoride regime, caries diagnosis, tooth surface
•
CHX mouthrinse has short-term effect; gel and varnish have larger effects (Ribeiro et al 2007)
Chlorhexidine !
Use in high-caries risk patients (Featherstone) ! rinse with 1 - 2 tsp one minute per day for one week ! repeat every 3 months as needed ! can be used more frequently (one week per month) in more resistant children ! brush or swab onto the teeth of young children to avoid ingestion
682
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Chlorhexidine •
Disadvantages • staining of teeth • taste disturbances • recolonization by MS within weeks of discontinuation
•
Still considered one of the most efficient tools in caries management in high risk patients
Other Antimicrobials !
Povidone-iodine 10% (Betadine)
!
Mouthrinses containing essential oils (Fine et al 2000; Zhang et al 2004) Cetylpyridinium chloride, triclosan, sanguinaria extracts, hexetidine, enzymes, metal ions, others
!
! broad spectrum topical iodophor microbicide ! topical use reduces risk for ECC (Lopez et al 1999)
683
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
CPP – APP: Recaldent •
Calcium phosphopeptide – amorphous calcium phosphate
•
Ca and PO4 ions stabilized into nanoclusters by CPP – milk-derived protein
•
Available as MI Paste and MI Paste Plus • Tooth Mousse in Europe, Australia
CPP - ACP Soluble Ca and PO4 do not concentrate in plaque or localize at tooth surface • CPP stabilizes Ca and PO4 along with F at tooth surface – binding to pellicle and plaque •
CPP – ACP bound to Mutans strep in plaque
684
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
CPP – ACP: In vivo, in vitro, in situ studies •
Demonstrated anticariogenicity in rat (in vivo)
•
Inhibition of demineralization / promotion of remineralization seen in several in vitro studies
•
Promotion of remineralization of subsurface lesions seen in in situ studies
•
Incorporation in chewing gum produced remineralization in in situ models
CPP – ACP Human Trials •
Increases in levels of Ca and PO4 in supragingival plaque with mouthrinse
•
CPP – ACP chewing gum slowed proximal caries progression and remineralized more lesions compared to placebo – radiographic assessment
685
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
CPP – ACP Human Trials •
RCT showed CPP-ACP more effective than F mouthrinse in remineralizing post-ortho white spot lesions
•
Multiple case reports • treatment of fluorosis • reversal of early lesions • stabilization of lesions
CPP - ACP •
Quality of existing studies: good
•
Need more human trials
•
Promising
686
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Remineralizer – CPP-ACP •
Can be applied by prophy cup, custom tray, finger
•
Also available in chewing gums
•
MI Paste Plus • contains fluoride in 5:3:1 formulation (5 Ca, 5 PO4, 1 F)
Managing Occlusal Surfaces of Young Permanent Teeth !
Pit and fissure decay ! occlusal surfaces comprise 12.5% of total surface area ! comprise 50-80% of decay in ages 5-17
!
Less decline of pit and fissure caries in recent years - relative F effectiveness
!
Relative increase in occlusal caries in recent years
687
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pits and Fissures Photomicrograph of toothbrush bristle and molar fissure
Photomicrograph of molar fissure pattern
Effectiveness of Sealants •
Systematic review • relative caries risk reduction on permanent 1st molars: 33% • effect was dependent on retention • incomplete evidence for permanent 2nd molars, premolars, primary molars, and glass ionomer cements Mejare et al 2003
688
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Effectiveness of Sealants •
Cochrane Review
•
After 4.5 years, sealed permanent molars of children ages 5-10 had caries reductions in over 50% of occlusal surfaces
•
Caries reductions ranged from 86% at 12 months to 57% at 48-54 months
Sealant Types ! ! ! ! ! ! ! !
Self-cure vs. light cure Filled vs. unfilled Fluoride containing Radiopaque Clear vs. opaque White, tinted, color-changing GIC, flowable composite, bonding agent, bonded amalgam Self-etching
689
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADA Recommendations (2008) •
Resin-based sealants first choice (high level of evidence)
•
GIC sealants may be used when moisture control is an issue (high level of evidence, but low strength of recommendation)
•
Hiiri et al 2006: • sealants provide better protection than fluoride varnish
ADA Recommendations (2008) •
Use of compatible 1-bottle agents (primer/adhesive) may be used between etching/sealant to enhance retention (mod high level of evidence)
•
Use of self-etching bonding agents may provide less retention than standard etching procedure (mod high level of evidence)
•
Borsatto et al 2007 • Er:YAG laser may improve sealant bond strength to primary teeth, but only if enamel is etched subsequently
690
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Concerns •
Sealing over decay • proven effective in arresting lesion
•
Systematic review (Griffin et al 2008) • sealing non-cavitated caries in permanent teeth effective in reducing caries progression
•
Routine mechanical preparation of enamel not recommended (ADA; mod high level)
ADA Recommendations for Use of Sealants (2008) •
Primary teeth • when tooth and/or patient is at risk for caries • low level of evidence
•
Permanent teeth (children/adolescents) • when tooth and/or patient is at risk for caries • high level of evidence
•
Placement over non-cavitated lesions • high level of evidence
•
Use 4-handed technique when possible • low level of evidence
691
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Fissure Diagnosis • •
•
Use care with explorer Probing can convert non-cavitated occlusal lesion into cavitated lesion (Künisch et al 2007) Use • air • visual exam • diagnostic aids (eg, QLF)
692
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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694
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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696
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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697
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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698
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Constance M. Killian, D.M.D.
Special Needs Definition of Persons with Special Health Care Needs: Individuals with a physical, developmental, mental, sensory, behavioral, cognitive, or emotional impairment or limiting condition that requires medical management, health care intervention, and/or use of specialized services or programs.
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Special Needs
General Considerations • May cause limitations in performing daily selfmaintenance • Persons with SHCN are at increased risk for oral disease • Disability impacted by severity of disease
Special Needs
Epidemiology The numbers are increasing... Nearly 1 in 5 Americans older than 5 years have a disability Nearly 2.6 million children ages 5-15 years have a disability
701
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Special Needs
Epidemiology Causes of Disability • Extreme pre-term birth (< 26 weeks) • Congenital disorders • Acquired disorders – accidents, diseases
5
Special Needs
Changing Patterns • History of care in institutions • Increasing numbers of children with
intellectual, physical, or developmental disability are surviving into adulthood
What does this mean to you?
702
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Special Needs
Healthy People 2010 Goal: To decrease to zero the number of persons under 21 years of age in congregate care facilities by the year 2010
Special Needs
Trends As more children with SHCN are living at home, they become part of the patient population in private practice
703
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Special Needs
Families of Children with SHCN Parents of these children are overwhelmed • • • •
Complex medical conditions Daily maintenance tasks No respite Complicated family dynamics
Special Needs
Principles of Providing Care Get to know the patient Get to know the patient’s family • Family circumstances • Experiences with medical/dental care
Get to know the patient’s condition • Thorough medical history
• Consultation with physician – get it in writing • Use internet/other resources
704
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Special Needs
Principles of Providing Care Be prepared !Communicate with caregiver !Plan for emergencies !Staff training
Special Needs
Principles of Providing Care • Listen and learn • Be flexible • Think multi-disciplinary when
treatment planning
705
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Special Needs
Principles of Providing Care • Be an educator • Discuss impact of medical condition on patient’s oral care • Establish dental home • Provide an atmosphere of increased awareness for all parents
Be Inclusive
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Special Needs
Principles of Providing Care
Your office can be the great equalizer
Special Needs
Principles of Providing Care Remember that “Attached to every tooth there is a person” Look beyond the condition to see the unique personality, needs and special gifts of each patient
707
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Asthma
Asthma Features • Chronic condition of respiratory system • Airway has increased responsiveness to stimuli • Characterized by wheezing, dyspnea, coughing and airflow obstruction • Prevalence is increasing – currently 7-10% of children • One of leading causes of hospitalizations • High costs - $ and lost work/school
708
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Asthma
Triggers • Allergens: dust mites, pollen, animals • Cigarette smoke (including second hand), ozone
Asthma
Pathogenesis Exposure to a trigger Mast cell degranulation Bronchoconstriction Decrease in expiratory airflow Progressive shortness of breath – wheezing, cough • Airway inflammation • Bronchial hyper-responsiveness • • • • •
709
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Asthma and the Airway
Asthma and the Airway
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Asthma
Classification • Mild • No night symptoms • Tolerates exercise • Wheezing < 2 days/wk
• Moderate • Some night symptoms • Limited exercise tolerance • Wheezing 2-5 days/wk
• Severe • Frequent night symptoms • Poor tolerance to exercise • Wheezing daily
Asthma
Goals of Therapy ! Reduce symptoms ! Maintain pulmonary function ! Prevent acute attack ! Avoid effects of medications
711
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Asthma
Medications
• Asthma therapy should be flexible and based on changes in symptoms • Albuterol – B2 agonist – Bronchodilator – relaxes bronchial smooth muscle – Used as rescue inhaler – Examples: Proventil, Ventolin
Asthma
Medications • Corticosteroids • Anti-inflammatory • Immunosuppressive • Maintenance medication • May be inhaled •
Fluticasone (Flovent), Budesamide (Pulmicort)
• May be systemic •
Prednisolone
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Asthma
Risks of Inhaled Corticosteroids • Overall low risk • Suppressed adrenal function • Decreased bone density • Increased risk for cataracts • Growth retardation • Control risks by reducing dose to minimal dose
that is effective
Asthma
Newer Classes of Medications • Long-acting B2 agonists (12 hour activity): bronchodilators • LTRA – Leukotriene receptor antagonists –decrease or block leukotrienes • Montelukast (Singulair )
• Anti IgE agents
713
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Asthma
Compliance with Medication
Compliance is critical, but especially with adolescents: the greatest number of asthma deaths occurs in ages 10-14
Asthma
Relevant Oral Findings • Decreased salivary flow • Increase in dental caries • Dental erosion • Increased calculus • Increased gingivitis
714
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Asthma
Relevant Oral Findings
Dentofacial findings • High palate • Increased anterior face height • Increased overjet • Greater incidence of posterior
crossbite
Asthma
Relevant Oral Findings
• Evidence of steroid use • Candidiasis • Tongue enlargement • Pharyngeal irritation
715
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Asthma
Dentistry and the Patient with Asthma What to Ask… • • • • • • • • •
Medications used Triggers Last asthma attack Frequency of attacks Ever hospitalized for attack? Last visit to ED for asthma History of needing mechanical ventilation Recent use of oral steroids How often is inhaler used/refilled - >1 canister/month?
Asthma
Dental Treatment and Asthma Dental treatment can result in 15% decreased lung function • Dental treatment can provide triggers… • • • • •
Prolonged supine position Position of dental instruments Tooth dust Sealant materials Aerosols
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Asthma
Dental Management of Asthma Patients • Confirm patient has taken medication • Have patient bring inhaler • Avoid triggers as much as possible • Use rubber dam
Asthma
Adjunctive Therapy for Dental Care • Nitrous oxide appropriate with mild/moderate
asthma • Sedation: avoid narcotics, barbiturates • Be prepared to rescue patient
717
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Asthma
Management of Acute Asthma Attack • • • • • • •
Discontinue treatment Remove everything from mouth Position patient for comfort Apply pulse oximeter B2 rescue inhaler Oxygen If O2 < 91%, struggling to breathe • Epinephrine 0.01mg/kg • Call 911
Congenital Heart Disease
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Congenital Heart Disease Incidence of Congenital Heart Disease is 8-10 per 1,000 live births
Congenital Heart Disease
Heart Murmurs • Related to increased blood flow velocity
across valve • Common – present in 80% of all children • Systolic murmurs may be innocent • Diastolic murmurs and continuous
murmurs are abnormal
719
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Anatomy of the Heart
Congenital Heart Disease
Cardiac Defects
Increased pulmonary blood flow • L to R shunt: ASD, VSD, PDA, AV
Canal • Increase in pulmonary blood flow at
expense of systemic circulation • Appears as CHF over time
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Anatomy!of!the! Heart:!Increased! Pulmonary!Flow Example:!VSD
Congenital Heart Disease
Cardiac Defects Decreased pulmonary blood flow • R to L shunt: Less blood to lungs • Example: Tetrology of Fallot • Patients appear cyanotic • High risk of endocarditis
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Decreased! Pulmonary!Flow Example:!Tetrology of!Fallot 1.!!Pulmonary!stenosis 2.!Right!ventricular!!! hypertrophy 3.!Overarching!aorta 4.!VSD
Congenital Heart Disease
Cardiac Defects Obstructive defects • Anatomic narrowing: coarctation of aorta,
aortic stenosis, pulmonic stenosis • Valvular, subvalvular or supravalvular • Appears as CHF over time
722
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Congenital Heart Disease
Cardiac Defects
• Primary pump failure • Dilated cardiomyopathy • Hypertrophic cardiomyopathy : can result in syncope, sudden death
Congenital Heart Disease Cardiac Defects Hypertrophic Cardiomyopathy • Thickening of cardiac muscle • Most often affects ventricular septum
48
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Congenital Heart Disease
Cardiac Defects Congestive Heart Failure Management with medications
• Remove accumulated fluid – e.g. diuretics • Improve cardiac function – e.g. digoxin • Improve tissue oxygenation- e.g. warfarin to increase PT • Reduce demands on heart – ACE inhibitors to decrease BP
Management with surgery
Congenital Heart Disease
Management of Cardiac Conditions • Valve stenosis: corrected by balloon valvuloplasty • Condition improves as leaflets of valve are separated • Valve is able to open
724
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Management of Cardiac Conditions Open heart surgery • ASD/VSD repair – patch closure • Shunts • Valve replacement
Congenital Heart Disease
Management of Cardiac Conditions Valve Replacement: Bioprosthetic valves • Porcine, bovine, human • Benefits – No need for anticoagulants – Good hemodynamics
725
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Management of Cardiac Conditions Valve Replacement: Mechanical valves • Doesn’t grow with patient • Need anticoagulants • Readily available, replacements available
Mechanical and Tissue Heart Valves
726
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Oral Care for Cardiac Patients • Medical history • • • • • • •
Type of defect Hospitalizations – when, why Surgery – when, type Medications Any prosthetic valves Any limitations on activities Hypertension
Congenital Heart Disease
Oral Care for Cardiac Patients Oral findings • Increased caries • Poorer oral health than siblings • Increase in untreated caries in cases of
severe CHD • Gingival bleeding
727
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Infective Endocarditis (IE) • Low incidence in general population • Less frequent in children • Microbial infection – affects valves, muscle, defects • Strep viridens most common microorganism ! Symptoms – may appear as other infection ! Fatigue, fever, rash, anorexia ! 7-14 day typical incubation period, but may take up to 4 weeks
Congenital Heart Disease
Sequence of Events in IE • Clinical manifestations of IE related to host’s immune response: immune cells, platelets and fibrin sent to site of cardiac defect/valve • Formation of non-bacterial thrombotic endocarditis (NBTE) at site of defect/valve • Bacteremia • Bacteria adhere to NBTE & proliferate there, forming “vegetations” • Vegetations may break off and enter circulation
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Risk of Transient Bacteremia • Dental procedures – done infrequently – Extraction: 10-100% – Perio surgery: 36-88% – Scaling/Root planning: 8-80% – Teeth cleaning: 40% – Rubber dam placement: 9-32%
! Routine daily procedures – done much more often – Toothbrushing/flossing: 20-68% – Toothpicks: 20-40% – Chewing food: 7-51%
Congenital Heart Disease
Risk of Transient Bacteremia Antibiotic Prophylaxis against Infective Endocarditis: 2007 AHA Guidelines
A Change in Emphasis
729
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Summary of Changes – See Appendix • Bacteremia resulting from daily activities is more likely to cause IE than that of dental procedures • Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities • Only very small number of IE cases might be prevented by AP, even if 100% effective
730
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Summary of Changes – See Appendix AP only recommended for cardiac conditions associated with the highest risk of adverse outcome from endocarditis (See Appendix): • Prosthetic heart valve • Previous infective endocarditis • Congenital heart disease – limited to: – Unrepaired cyanotic CHD – Completely repaired congenital heart defect : AP needed during first 6 months after procedure – Repaired CHD with residual defects • Cardiac transplantation recipients who develop cardiac valvulopathy
Congenital Heart Disease
Summary of Changes – See Appendix • AP recommended for procedures that
involve manipulation of gingival tissues or periapical region of teeth or perforation of oral mucosa only for high risk patients
• AP recommended for procedures on
respiratory tract or infected skin, skin structures, or musculoskeletal tissue only for high risk patients
731
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Congenital Heart Disease
Considerations for Antibiotic Prophylaxis ! See Appendix for specific recommendations ! Single dose one hour pre-op ! Patient already on antibiotic ! Patient taking parenteral antibiotic therapy
Genetics and Congenital Disorders
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
General Considerations Role of the Pediatric dentist • Be familiar with molecular basis for disease • Recognition of the clinical expression • Be a source of information for oral health care issues
Genetics and Congenital Disorders
Principles • Understand the disorder and its dental
implications • Consult with medical colleagues • Provide information • Develop short-term and long-term plan for oral health of the patient
733
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
Diagnosis of Genetic Disorders Phenotype/Genotype and the Human Genome • Diagnosis previously made solely by identification of dysmorphic features, pattern recognition (phenotype) • Human genome project allows for identification by genetic findings (genotype) • Relationship between phenotype and genotype is not always straightforward
Genetics and Congenital Disorders
Diagnosis of Genetic Disorders Genetic disorder may result from spontaneous mutation with no familial inheritance pattern
734
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
Clinical Application Molecular genetics of a syndrome • Identify syndrome w/familial pattern • In-depth family history • Linkage studies to sequence gene in
affected/unaffected family members • Identify and positionally clone the mutation • Determine the function of the gene and understand how mutation alters this function
Genetics and Congenital Disorders Identification of Dysmorphic Features • Pediatric dentist can provide information to other professionals to aid in diagnosis of genetic disorder • Pediatric dentist can consult various online sources for information about inheritance of specific syndromes – National Center for Biotechnology Information – Online Mendelian Inheritance in Man – National Human Genome Research Institute
735
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
Clinical Application Treatment will primarily be determined by the clinical features and patient’s needs: • • • •
Behavioral Physical features Medical aspects Multidisciplinary approach to dental care – think about orthodontic issues early on and incorporate care into overall treatment plan
Genetics and Congenital Disorders
Modes of Inheritance Single Gene Inheritance: caused by mutation in a single gene Chromosomal anomalies ! Autosomal Dominant Transmission ! Autosomal Recessive Transmission ! X-linked Recessive Transmission !
736
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
Modes of Inheritance Multifactorial Inheritance: caused by interaction between genetic and environmental factors • •
Cardiovascular disease Diabetes
Genetics and Congenital Disorders
Chromosomal Anomalies • Defect in the chromosome can result in ! Extra copies of chromosome– Trisomy 21 ! deletion of chromosome – 22q11.2 ! translocation of part of a chromosome
• Multiple physical defects • Mental/developmental delay
737
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Chromosomal Anomalies
Down Syndrome
• Trisomy 21 – chromosomal sporadic mutation
Down Syndrome
Characteristic Physical Features • Hypotonia • Mental deficiency – varying degrees • Increased incidence of cardiac defects • Increased incidence of hypothyroidism • Increased incidence of ALL
738
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Down Syndrome
Dental/Craniofacial Features • Small ears • Inner epicanthal folds • Up-slanting palpebral fissures • Relative macroglossia, fissured tongue • Class III orthognathic tendency • Microdontia • Hypodontia • Decreased risk for dental caries • Increased risk for periodontal disease
Down Syndrome
Periodontal Disease in Down Syndrome • Prevalence: 50-90% , all under age 30 • Prevalence increases with age • Primary dentition involved in 36%
patients • Greater in Down than in general population • Lower prevalence for Down at home • Higher prevalence of ANUG in institutionalized Down
739
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Down Syndrome
Periodontal Disease in Down Syndrome Mechanism of Periodontal Disease in Down Syndrome • Calculus not remarkable • Bacteria not different from other MR • Pathogens colonize earlier than in non-Down • Vasculature: abnormal capillary fragility • B-Cells normal • T-Cells dysfunctional: may have diminished
ability to recognize and respond to specific antigens
Down Syndrome
Plan for Dental Treatment If considering sedation or general anesthesia, consider specific issues related to patient’s medical condition • Atlanto-axial instability • Bradycardia • Airway challenges
740
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
Autosomal Dominant Tranmission • Gene responsible for phenotype located on one of 22 pairs of autosomes • Expressed in individuals who have just one copy of the mutant allele • Males/Females equally affected • Offspring of affected individuals have 50% chance of inheriting mutant allele
741
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Dominant Transmission
Dentinogenesis Imperfecta Type 2 • Physical findings normal (differs from OI –
DI Type 1) • Family usually aware of condition & its consequences • Early consultation to prepare for future needs
Autosomal Dominant Transmission
Dentinogenesis Imperfecta Type 2 Dental Findings • Primary and permanent dentition affected • Teeth blue-gray/brown • Teeth susceptible to severe wear • Pulpal obliteration/dental abscesses
742
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
743
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Dominant Transmission
Dentinogenesis Imperfecta Type 2 • Plan for dental treatment: Primary Dentition ! SSCs when molar wear is evident ! Pulp therapy/extractions as needed • Plan for dental treatment: Permanent Dentition • Possible bleaching • Composite veneers • Full coverage crowns • Endodontic therapy
Genetics and Congenital Disorders
Autosomal Recessive Tranmission • Gene responsible is located on one of 22 autosomes • Expressed only in individuals who have both copies of the mutant allele • If only one copy of mutant allele is present, individual is an unaffected carrier • Males/females equally affected • If 2 carriers mate, resulting offspring have: ! 25% chance of being unaffected ! 25% chance of being affected w/ expression ! 50% chance of being unaffected carrier
744
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Recessive Transmission
Cystic Fibrosis Epidemiology • 1/3,200 live Caucasian births • 2-4% of Caucasians are carriers • Chronic progressive disease • Shortened life expectancy
745
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Recessive Transmission
Cystic Fibrosis • Mechanism of CF • Abnormal CFTR protein • Abnormal ion transport • Decreased secretion of chloride • Increased absorption of sodium • Exocrine glands produce thick sticky secretions • Lungs, intestine, reproductive epithelium most affected
Autosomal Recessive Transmission
Cystic Fibrosis Diagnosis of CF • 10% detected at birth, most detected in
first 3 years of life • Genetic testing • Sweat chloride test for diagnosis
746
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Recessive Transmission
Cystic Fibrosis Symptoms of CF • • • • • • • •
Salty tasting skin 2-5 times normal amount of Na, Cl, K in sweat Failure to gain weight Abnormal bowel movements Recurrent wheezing, cough Recurrent pneumonia Nasal polyps Clubbing of fingers and toes
Autosomal Recessive Transmission
Cystic Fibrosis Respiratory Complications of CF Chronic lung disease ! Bronchiectasis – form of COPD ! Pneumothorax – collapse of lung ! Hemoptysis – coughing up blood ! Cor pulmonale- right side heart enlargement
secondary to pulmonary dysfunction ! Clubbing
747
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Recessive Transmission
Cystic Fibrosis Respiratory Treatments of CF Airway clearance techniques • Chest physiotherapy 1-3 times/day • Mechanical vest – no assistance needed • Flutter device – resembles pipe
Compliance is most difficult in adolescents – allowing for independence is the key
Respiratory therapies for Cystic Fibrosis
748
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Recessive Transmission
Cystic Fibrosis Respiratory Treatments of CF • Exercise – Improves cardiovascular fitness and muscle strength – Loosens mucous, stimulates coughing • Aerosols – Bronchodilators – Mucolytics - (Pulmozyme) – Decongestants – Antibiotics – (Tobramycin) • Oral antibiotics
Autosomal Recessive Transmission
Cystic Fibrosis Digestive System and CF ! Pancreatic enzymes blocked in duct ! 90% patients affected ! Malabsorption of fat and protein
Poor weight gain – High fat stools – Abdominal pain, excess gas –
749
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autosomal Recessive Transmission
Cystic Fibrosis Management of Digestive System ! Pancreatic enzyme supplements ! Vitamins - fat-soluble A,D,E,K ! Iron ! Increase caloric intake to 120-150%
RDA
Autosomal Recessive Transmission
Cystic Fibrosis Oral Findings in CF ! Increased enamel defects ! Decreased caries ! Increased calculus ! Salivary pH elevated ! Gingivitis ! Potential for mouthbreathing/malocclusion
750
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Genetics and Congenital Disorders
X-Linked Recessive Transmission • Mutation located on gene affecting the X chromosome • Females typically carriers •
If mother is carrier, daughter 50% chance of being carrier
• Males • •
If mother is carrier, son has 50% chance of inheriting defective gene and expressing disease All daughters of affected males are carriers
Common examples: Ectodermal dysplasia, Hemophilia
751
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
X-Linked Recessive Transmission
Ectodermal Dysplasia Genetic Features • X-linked recessive, autosomal dominant,
autosomal recessive
• Many forms of ED that can affect one or
more of ectodermally derived tissues
Characteristic physical features • Sparse hair • Dry skin • Absence of sweat glands – heat
intolerance
• Normal mental status
752
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
X-Linked Recessive Transmission
Ectodermal Dysplasia Dental/Craniofacial features • Hypodontia to complete
anodontia of primary and permanent teeth
• Dental agenesis results in
underdevelopment of alveolar ridges
Ectodermal Dysplasia
Long-term Prosthetic Plan Long-term prosthetic plan • • • •
Dentures Bone-grafts, implants Orthognathic implications Psychosocial implications as child matures
Resource information: National Foundation for the Ectodermal Dysplasias
753
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Coagulation Disorders Process of Hemostasis • Primary: Platelet aggregation – – – –
Injury causes platelets to aggregate Release of vWF and collagen fibers from endothelium Platelets adhere to subendothelial matrix-vWF-collagen Vasoconstriction occurs
• Secondary: Coagulation Cascade – – –
Extrinsic pathway activated when injury exposes blood to Tissue Factor Intrinsic pathway produces factor X Common pathway generates thrombin
754
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
The Cascade of Coagulation
Coagulation Disorders
Fibrinolysis How is the clot removed? • Plasmin dissolves fibrin clot • Plasmin is regulated by antiplasmin and
plasminogen activator inhibitor
755
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Medical History Pursue all positive responses to “bleeding problems” • • • • • • • • • • •
Age of onset Type of bleeding Spontaneous or induced How long does bleeding continue? How does bleeding stop? Any problems with surgery or venipuncture Current medications Overall health – liver disease, etc. Family history History of blood or plasma transfusions Inhibitor status
Coagulation Disorders
Anticoagulant Medications • Aspirin • NSAID • Warfarin (Coumadin) – inhibits
production of Vit K-dependent factors
756
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Screening Lab Tests • PT – Extrinsic Path: tests for Factors VII, X, V, thrombin, fibrinogen • PTT –Intrinsic Path: tests for Factors VIII, IX, X, XI, V, thrombin, fibrinogen • Platelet count: platelet phase • Platelet function: platelet phase • Bleeding time: platelet phase, vascular
Coagulation Disorders
Patients at Moderate Risk for Bleeding • Family history • Abnormal bruising • Liver disease • ASA/NSAID use
–Juvenile rheumatoid arthritis
757
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Management of Moderate Risk Patients • Detailed medical history • Physician consult • Lab tests: PT, PTT, Platelet function, Platelet count • Optimize patient’s hematologic condition pre-op
Coagulation Disorders
Patients at High Risk for Bleeding • Known bleeding disorder • Taking oral anticoagulants – anti-Vit K (Coumadin) – Thrombotic disease – Factor V Leiden thrombophilia – Cardiac arrythmia • Use of heparin in last four hours
758
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Management of High Risk Patients • Consult with hematologist • Lab tests: PT, PTT, Platelet function,
Platelet count • Have patient optimized pre-op • Plan for post-op management
Coagulation Disorders
Dental Procedures and Risk of Bleeding Low • Supragingival restorations or prophylaxis • Infiltration anesthesia
Intermediate • • • •
Subgingival restoration Single extraction Endodontic treatment Nerve blocks
High • Multiple extractions • Periodontal surgery • Gingival curettage
759
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders Primary Defect • Defects in platelet number/function • Von Willebrand Disease
Clinical manifestations • • • • •
Longer bleeding time Bleeding from superficial and deep cuts Petechiae Small, multiple ecchymoses Spontaneous bleeding
Coagulation Disorders
Type of Defect Secondary defect • Defect in the Coagulation pathway • Hemophilia A & B
Clinical manifestations • No significant bleeding after superficial cuts • Significant bleeding after deep cuts • No petechiae • Large, wide-spread ecchymoses • Hematoma, Hemarthrosis • Spontaneous bleeding
760
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
von Willebrand Disease • • • • • • • •
Autosomal dominant inheritance Most common inherited coagulation disorder vWF may be deficient or defective Often detected after prolonged bleeding episode Low levels of vWF Low levels of factor VIII Prolonged bleeding time Abnormal platelet function test
Coagulation Disorders
von Willebrand Factor What is von Willebrand Factor? • Plasma protein produced in endothelial cells of vessels • Functions as a bridge between platelets and injury site in vessel – helps in platelet plug formation • Protects factor VIII from quick degradation
761
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Management of von Willebrand Disease Patients with von Willebrand may respond to desmopressin (DDAVP) • Synthetic peptide • For mild hemophilia A or vWD • Causes rapid release of factor VIII and vWF • 30-45 minutes to take effect • IV or subcutaneous injection • Stimate – nasal spray
Coagulation Disorders
Management of von Willebrand Disease Amicar (e-aminocaproic acid) effective for all types in stabilizing clot • Antifibrinolytic – inhibits activation of
plasminogen to plasmin • 2 hours to peak effect • Give IV or PO: 50mg/kg q6h until healed (usually 7 days) • May be given alone or with DDAVP
762
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Thrombocytopenia • Insufficient number of platelets • May be due to low production of platelets – Aplastic anemia – Cancer in bone marrow • May be due to increased breakdown of platelets – Idiopathic thrombocytopenic purpura (ITP) – Drug-induced immune thrombocytopenia
Coagulation Disorders
Thrombocytopenia Clinical manifestation ! Bruising ! Epistaxis, gingival bleeding ! Petechiae
Lab tests & findings ! CBC – low platelets ! PTT, PT - normal
Consult with physician prior to any procedures likely to induce bleeding
763
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Hemophilia • X-linked recessive inheritance • 1/3 cases – new mutations • Hemophilia A – Factor VIII – most
common (85%) • Hemophilia B – Factor IX (15%)
Coagulation Disorders
Hemophilia Classification of severity of hemophilia
• Hemophilia A Severe - < 1% Factor activity (70%) • Moderate 1-5% Factor activity (15%) • Mild >5% Factor activity (15%) Hemophilia B • Severe - < 1% Factor activity (50%) • Moderate 1-5% Factor activity (30%) • Mild >5% Factor activity (20%) •
•
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Coagulation Disorders
Hemophilia Bleeding with hemophilia • Normal platelet plug forms • Delayed formation of fibrin clot • Types of bleeding – Deep bleeding into joints or muscles – Increased bleeding from open wounds
Coagulation Disorders
Hemophilia - Complications Inhibitors • Antibodies that block activity of clotting factors – 15% of severe hemophilia A patients – 2.5% of hemophilia B patients
• Emerge after variable number of factor exposures • Treatments – High dose of clotting factor – Bypassing agents – Efforts to induce immune tolerance
765
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Hemophilia - Complications • Arthropathy • Bleeding into CNS or
airway • HIV infection • Hepatitis
Coagulation Disorders
Hemophilia - Treatment General Prophylaxis ! Goals
Decrease joint disease – Decrease hospitalizations – Decrease time lost from school or work ! Use clotting factor 2-3 times/week ! Prevent bleeds –
! Possible need for indwelling catheter for young patients
! High cost - $100,000/year
766
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Hemophilia - Treatment Management of coagulation disorders • Replacement with recombinant factors VIII and IX
Evolution of Factor VIII
Coagulation Disorders
Hemophilia - Treatment Management of coagulation disorders: DDAVP • Synthetic analogue of vasopressin that causes a rise in levels of Factor VIII and vWF • Peak levels obtained ~ 1 hour post-administration
767
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Hemophilia - Treatment Management of coagulation disorders: Antifibinolytics • Prevent clot dissolution • Amicar: e-aminocaproic acid • Cyklokapron: tranexamic acid Aminocaproic Acid (Amicar)
Coagulation Disorders
Hemophilia & Dental Treatment Pre-treatment planning for dental treatment • • • • • • • • •
Consult hematologist Type and severity of hemophilia Medications Type of treatment for bleeding disorder Contact info for hemophilia treatment center Inhibitor status Infectious disease status History of joint replacement? Venous access device present?
768
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Coagulation Disorders
Hemophilia & Dental Treatment Management of hemorrhage • Need to have Factor level to achieve/maintain
clot • Goal: 30-40% of normal • 1 unit factor VIII/kg = 2% increase in Factor VIII
level • 1 unit factor IX/kg = 1% increase in Factor IX
Hemostasis
769
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Coagulation Disorders
Hemophilia & Dental Treatment Local measures for hemorrhage control • Pressure • Sutures – absorbable if possible • Collagen sponge – increases platelet aggregation • Gelfoam – absorbs blood, forms matrix • Bone wax • Thrombin – helps conversion of fibrinogen to fibrin • Electrocautery • Epinephrine – re-bleeding likely to occur
Coagulation Disorders
Hemophilia & Dental Treatment Dental management of patients with hemophilia Focus on prevention – caries, gingival tissues Consultation with hematology team Plan for management of hemophilia Plan for all dental treatment in one visit Fabricate splints for extractions Local measures: collagen, gelfoam, topical thrombin, soft diet – 10 days • Management of break-through bleeding • Management of liver clot from slow bleed • • • • • •
770
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Coagulation Disorders
Thrombotic Disorders Acquired • • • •
Short-duration Pregnancy Surgery Immobilization
Inherited • Related to impaired function of protein C-
anticoagulant system
• Factor V Leiden – Incidence 5% in North America – Results in increase in prothrombin
Coagulation Disorders
Thrombotic Disorders Management Acute • Heparin for several days, followed by Warfarin for 3-6 months Long-term • Anti-coagulant therapy
771
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Sickle Cell Anemia Sickle Cell Disease • Autosomal recessive hemoglobin defect • Genotype determines symptoms – Heterozygote: HbA and HbS • 8-10% African Americans • Sickle cell trait – Homozygote: HbSS • 1 in 500 African Americans
Sickle Cell Anemia
Diagnosis • Blood sample collected • RBCs are exposed to deoxygenating agent • Sickling of cells occurs if trait or disease is present – Homozygous – rapid rate of sickling; almost all red blood cells involved – Electrophoresis confirms diagnosis
772
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Sickle Cell Anemia
Hemoglobin S
Sickle Cell Anemia
Hemoglobin S Sensitive to O2 demands and supply • Systemic disease • Dehydration • Exposure to cold • Rigorous exercise • Infection • Acidosis • Stress
773
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Sickle Cell Anemia
Medical Findings • Anemia due to decreased survival of • • • •
sickled RBC’s Chronic anemia: HbG 6-9 g/dl; Hct – 20 Delayed growth and puberty Susceptibility to sepsis Bone pain – sickled RBC trapped in bone sinusoids
Sickle Cell Anemia
Medical Findings • Hand/foot syndrome – when small vessels blocked • Chest syndrome – Sickled RBC block circulation in alveoli – Severe pain, cough, fever, dyspnea • Abdominal pain – Liver, spleen, kidney damage • Aplastic crisis • Thrombotic crisis
774
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Sickle Cell Anemia
Morbidity/Mortality • Pneumococcal infections –
early treatment with antibiotics decreases incidence • Morbidity related to blockage of various organs • Life expectancy: late 40s
Sickle Cell Anemia
Medical Management of Patients ! Early diagnosis ! Avoid sickling-inducing conditions –Dehydration –Acidosis –Cold exposure ! Blood transfusions regularly
775
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Sickle Cell Anemia
Crisis Management • Bed rest to decrease oxygen use • Hydration • Electrolyte replacement • Analgesics • Transfusion to treat anemia • Antibiotics
Sickle Cell Anemia
Oral Findings • • • • • • • •
Pale mucosa Enamel hypoplasia Dental or jaw pain (from infarcts) Delayed eruption Pulp calcifications Mandible – decreased trabeculae Class II – protrusive maxilla Decreased caries when taking antibiotics
776
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Sickle Cell Anemia
Dental Management of Patients • • • • • • • •
Prevention of dental disease Antibiotic prophylaxis – uncertain value AM appointments – keep brief Local anesthesia with vasoconstrictor is okay N2O – minimum of 50% O2 to avoid hypoxia Acetaminophen for pain Considered ASA III Avoid elective surgery – treat infections vigorously
Diabetes
777
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Diabetes
Type I (Insulin-Dependent) Diabetes • Destruction of pancreatic beta cells leads to absolute insulin deficiency • Most common form of pediatric diabetes: 70% • Peak onset – Girls: 10-12 years – Boys 12-14 years • Causes – Genetic, environmental, autoimmune factors
Diabetes
Symptoms of Type I Diabetes • • • • • •
Frequent urination Extreme increase in appetite and thirst Weight loss Fatigue Weakness Symptoms develop over a short period of time
778
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diabetes
Type II (Non-Insulin-Dependent) Diabetes • 30% of pediatric diabetes • Increasing incidence in children &
adolescents • Body doesn’t use insulin properly • Risk factors – major one is obesity
Diabetes
Symptoms of Type II diabetes • • • • • • • •
Increased appetite and thirst Increased urination Fatigue Blurred vision Dry, itchy skin Tingling or numb extremeties Nonhealing skin infections Acanthosis nigricans – cutaneous marker of insulin resistance – at nape of neck
779
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Diabetes
Medical Treatment Goals • Eliminate hyperglycemia symptoms • Stabilize blood glucose • Restore normal body weight • Prevent long-term complications
Diabetes
Management of Type I Diabetes • Frequent glucose monitoring (4 times/day or more) • Diet • Medications – injected insulin • Insulin pump • Pancreatic islet cell transplant
780
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diabetes
Management of Type II Diabetes • • • • •
Weight loss Small, frequent meals Exercise Daily glucose monitoring Medications – Oral hypoglycemics
– Injected Insulin • Long-term compliance difficult
Management of Diabetes
781
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Diabetes
Diet Management Glycemic Index Goal is to eat low-to medium GI foods Refined grains, potatoes, sucrose - high GI Non-starchy vegetables, fruits, legumes, nuts - low GI • Fat and protein have minimal effect on blood glucose • • • •
Diabetes
Oral Findings • Increased incidence of periodontal • • • •
disease Prolonged infections Xerostomia Delayed wound healing Altered sensations: numbness, burning, taste
782
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diabetes
Periodontal Disease and Diabetes • More gingival bleeding in diabetic children than in healthy counterparts • Diabetic children: lifelong increased risk of PD • Plaque Index not correlated with Gingival Index • Level of diabetic control is more important than plaque control in the severity of the gingival inflammation • Good metabolic control helps address periodontal considerations
Diabetes
Periodontal Disease and Diabetes Mechanism of periodontal changes • Early acute inflammatory response • HgA1C elevated • HgA1C levels positively correlate with
gingival bleeding levels – this implies a relationship between periodontal microvasculature and metabolic control
783
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diabetes
Dental Management of Patients AM appointments best Normal insulin dose + normal meal Ask about history of hypoglycemia Bring glucometer to appointment, check pre-op • Have source of glucose available • • • •
Diabetes
Dental Management of Patients Prevention is to be maximized • Incorporate periodontal exam/screening into
routine care
• Discuss relationship between glycemic
control and periodontal disease
• Manage infections aggressively: consider
antibiotics
784
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diabetes
Hypoglycemia Symptoms • Mild: hunger, weakness, increased pulse,
sweating
• Moderate: incoherence, uncooperativeness,
belligerence
• Severe: LOC, tonic or clonic movements,
hypotension, hypothermia
Diabetes
Hypoglycemia Management • Treat immediately – Don’t wait • Administer glucose in some form • Retest blood sugar • Repeat in 15 minutes if symptoms don’t
improve
785
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Diabetes
Long-Term Complications Caused by chronic hyperglycemia • • • • • • •
Retinopathy Nephropathy Neuropathy Peripheral vascular disease Hypertension Atherosclerosis Coronary artery disease
Gastro-Esophageal Reflux Disease
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Gastro-esophageal Reflux Disease
GERD Malfunctioning or weak LES Hiatal hernia Incidence: 5-7% of population Symptoms + tissue damage: esophagitis, erosive GERD • Symptoms + no tissue damage: non-erosive GERD • • • •
Anatomy of GERD
787
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GERD
Symptoms ! Chronic heartburn ! Acid regurgitation ! Belching ! Painful swallowing ! Chronic sore
throat ! Laryngitis ! Sour taste
GERD
Untreated • • • • • • • •
Persistent discomfort Burning/scarring of esophagus Malignant transformation Apnea Chronic cough Asthma Recurrent pneumonia Poor weight gain
788
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
GERD
Diagnosis • • • • • • •
History 2 week trial of medication pH monitoring of esophagus Barium swallow – upper GI series Endoscopy Ultrasonography Laryngoscopy
GERD
Oral Signs/Symptoms • Difficult or painful swallowing • Gingival inflammation • Enamel erosion – Maxillary palatal surfaces affected first – Loss of hard tissue by chemical process
789
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
790
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
GERD
Treatment Lifestyle modification • Upright until meal digested • Decrease portion size • Restrict food choices • No exercise after meals • Reduce body weight
GERD
Treatment
Avoid foods that aggravate GERD • Caffeine-containing sodas • Chocolate • Peppermint • Spicy foods • Acidic foods • Fried, fatty foods • Alcohol
791
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
GERD
Treatment Medications • Antacids – neutralize stomach acid • Foaming agents – cover stomach contents • Proton pump inhibitors – impede acid production • Prokinetics – strengthen sphincter
GERD
Treatment Surgery • Fundoplication – 90% cure rate • Stretta procedure: electrosurgery- induced scarring of GEJ • Endocinch procedure: sutures to reduce LES opening • Enteryx procedure: inject polymer into LES
792
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
GERD
Dental Considerations • Children with GERD have increased risk of erosion • Higher salivary micro-organism colonization in GERD children increases caries risk • Consider evaluation for GERD when dental erosion is present in asymptomatic children
Seizure Disorders
793
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
General Considerations • Epilepsy = 3 or more recurrent seizures • Affects 1% of general population • Majority: no identifiable etiology • Involves spontaneous uncontrollable
excessive discharge of cerebral neurons
Seizure Disorders
Seizure Classification New terminology • • • •
Partial: simple or complex (40%) Generalized: convulsive or nonconvulsive (40% ) Unclassified Status epilepticus – seizure lasting > 30 minutes
794
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Generalized seizure
Partial seizure
Seizure Disorders
Partial Seizures - Simple • Originate from localized area of brain • Patient remains conscious • Motor, autonomic, sensory, or psychic symptoms – Localized muscle twitching – Localized numbness or tingling – Chewing, smacking lips – Flashes of light – Feeling of dissociation from body
795
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Partial Seizures - Complex • • • •
Originate from localized area of brain May be preceded by aura 1-2 minute loss of consciousness Motor, autonomic, sensory, or psychic symptoms – – – – –
Localized motor activity Paresthesia Overwhelming sense of fear Visual disturbances Distorted perceptions
• Confusion continues 1-2 minutes postictal
Seizure Disorders
Generalized Seizures • Involve entire brain • Classified by presentation ! Absence ! Myclonic ! Tonic-Clonic ! Atonic ! Clonic ! Tonic
796
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Seizure Disorders
Generalized Seizures • Absence seizures (formerly termed petit mal) ! 10-30 second LOC ! Brief eye or muscle fluttering ! Sudden stop of activity ! Onset generally 4-10 year ! 50% develop tonic-clonic seizures at puberty ! Misdiagnosed as behavior or learning problems
Seizure Disorders
Generalized Seizures Tonic-Clonic seizures (formerly termed grand mal) ! Aura - hours to days before seizure ! LOC leads to falling ! Tonic phase: muscle rigidity for 10-20 seconds ! Clonic phase: 2-5 minutes of muscle contractions ! Urinary and/or fecal incontinence ! Postictal period 10-30 minutes ! Full recovery – 3 hours
797
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Other Generalized Seizures Atonic: brief loss of muscle tone May/may not lose consciousness ! Many injuries from falls !
Clonic: contraction/relaxation Tonic: persistent contractions
Seizure Disorders
Unclassified Seizures • Neonatal seizures • Severe myoclonic epilepsy in infancy • Febrile convulsions • Special syndromes
798
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Seizure History Questions to ask ! Age of onset ! Type ! Duration ! Triggers ! Frequency – date of last seizure ! Medications and compliance ! Control – date of last hospitalization for seizure ! Diet
799
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Medical Management Anti-convulsive medications Ketogenic diet – used for difficult-to-control seizures ! High in fat (3:1 ratio of calories) ! Adequate in protein ! Low in carbohydrate ! Vitamin/mineral supplements indicated ! Avoid liquid and chewable medications – contain
carbohydrates
800
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Medical Management Surgery Hemispherectomy ! Vagus nerve stimulator ! Section corpus callosum !
Alternative /Complementary medicine
Seizure Disorders
Medical Management Medications • Comprehensive descriptions in Manual • Choice of medication based on type of seizure • Medications may be changed based on patient response • Basic principles • Consult with physician/neurologist • Know medication actions • Know medication interactions • Know medication side effects
801
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Medical Management Medications Common side effects of seizure medications • Lethargy • Dizziness • Ataxia • Potential for drug interactions
Some dental effects of seizure medications • Xerostomia (Tegretol, Neurontin) • Gingival bleeding (Depakene) • Gingival hyperplasia (Dilantin)
Seizure Disorders
Medical Management Medications Dilantin-induced gingival hyperplasia
802
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Medical Management Medications Dilantin-induced Gingival Overgrowth • Prevalence of gingival enlargement: 50% • Overgrowth is fibroepithelial in nature • Increase in plaque and inflammation related to increase in dilantin-induced gingival overgrowth
Seizure Disorders
Dental Considerations for Patients • Consider anxiety management • Caution with sedation due to effects of medications • Schedule when well-rested • Make sure medications were taken • Be aware of medication side effects • Be prepared to manage seizure
803
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Seizure Disorders
Seizure Management • • • • • •
Note time that seizure begins Stay calm Move onlookers away Position patient to prevent injury Post-ictal airway support Seizures > 5 minutes, activate EMS: Status epilepticus
Attention Deficit Hyperactivity Disorder ADHD
804
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Attention Deficit Hyperactivity Disorder
ADHD Components of attention ! Focus: ability to spotlight ! Shift: flexibility ! Sustenance: vigilance
over time
Prefrontal brain functions ! Maintain attention ! Self-regulate impulsivity ! Delay gratification
ADHD
Diagnosis ADHD not considered a developmental disorder • Psychiatric diagnosis • Incidence 6-16% • Serious and persisting difficulties
Inattention – Hyperactivity – Impulsivity –
805
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Possible Etiologies of ADHD • Genetic predisposition • Brain size – 3 to 4% smaller in ADHD • System dysfunctions !
Neurotransmitter deficiencies
• Environmental toxins • Severe head injury • History of childhood cancer
ADHD
Effects of ADHD • Psychological impact • Education • Occupational adjustment • May be underachievers • May develop significant social/psychiatric
dysfunction
806
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Common Behaviors and Symptoms Inattentive
ADHD
Common Behaviors and Symptoms
Hyperactivity
807
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Common Behaviors and Symptoms
Impulsivity
AHDD
Diagnosis of ADHD Behaviors of inattention, impulsivity, hyperactivity must: ! Occur in more than one setting (home/school) ! Be more severe than in other children same
age ! Start before 7 years of age ! Continue for >6 months ! Make it difficult to function in various settings
808
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Types of ADHD • Inattentive only (formerly ADD) • Hyperactive/Impulsive • Combined Inattentive/Hyperactive/Impulsive
ADHD
Co-existing Conditions (Comorbity) Oppositional defiant disorder/Conduct disorder (35%) Depression (18%) Anxiety disorders (25%) Learning disabilities
809
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Childhood Impairments • Poor schoolwork completion • Increased learning disabilities • Conduct problems • Peer rejection • Conflict with parents and teachers • Low self-esteem • Poor coordination
ADHD
Adolescent Impairments • • • • • • • •
Failed a grade Increased dropout rate School suspensions Serious antisocial behavior Alcohol or drug use Serious auto accidents Low self-esteem Trouble keeping friends
810
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Safety Concerns ADHD – requires close supervision
ADHD
Treatment of ADHD: Medical/Behavioral • Treatment plan as for other chronic conditions • Long-term management: Set goals, assess outcomes • Teamwork – Doctors, teachers, parents, caregivers, etc. • Medications • Behavior therapy • Parent training • Counseling
811
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Medications Dosages not based solely on weight, but also on patient response to medication
ADHD
Medications - Stimulants Methylphenidate (Ritalin, Concerta) • • • • • • •
Non-amphetamine CNS stimulant Xerostomia Tachycardia Nervousness Anorexia Insomnia Potentiates arrythmogenic effects of tricyclic antidepressants (TCAs)
812
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Medications - Stimulants Dextroamphetamine (Adderall) • • • • • • • • •
Amphetamine CNS stimulant Xerostomia Altered taste Bruxism Hypertension Nervousness, insomnia Anorexia Potentiates arrythmogenic effects of TCAs Meperidine contraindicated
ADHD
Medications – Non-stimulants Amoxetine HCL (Strattera) •
• • • • •
Selective nor-epinephrine reuptake inhibitor Xerostomia Anorexia Fatigue Elevated BP Avoid levonordefrin
813
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Medications – Non-stimulants Clonidine (Catapres) • • • • • •
Anti-hypertensive Xerostomia Dysphagia Sialadenitis Potentiates CNS depressants Cardiac arrythmias
ADHD
Medications – Trends • Between 1991 and 1995, use of stimulants in 2-4 year old children tripled • Use of these medications in children < 6 yrs is “off-label” • Questions of efficacy and safety • Difficult to assess changes in developing personality due to psychotropic drugs • Questionable validity of diagnosis of ADHD, mood disorders in very young children
814
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Behavioral Therapy • Positive reinforcement: reward desired behavior • Time out: remove access to activity due to unwanted behavior • Response-cost: withdraw rewards due to unwanted behavior • Token economy: child receives tokens when displaying desired behavior; tokens later exchanged for meaningful object/privelege
ADHD
Additional Behavioral Therapies • Keep child on a schedule • Cut down on over-stimulating distractions • Provide an organized environment • Reward positive behavior • Set small, attainable goals • Limit choices • Use calm discipline
815
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Dental Management of Patients Behavioral aspects ! Know definitive diagnosis and treatment plan
for patient
! Use behavioral approaches that reinforce
those being used in long-term management plan
! Immediate positive reinforcement ! Short appointments ! Don’t treat on drug holidays
ADHD
Dental Management of Patients • Increased bruxism • Involve parent in oral hygiene • Remember that patient has ADHD • Update history/progression of ADHD
since last dental visit
816
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
ADHD
Dental Management of Patients • Look up medications – side effects • Increased risk of dental trauma • •
Poor coordination Impulsivity
Developmental Disabilities
817
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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819
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Steven M. Adair, DDS, MS Medical College of Georgia
•
Dental lamina
•
Bud stage
•
Cap stage
•
Bell stage
•
Advanced bell stage
•
Hertwig’s epithelial root sheath
820
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Initiation - seen at 37-42 days in utero • dental lamina inductive activity • anomalies: tooth number
•
Proliferation • bud, cap, early bell, late bell stages • anomalies: size, proportion, number, twinning
821
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Histodifferentiation • cap, early and late bell stages • differentiation of odontoblasts and ameloblasts • anomalies: AI type I (hypoplastic), AI type IV, dentinogenesis imperfecta
•
Morphodifferentiation • bud, cap, early and late bell stages • basic form and relative size established; DEJ outline established • anomalies: size and shape
822
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
o
Apposition • matrix deposition for hard tissues • anomalies: enamel hypoplasia, dentinal dysplasia, hypercementosis, enamel pearls
•
Mineralization and Maturation • occurs in immediate and maturation phases • removal of H2O/organic material, add’l mineralization • outward from DEJ, from incisal to cervical • anomalies: AI II, III, IV, fluorosis, interglobular/sclerotic dentin and localized hypomineralization
823
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Lines of apposition and maturation seen via tetracycline staining
•
Incidence 0.3-3%; males 2:1 females
•
Permanent dentition 5:1 primary dentition
•
90—98% in maxilla
824
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Supplemental
“normal” morphology
Supplemental permanent?
Supplemental primary incisor
825
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•Rudimentary
conical tuberculate molariform
826
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
827
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
828
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Apert
•
Cleidocranial
•
Down
•
Sturge-Weber
•
Orofaciodigital syndrome I
dysplasia •
Gardner
•
Hallerman-Strief
•
Crouzon
•
Cleft lip and palate
•
Incidence 1.5-10%, excluding 3rd molars (0.09-0.4% for primary dentition)
•
Frequency: 3rd molar, mandibular 2nd premolar, maxillary lateral incisor, maxillary 2nd premolar
•
Significant correlation b/t missing primary tooth and missing permanent successor
•
Familial tendency
829
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Problems may arise from
• • • •
failure of induction abnormality of lamina insufficient space physical obstruction of lamina
830
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Bilateral
831
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Missing primaries
No (?) permanent teeth
•
Ectodermal dysplasia
•
Incontinentia pigmenti
•
Crouzon
•
•
Achondroplasia
Orofaciodigital syndrome I
Chondroectodermal dysplasia
•
•
Hallerman-Strief
•
Reiger
•
Extremely talented/rich former NBA players
•
Seckel
Other ectodermal organs sometimes affected: salivary glands, skin (sweat glands), hair, nails – not part of ectodermal dysplasia
832
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
True generalized • small/large teeth in normal jaws
•
Relative generalized
• normal or slightly small teeth in large jaws • normal or slightly large teeth in small jaws
•
Single tooth macrodontia rare • rule out fusion, gemination
•Frequency –lateral incisors –second premolars –third molars
True localized
833
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Barrel-shaped lateral Peg lateral on right, missing lateral on left
Microdont molars and 3 premolars
Relative generalized
834
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Ectodermal dysplasia
•
Chondroectodermal dysplasia
•
Hemifacial microsomia
•
Down syndrome
•
Crouzon
•
Hemifacial hypertrophy; accelerated eruption on affected side
•
Crouzon
•
Otodental syndrome • macrodontia of posterior teeth • globodontia, molar fusion
835
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Photos courtesy of Dr. Lourdes Santos-Pinto
836
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Gemination • incidence ~0.5%; more common in primary dentition • may retard eruption of permanent successor • clinical diagnosis: extra crown (assumes normal complement of other teeth)
837
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Single pulp canal; extra crown (depends on clinical appearance)
•
Twinning • complete cleavage of single bud • mirror image “supernumerary” tooth
838
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Fusion • incidence roughly 0.5%, more common in primary dentition • union by dentin; separate pulp chambers/canals • may retard eruption of permanent successor • clinical diagnosis: normal complement of crowns (unless fusion with supernumerary)
839
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Concrescence • fusion occurs after root formation complete • etiology: trauma?, crowding? • may occur pre- or post-eruption
840
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Dens-in-dente (dens invaginatus)
•
Dens evaginatus (talon cusp)
•
Taurodontism
•
Dilaceration
•
“Tooth within a tooth”
•
Incidence 1-7.7%; rare in African-Americans
•
4 classes
crown only
841
part of root
entire root
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Maxillary lateral most affected; both dentitions
•
Etiology: invagination of inner enamel epithelium
•
Hertwig’s epithelial root sheath involved in severe cases
•
Treatment • • • •
conventional RCT MTA/RCT combined RCT/surgery intentional replantation
842
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
3 types:
•
• I – talon • II – semi-talon • III – trace talon
•
Incidence 1-8%
•
Higher in some racial groups
•
77% occur in permanent teeth
•
94% are maxillary incisors
•
55% are lateral incisors
•
May be uni- or bilateral
•
65% in males
843
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Evagination of enamel epithelium
•
Pulp tissue within extra cusp
•
Seen in lobodontia (“wolf teeth”)
•
Failure of proper invagination of Hertwig’s epithelial root sheath
•
“Bull’s teeth”
•
Incidence 0.5-5.6%; higher in some groups
•
Genetic advantage to groups that use teeth as tools (?)
844
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Klinefelter
•
Trichodento-osseous
•
Orofaciodigital II (Mohr)
•
Ectodermal dysplasia (hypohidrotic)
•
Amelogenesis imperfecta type IV
•
Down syndrome
•
Etiology: trauma, especially intrusion injuries to primary dentition
•
Syndrome with dilaceration: lamellar ichthyosis
845
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Enamel defects • amelogenesis type I • amelogenesis type IV (discussed under Maturation)
•
Dentin defects • dentinogenesis types I, II, III
846
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Heritable enamel defect
•
Reported incidence varies from 1:14,000 to 1:4000
•
Multiple inheritance patterns
•
4 major types (Witkop), 14 subgroups
•
Distinguished from other enamel defects: • confined to distinct patterns of inheritance • occurs apart from syndromic, metabolic, or systemic conditions
•
Insufficient quantity of enamel (matrix)
•
Both dentitions affected
•
Most subgroups autosomal dominant
•
Most frequently reported type (?)
Anterior openbite in 44% “vertical dysgnathia”
847
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
848
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
849
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Heritable defect of predentin matrix • normal mantle dentin • amorphic and atubular circumpulpal dentin
•
Incidence 1:8000
•
Three types as defined by Shields
850
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Mantle: outer layer of primary dentin Primary: develops before and up to root completion (Circumpulpal = primary – mantle)
Secondary: develops after root completion
Tertiary: develops in response to trauma/caries Predentin: innermost layer
•
Occurs with osteogenesis imperfecta (IB & IVB)
•
Dental manifestation of type I collagen defect
•
Primary teeth more severely affected
•
Permanent teeth - central incisors and 1st molars
851
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Least severe form
•
Amber translucence
•
Periapical radiolucencies, alveolar abscesses
•
Autosomal dominant
•
Rapid attrition
•
Pulpal obliteration – occurs soon after eruption of prior to eruption
•
Degree of expressivity is variable intra- and interpatient
•
Bulbous crowns, short roots
•
Occurs alone - no osteogenesis imperfecta
•
Attributed to mutations of DSPP gene
•
Nearly complete penetrance; more consistent expressivity w/in a family
852
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Both dentitions equally affected
•
Same characteristics as DI-I
•
Irregular or tubular pattern
•
Autosomal dominant
•
Rare; most severe; Brandywine triracial isolate
•
Bell-shaped crowns, opalescent hue
•
Shell teeth (esp. primary teeth, short roots, enlarged pulp chambers), only mantle dentin
•
Rapid wear of primary and permanent teeth
•
Permanent pulps obliterated; multiple pulp exposures in primary teeth
•
Regular tubules
•
Enamel pitting
853
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Enamel hypoplasia • systemic • local
•
Enamel pearls
854
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Physiologic • developmental, ingestional
•
Infectious
•
Traumatic
•
Iatrogenic Jorgenson & Yost
•
Potential marker for celiac disease
•
Predominant locations: • upper/lower • primary/permanent • centrals/laterals
•
55% of celiac patients vs 18% of controls
Bossu et al 2007; Wierink et al 2007
855
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Cells of epithelial root sheath may remain attached to dentin
•
May differentiate into ameloblasts and produce enamel
•
Enamel pearls may contain dentin and pulp
•
Dentin dysplasia - 2 types (Shields)
•
Regional odontodysplasia
•
Others
856
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Short, blunted roots, or rootless
•
Obliterated pulp chambers
•
Multiple periapical radiolucencies
•
Severe mobility and malalignment
•
Autosomal dominant - root sheath problem
•
Prevalence 1:100,000
“rootless” teeth
857
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Coronal and root dentin dysplasia
•
Primary teeth affected
•
Amber color - looks like DI-II
•
Permanent teeth appear normal clinically, but demonstrate thistle-tube shaped pulps, multiple pulp stones
•
Characteristics of DI-II sometimes seen
Kim & Summer 2007
858
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
•
• •
•
•
“Ghost teeth” - localized arrest in tooth development Thin enamel, diffuse shell appearance Large pulps, little dentin Affects primary and/or permanent dentitions 80% involve central incisors No known etiology or inheritance pattern
859
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
860
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Vitamin D-resistant rickets
•
Ehlers-Danlos syndrome
•
Hypoparathyroidism
•
•
Pseudohypoparathyroidism
Epidermolysis bullosa
•
Osteogenesis imperfecta
•
Albright’s hereditary osteodystrophy
•
Hypercementosis
•
Hypophosphatasia - 4 types • little cementum produced (controversial) • autosomal recessive • early exfoliation of primary teeth (little or no resorption)
•
Epidermolysis bullosa
•
Cleidocranial dysplasia
861
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Hypophosphatasia
Cleidocranial dysplasia
•
Enamel hypomineralization - systemic and local
•
Hypomineralized permanent first molars
•
Amelogenesis imperfecta type III
•
Enamel fluorosis
862
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
See etiologies for enamel hypoplasia previously discussed – similar etiologies
•
Hypomineralization of 1-4 permanent first molars
•
Frequently assoc w/ affected permanent incisors
•
Prevalence 4-25% (Europe)
•
Varies with birth cohorts, suggesting potential environmental factors
863
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Called “cheese molars” by the Dutch
•
Possible problem with ameloblast function and/or mineral uptake
•
Associated with • • • • • •
febrile illness confounding factors antibiotics nutritional deficiencies preterm birth dioxin compounds in breastmilk others – see manual; William et al 2006
864
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Most common type (?)
•
Deficit in mineralization of normal matrix
•
Normal thickness, but soft; yellow to yellow-brown
•
Pronounced thermal sensitivity
•
Reduced radiographic distinction between enamel and dentin
•
Anterior openbite in 64% (Rowley et al)
•
High calculus formation (rough enamel)
•
Delays in eruption
•
Inheritance patterns: autosomal dominant and recessive
865
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Defect of mineralization (subsurface)
•
Thin, paper white opaque lines corresponding to perikymata
•
Entire surface chalky white
•
Porosity leads to staining
•
Pitting, enamel loss in severe cases
866
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
• •
Amelogenesis imperfecta type II Amelogenesis imperfecta type IV
867
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Normal enamel thickness, but undermineralized, low radiodensity
•
Less severely hypomineralized than hypocalcified type
•
Brown, porous surface, soft, chips away (rather than wears away)
•
Persistence of organic content
•
X-linked recessive
•
Subgroups • pigmented - autosomal recessive • X-linked recessive • snow capped - autosomal dominant?
868
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Brown, porous surface
• •
• •
Distinct from trichodento-osseous syndrome Mottled yellow-brown enamel with pits
Molars are taurodont Subgroups
• hypomaturation-hypoplastic • hypoplastic-hypomaturation • both autosomal dominant
869
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Blood-borne pigments • • • •
porphyria: purplish-brown bile duct defects: green neonatal hepatitis: black, gray Rh incompatibility: blue-green, brown • anemias: gray • dental trauma: red, gray, black
870
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Trauma
•
Hypoplasia/hypocalcifi-cation disorders • amelogenesis imperfecta
•
Dentinogenesis imperfecta • dental caries • enamel and dentin dysplasias
•
Systemic fluoride
•
Mechanisms of tooth bleaching • H2O2 oxidizes wide variety of organic / inorganic compounds that cause staining • bleaching can occur in solution or on a surface • mechanisms of H2O2 bleaching not well understood
871
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Mechanisms of tooth bleaching
• peroxide diffuses into / through enamel to reach dentin and pulp • levels of peroxide in pulp insufficient to inactivate pulpal enzymes • color changes occur throughout dentin
•
Type of bleach • hydrogen peroxide • carbamide peroxide • adduct of urea & H2O2 breaks down on contact with water into those components • 10% carbamide peroxide = 3.6% hydrogen peroxide
• sodium percarbonate • used in silicone polymer that is painted onto teeth •
Concentration of bleaching agent
•
Time
872
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Temperature • rise of 10º C doubles rate of reaction
•
Light • halogen, plasma arc, lasers, LEDs • light source may energize stain to accelerate bleaching process, but actual effect is controversial
•
Type of stain • eg, tetracycline
•
Effect of plaque and pellicle • appear to be minimal
•
In-office procedures • internal bleaching (incl. “walking bleach”) for endodontically treated teeth • external bleaching: 25-38% carbamide peroxide with / without heat / light
•
Vital nightguard bleaching • 10% carbamide peroxide in custom trays
•
OTC products • bleaching strips, paint-on gels, userfabricated or user-modified trays
873
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Transient tooth sensitivity • reduce duration / frequency of bleaching sessions • use desensitizing toothpaste • discontinue bleaching (rare)
•
Gingival irritation • usually caused by improperly made tray
•
Use of acidified pumice • manual or handpiece-driven rubbing
•
Can remove stains if discoloration is less than a few tenths of a mm deep • cannot know depth of stain until microabrasion is attempted
874
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Best for isolated brown or white areas in otherwise normal enamel (eg, fluorosis)
•
If combined with bleaching, generally attempt microabrasion first
•
Microabrasion followed by bleaching can improve tooth discoloration prior to composite or other veneer
•
Generally contain abrasives designed to remove surface stains
•
Some contain peroxide bleaching agents
•
No evidence of efficacy for internal stains
875
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
• • •
Root growth Hydrostatic pressure Bone remodeling
•Periodontal ligament traction •Connective tissue proliferation at pulp apex
•
Hormonal control (growth and thyroid) • circadian rhythms in eruption reflect rhythmic activity of PDL • more eruption seen in evening during sleep • corresponds to release of growth hormone factor
876
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Children with height for age deficits at 6 months • fewer pairs of erupted primary teeth at 6 & 12 mos • less likely to have some permanent molars erupted at age 6
•
Physical control • teeth undergo periods of eruption and intrusion
•
Most favorable in primary dentition: ABDCE
•
Most favorable in permanent dentition Maxilla: 6 1 2 4 5 3 7 8 Mandible: 6 1 2 3 4 5 7 8
•
Sequence more important than timing
877
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Genetic • strong correlation in twin studies • AfrAmer earlier than whites (?) • females ahead of males
•
Environmental • low birth weight/prematurity delays eruption • nutrition – little/no effect • SES – may hide confounding variables
•
Systemic • high correlation with hypopituitarism and hypothyroidism • low correlation with growth hormone production
•
Root development
•
Amount of overlying bone
•
Presence of infection
•
Timing of primary molar loss: • before age 5/prior to crown completion - delays premolar • after age 8/after crown completion - accelerates premolar
878
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Erupt prior to 3 months of age
•
Natal – present at birth
•
Neonatal – present w/in first 30 days
•
Natal 3:1 neonatal
•
Incidence 1:716-3500
•
Positive family hx 1518%
•
90% are true primary teeth
•
Etiology unknown
•
Most are poorly formed
•
Most may exfoliate early (?)
879
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
880
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
biting, drooling
•
gum rubbing, sucking
•
irritability, wakefulness
•
ear rubbing, facial rash
Macknin et al 2000
881
#
decreased appetite for solid foods
#
mild (<102) temperature elevation
#
no combination could predict teething
#
symptoms occurred in <35% of infants
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Wake et al Pediatrics 2000
•
Did not confirm strong associations between tooth eruption and a range of teething symptoms
•
Stated that weak associations may exist
•King et al. 1992 –HSV-1 found in 9 of 20 infants with teething difficulties
•Other studies have implicated HHV-6
882
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
No evidence available to suggest signs/symptoms specific to teething to allow confident diagnosis without excluding other organic pathology
•
Tighe & Roe 2007
•
Local causes • • • •
•
trauma impaction ankylosis supernumeraries
Systemic causes
• syndromes • hypothyroidism, hypopituitarism
•
Genetic conditions
883
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Malfunction of eruption mechanism causes nonankylosed tooth to fail to erupt
•
Teeth can partially erupt
Frazier-Bowers et al 2007
•
Only posterior teeth affected
•
Result is posterior openbite
•
Type 1: eruption failure occurs at/near same time for all teeth in affected quadrant
884
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Type 2: gradient in time of failure; some further development of teeth posterior to affected tooth
•
Rarely symmetric, frequently unilateral
•
Can affect any or all quadrants
•
Abnormal or lack of response to orthodontic force
•
Non-ankylosed tooth with PFE likely to become ankylosed when force applied
Frazier-Bowers et al 2007
•
Local causes • loss of primary predecessor
•
Systemic causes • hyperthyroidism • syndromes • others: see Table
885
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
• •
•
•
Diseases of bone Diseases of periodontium Diseases of metabolism Deviations of growth
• •
•
•
•
Type of dentigerous cyst
•
Either dentition
•
No sex predilection
•
Usually asymptomatic
•
No treatment usually required
•
R/O hemangioma
886
Diseases of blood Physical and chemical injuries Benign and malignant tumors Dental anomalies
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Spicule of bone on occlusal surface of erupting molar
•
•
Incidence 2-3% (25% in CLP)
•
Associations (Pulver): • • • • • •
•
larger maxillary teeth larger affected Es and 6s smaller maxilla small SNA abnormal eruption angle of 6 delayed calcification of some 6s
Self-correction 66% (22% in CLP)
887
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Ectopic #3 and #30 Self-correction
Canine resorption
888
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Fusion of cementum with alveolar bone
•
May occur prior to full eruption
•
Clinically: “submerged” tooth
•
Etiology: unknown
•
Possible extrinsic factors: • trauma; tooth replantation • disturbed local metabolism; localized infection • chemical or thermal irritation
•
Possible intrinsic factors • genetic gap in PDL • aberrant deposition of cementum or bone
889
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Prevalence 1.3-38.5%
•
Most often affected teeth: lower D, lower E, upper D, upper E
•
Multiple teeth as frequent as single
•
Deflected eruption paths
•
Impacted premolars
•
Loss of arch length
•
Supraeruption of opposing teeth (especially maxilla)
890
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Prevalence • 44-97% in 6-year-olds • 33-46% in 9-year-olds • 7-20% in 14-year-olds
•
Racial distribution • higher in African Americans, Mediterranean whites • higher in females at younger ages (?)
• •
• •
Normal development Excessive skeletal growth Pernicious habits Deficiency of tooth material
•
Physical impediment to closure • mesiodens, retained primary teeth • interruption of transseptal fibers
•
• spaced dentition, missing teeth, xs ob and/or oj, others
Artificial • RPE • Milwaukee brace
891
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
•
Usually a combination of orthodontics and bond-o-dontics
892
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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893
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Constance M. Killian, D.M.D.
Topic Outline Considerations Decision to Use General Anesthesia Planning for General Anesthesia Pre-GA Overall Assessment GA-Specific Assessment Day of Procedure Pre-operative Procedures Intra-operative Procedures Post-operative Management
894
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
General Considerations
Who benefits from GA for dental treatment?
Indicated for the OR?
895
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
General Considerations
How can pediatric dentists interface with hospitals?
General Considerations
GA must be seen as part of a long-term comprehensive treatment plan
896
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
General Considerations
Hospital Dentistry: Communication is critical
Patient Considerations •A patient needing dental treatment presents
at your office as any of the following: • • • •
Pre-cooperative Uncooperative or combative Medically compromised Developmentally delayed
How do you decide if you should take the child to the OR for treatment?
897
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Decision to Use General Anesthesia Extent of treatment needs
Decision to Use General Anesthesia The General Health of the Patient
898
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Decision to Use General Anesthesia • Other options available for treatment • Traditional behavior management techniques • Alternative Restorative Technique (ART)
Decision to Use General Anesthesia •
Will the patient be able to cooperate for the needed treatment without GA?
•
Ask parent about previous experiences
899
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Decision to Use General Anesthesia • What is the patient’s dental history? • Radiographs? • Previous treatment? • Conditions of previous treatment
Decision to Use General Anesthesia • What are the parental expectations? • What are the parental fears? • Communication is essential
900
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Decision to Use General Anesthesia Indications for GA • • • • •
Young age Uncooperative/combative behavior Developmental disability Medical disability Extensive dental disease
Decision to Use General Anesthesia Contraindications to GA • Minimal dental disease • Certain high-risk medical conditions
901
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Decision to Use General Anesthesia Consider the following as they relate to the child: • Indications for GA? • Any contraindications to GA? • Any attempts made to provide treatment
without GA? • Do the benefits of GA for this child’s dental treatment outweigh the risks?
Decision to Use General Anesthesia The Bottom Line
• Recommendation for GA must be justified • Justification for GA must be documented • Provide information for informed consent
902
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
What are the risks of treatment with GA? Physical/Medical risks • Intraoperative incidence of adverse
respiratory events – 22% • 44% of post-operative patients have some symptoms • Post-operative complications studied in 90 children • Pain, agitation, sleepiness, sore throat • Pain at home (more reports in children
>4yo)
What are the risks of treatment with GA? Physical/Medical risks • Risk of serious complication such as brain
damage or death, although rare • Mortality risk in 22,000 GA dental cases was studied – no deaths reported • Undetermined potential risk to developing brain of young child
903
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
What are the risks of treatment with GA? • Behavioral • Fingernail biting • Fear of dark • Needing more parental attention
What are the risks of treatment without GA? • Procedure cannot be completed • Treatment is compromised • Increased risk of injury • Patient may be reluctant to return for future
visits • Increased number of appointments
904
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
What are the risks of no treatment? • A false sense that there is no problem with
not getting the indicated dental treatment • The severity of the disease increases • Decreased quality of life
What are the benefits of GA? • Pain-free delivery of dental care • Dental treatment can be performed under
optimal conditions • Improved behavior of the child at follow-up dental visits • Less cost than multiple sedation visits
905
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
What are the responsibilities associated with GA? Responsibilities of the Pediatric Dentist • Educate regarding etiology of oral disease • Inform parent of need for comprehensive
care • Obtain a thorough pre-op history and assessment • Communicate with medical colleagues about the child • Assist parent in coordinating care
What are the responsibilities associated with GA? • Responsibilities of the Pediatric
Dentist
• Provide pre-op and post-op instructions
regarding the procedure • Stress the need for post-op follow-up care • Provide preventive oral health information • Consider combining procedures under GA
906
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
What are the responsibilities associated with GA? Responsibilities of the Parent/Guardian • Provide accurate and thorough • • • •
information about child Follow pre-op and post-op instructions Keep follow-up appointment Learn about etiology of oral disease Become a committed partner in the preventive plan
Planning for General Anesthesia The Pre-GA Appointment
Overall Planning/Assessment !Clarify the relationship of the patient and guardian !Verify that the individual has the ability to understand the issues related to treatment and consent
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
The Pre-GA Appointment • Review the medical history • Assess overall health • Consult with medical specialists as
indicated • Contributing factors to avoidable mortality and morbidity
The Pre-GA Appointment Examine the patient • Document behavior • Extraoral assessment • Intraoral assessment • Document justification for GA
908
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Mallampati Classification
The Pre-GA Appointment Create a problem list and treatment plan • Treatment plan for long-term success • More aggressive restorative procedures • Sealant success limited in patients with high DMFT • SSCs most successful restorative OR procedure • Patients with developmental disabilities have higher failure rate of SSCs • High % of patients having GA have recurrent oral disease
909
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
The Pre-GA Appointment Create a problem list and treatment plan • Plan for alternatives to original treatment plan • Discuss all of the above with the parent/guardian • Describe the appearance of proposed treatment
Obtain informed consent
Assess health and airway status Overall health status – ASA Classification • • • • • •
P1 (ASA I ) – normal healthy patient P2 (ASA II) – patient with mild systemic disease P3 (ASA III) – patient with severe systemic disease, not incapacitating P4 (ASA IV) – patient with severe systemic disease that is a constant threat to life P5 (ASA V) - moribund P6 (ASA VI)- on support, awaiting organ removal
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Assess health and airway status ! Previous history of GA and any
complications ! Known difficult airway ! History of premature birth ! MH-susceptible or 1st degree relative with MH-susceptibility
Assess health and airway status • Physical limitations of the patient • CP • Atlanto-axial instability – Down syndrome • Obesity • Mental Disability – may be difficult to induce anesthesia • Conditions that cause limited opening
911
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Assess health and airway status Possible causes of airway/anesthesia problems
Respiratory problems • Asthma – note last attack, last ER visit, last hospitalization • Reactive Airway Disease • Bronchopulmonary dysplasia • Current/Recent URI/LRI • Obstructive sleep apnea
Assess health and airway status Possible causes of airway/anesthesia problems
Congenital syndromes/conditions • • • • • •
Trisomy-21 Pierre Robin Crouzon Treacher Collins History of repaired cleft palate JRA: decreased cervical mobility
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Assess health and airway status Possible causes of airway/anesthesia problems
Cardiac conditions • Congenital heart disease • Document need for SBE prophylaxis
Neurologic conditions • • • •
Seizure disorder V-P shunt present? CP Myopathy
Assess health and airway status • Possible causes of airway/anesthesia
problems • Obesity
• GERD • Obstructive Sleep Apnea
• Oncological disease • History of organ transplantation • Bleeding disorders • History of pseudocholinesterase deficiency
913
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pre-GA Appointment • Order H&P • Order lab tests as needed • Order any consults as needed
Decision: Hospital Admission vs. Same-Day Procedure •Facility factors •Personnel factors •Patient factors: ASA Classification
State requirements and hospital/facility protocols are the ultimate determinants of admissions requirements
914
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Preoperative Instructions • Individualized to the patient • Information regarding URI • Information regarding infectious disease
exposure • NPO Guidelines
Preoperative Instructions NPO Guidelines • No solids for 6 hours • No formula for 6 hours • No breast milk for 4 hours • No clear fluids for 2 hours 44
915
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pre-GA Appointment Discussion of Risks of Complications • Don’t be afraid to discuss risks • Common assessment of risk of complications: • 1:3 – sore throat • 1:4 – nausea and vomiting • 1-2:1000 – awareness during anesthesia • 1.4:10,000 – cardiac arrest • 1:20,000 – death • 1:30,000 severe damage to teeth • 1:80,000 brain damage
Pre-GA Appointment Advise parents that procedure may be cancelled at the day of procedure • Fever • NPO violation • Exposure to infectious disease • Wheezing • Cough or runny nose • Recent URI/LRI
916
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Day of Procedure Pre-operative Procedures Meet the family and patient Pre-operative Note • • • • • •
Summarize medical history Describe procedures planned State rationale for GA List/summarize consults obtained Consent obtained Name of surgeon/assistant
Day of Procedure Pre-operative Procedures Pre-operative anxiolytic medication Typically midazolam – 0.25-0.5mg/kg to 10mg max • For combative patients – IM Ketamine 23mg/kg with atropine and midazolam • IV or Mask induction can begin when the patient is sedated •
917
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Intra-operative Procedures Monitors • EKG • BP • Pulse Oximeter • Capnography Device • Precordial Stethoscope • Temperature measuring device • Bispectral Index
Intra-operative Procedures Heating/cooling blankets should be available Neuromuscular blocking agents • Avoid succinylcholine – may cause fatal hyperkalemia • Vecuronium, rocuronium (intermediate-acting) • Mivacurium (short-acting)
918
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Intra-operative Procedures Induction of Anesthesia !By mask !Sevoflurane !Intubation – nasotracheal vs. endotracheal
Intubation
919
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Intra-operative Procedures Induction Complications !Difficult IV access !Compromised airway !Traumatic intubation !Aspiration !Laryngospasm !Malignant Hyperthermia
Malignant Hyperthermia: Overview • Skeletal muscle disorder: hypermetabolic • • • •
state Autosomal dominant inheritance pattern No clinical signs of the condition Triggered by volatile anesthetic gases Testing for susceptibility
920
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Malignant Hyperthermia: Signs • Unexplained increase in CO2 • Unexplained tachycardia • Hypertension • Skin mottling • Muscle rigidity • Hyperthermia • Hyperkalemia-induced arrythmias • Disseminated intravascular coagulation
Malignant Hyperthermia: Treatment ! Discontinue triggering agents ! Monitor and treat metabolic acidosis ! Hyperventilate with 100% oxygen ! Sodium dantrolene 2.5mg/kg IV ! Cooling blanket
921
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Intra-operative Procedures Patient Preparation Patient Preparation • • • • •
Padding under pressure points Placement of shoulder roll Eye protection Stabilize head and naso/endotracheal tube Drape head and body
Before Placing Rubber Dam • • • •
Place throat pack Record radiographs Prophylaxis Overall Examination of oral cavity
Standard headrest
Simple towel headrest
922
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Ready to Go
Radiographs in the OR
923
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Be prepared
Intra-operative Procedures Patient Preparation Place Rubber Dam • • • • • • • • •
Perform dental examination Confirm treatment plan Complete operative dentistry Advise anesthesiologist 10 minutes from completion Apply Fluoride varnish Extractions Impressions for any appliances Check mouth and remove throat pack Case Completed
924
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Ongoing Monitoring by Anesthesia
Intra-operative Procedures Complications • Tube problems • IV disconnected • Bleeding • Edema • Arrythmia
925
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Intra-operative Procedures • Extubation • Transport to PACU • Dictate operative report
Post-operative Considerations Nausea/Vomiting • Provide pain relief • Have patient avoid drinking • Antiemetics act independently – use a
single agent • Prophylactic antiemetics preferred over treating nausea/vomiting • Consider propofol IV instead of volatile agents
926
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Post-operative Procedures Pain Management Non-opioid analgesics !Tylenol (Rectal) !IV Ketorolac
Post-operative Orders • Vital signs every 15 minutes until stable • Pain medications • Medications for nausea and vomiting • Ice as needed • Restraint as needed • Disconnect IV when taking oral fluids • Discharge when criteria are met
927
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Post-operative Complications ! Nausea/Vomiting ! Unexpected drowsiness ! Pain requiring medication ! Sore throat ! Hoarseness/croup ! Swelling ! Bleeding ! Fever
Post-operative Visit with Parents • • • • • • • •
Describe patient’s condition and location Speak in lay terms Review discharge criteria Review home care instructions Give contact information for emergencies Verify family contact information Review importance of preventive follow-up Set up follow-up appointment
928
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Post-operative Progress Discharge Criteria ! Vital signs normal ! Able to maintain airway ! Ambulatory ! Awake, alert, appropriate ! Can take fluids orally ! Pain/bleeding controlled ! No vomiting
Post-Anesthesia Recovery Score PARS used in PACU Evaluates patient status based on different organ systems ! Maximum score is 20 ! Score of 18 or higher = ready for discharge !
929
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Follow-up Care
• Low follow-up appointment rate: 54-60% • Future well care: 13-31% • Recare interval based on caries risk
Risk of Repeated Dental GA Risk factors ! 100% involvement of maxillary incisors at initial
GA ! Continued use of bottle at time of GA ! Poor cooperation in dental/medical setting ! Difficult personality as described by parents
930
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Closing Thoughts Dental care delivered under general anesthesia in a hospital setting can be the beginning of a lifetime of oral health. It takes many people, many efforts, a great investment of time and money, and involves significant risk. As child advocates and health providers, we must educate parents and the public of the value and importance of the efforts made on behalf of the child as we welcome them to their dental home.
931
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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932
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Developmental Disabilities
General Considerations ! Physical or mental
disabilities ! Functional limitations ! Need for enhanced services ! Persistent dependency ! Expense: long-term care, medications ! Parent stress higher
Developmental Disabilities
Questions to Ask • Overall family functioning – caretakers • Level of receptive/expressive function • Educational situation • Diet and oral hygiene • Input for behavior management
933
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Build confidence
Engage the child
Promote independence
Provide support and education
934
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Assessing Patient Abilities
935
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
936
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cerebral Palsy
General Considerations • Disorder of movement and posture • Result of injury to brain motor areas • Motor problems • Static/non-progressive • 300,000 U.S. children affected
Cerebral Palsy
Criteria Posturing/abnormal movements Oropharyngeal problems Strabismus Increased or decreased muscle tone • Evolutional responses • Increased deep tendon reflexes • • • •
937
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cerebral Palsy
Subtypes of CP Hemiparesis ! Asymmetric CNS damage ! Uneven strength/poor balance ! Progressive scoliosis
Spastic diplegia and quadriplegia Athetoid or ataxic: involuntary movements Hypotonic
Cerebral Palsy
CP Associated Findings • Strabismus • Refractive errors • Hearing loss • 50% Mental retardation • Behavioral problems
938
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cerebral Palsy
CP Oral Findings • Increased DMFS of permanent teeth • Enamel erosion • Poor gingival health • Malocclusion – High overjet, less crowding • Delayed permanent molar eruption • Tongue thrust • Bruxism • Increased gag reflex
Cerebral Palsy
CP Oral Findings Dysfunctional swallow Drooling: impacts socialization ! Can be treated with botox in
submandibular gland ! Can be treated with transdermal scopolamine ! Can be treated with maxillary appliance
939
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Cerebral Palsy
Dental Management of Patients Infant dental program to start prevention Communication challenges Feeding issues ! May have gastronomy tube ! GERD ! Role of diet and caries ! Caution with sucrose in medications
Cerebral Palsy
Dental Management of Patients Medications ! Baclofen – muscle relaxant ! Botox Consider chlorhexidine to aid in gingival health Treatment needs
940
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders ASD
Autism Spectrum Disorders ASD Autism: Neurodevelopmental disorder in which social interaction, language, behavior, and cognitive function are severely impaired
941
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Epidemiology and Etiology 10-20 cases of classic autism/10,000 live births 30-50 cases of ASD/10,000 live births Cause is unknown Role of genetics: genetic expression influenced by environment • No ethnic differences • 3% of families have > 1 child with autism • Increased risk with some conditions –Down syndrome: 7-15% –Deaf patients: 15% • • • •
Autism Spectrum Disorders
Early Signs of Autism • • • • • •
No babbling or gesturing by 12 months No words by 16 months No social interaction – smile, eye contact Restricted interests and activities Lack of imagination in play Compulsive behaviors may be evident
942
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Categories of Autism • Classic autism – most severe • Asperger Syndrome • Pervasive Developmental Disorder, not otherwise specified
Autism Spectrum Disorders
Characteristics of Classic Autism • Impaired social interaction • Impaired verbal and nonverbal communication • Restricted, repetitive patterns of behavior • Poor body awareness/clumsiness ! Slapping, tapping • Conduct problems • Familial pattern • Distorted sensory input
943
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Asperger Syndrome • Normal curiosity, adaptive behavior and self-help skills during first 3 yrs • Qualitative impairment in social interaction • No delay in language/cognition • More common than classic autism • Lack of demonstrated empathy • Impaired non-verbal contact • Physically clumsy
Autism Spectrum Disorders
Affected Areas of Brain • • • •
Frontotemporal region Synapse dysregulation Amygdala and associated limbic regions Cerebellum
944
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Deficits in Autism • Ability to recognize and understand mental states of self and others and use this to predict behavior • Executive function • Central coherence
Autism Spectrum Disorders
Effects of Autism on Family • Increased stress • Increase in negative outcomes for
siblings • Loss of employment/income • Lost leisure time • Increased familial conflicts
945
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Medical Management of ASD Goals • • •
Minimize core features of ASD Minimize family stress Maximize functional independence and quality of life
Autism Spectrum Disorders
Educational Management of ASD • The earlier the better – by 2 years of age • Intensive intervention schedule • 25 hours/week • 12 months/year • Low student/teacher ratio • Family involvement
946
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Educational Management of ASD • Focus on structure, routine, few distractions • Apply skills to new situations • Educational goals ! Improve social skills ! Improve speech/language ! Increased responsibility & independence ! Improve occupational skills ! Achieve academic goals
Autism Spectrum Disorders
Medical Treatment of ASD Medications – used to treat specific behaviors ! Hyperactivity – methylphenidate (Ritalin, Concerta) –
calm hyperactivity ! Repetitive behaviors – fluoxetine (Prozac) – decreases compulsive behaviors, self-mutilation ! Aggressive behaviors – carbamazepine (Tegretol), risperidone (Risperdal)
947
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Side Effects of Medications for Autism Methylphenidate (Ritalin, Concerta) - stimulant ! Tachycardia ! Nervousness ! Anorexia ! Insomnia ! Xerostomia
Autism Spectrum Disorders
Side Effects of Medications for Autism Fluoxetine (Prozac) – selective serotonin reuptake inhibitor (antidepressant) ! ! ! ! ! ! ! ! ! ! !
Diarrhea, nausea Somnolence Dizziness Increased bleeding time Potentiates CNS dpressants Erythromycin inhibits metabolism Xerostomia Altered taste Bruxism Stomatitis, glossitis Gingivitis
948
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Side Effects of Medications for Autism Risperidone (Risperdal) - antipsychotic ! Potentiates CNS depressants ! Xerostomia ! Dysphagia ! Altered taste ! Stomatitis ! Gingivitis ! Tongue edema ! Facial edema
Autism Spectrum Disorders
Side Effects of Medications for Autism Carbamazepine (Tegretol) – anticonvulsant ! Decrease WBC, Increase platelets – longterm use;
! ! ! !
caution with use of aspirin, NSAIDs – risk of increased bleeding Erythromycin inhibits metabolism Xerostomia Stomatitis, glossitis Carbohydrate craving
949
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Caries, Oral Hygiene, Diet
• Caries rate: similar or less than healthy population • Oral hygiene: difficulty accepting brushing/flossing • Diet: food often used as reward
Autism Spectrum Disorders
Dentistry and Autism • Make initial encounter benign and relaxing • Presence of parents is helpful • TSD useful • Use same treatment room • Keep visits short • Use short, clear commands • Positive and negative verbal reinforcement • Music/DVDs can be used as distractors • Use desensitization – build gradually on interventions
950
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Dentistry and Autism Protective stabilization may be needed Multiple short visits may be needed Consult with psychiatrist treating patient GA may be needed as adjunctive therapy for treatment • End on a positive note • • • •
Autism Spectrum Disorders
Dentistry and Autism Screening for 5 risk factors can help predict uncooperative behavior Age (<4 or 4-7) Reading (no vs. yes) • Toilet trained (no vs. yes) • Concurrent medical diagnosis (yes vs. no)* • Expressive language used (no vs. yes) Presence of >2 of any of the above risk factors is strongly associated with uncooperative behavior • •
Marshall, Sheller et al, 2007
951
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
952
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
953
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Oral Findings • Evidence of erosion • Evidence of bruxism • Macrocephaly • Possible bruising/abrasions on
head
954
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Autism Spectrum Disorders
Long-term Considerations for Oral Health • Maximize prevention • Topical fluoride use daily • Decrease cariogenic behaviors – food
choices, frequency
• Increase frequency of recall visits • Caution in allowing patient autonomy in
home care
HIV Infection
955
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
General Information ! 40,000 new cases yearly in U.S. ! HIV targets cells with CD4 receptor proteins ! Greatly decreased cellular immunity ! Decreased humoral immunity
HIV Infection
Pediatric HIV Sources • Perinatal transmission • Blood products • IV drug abuse • Unprotected sexual
activity
956
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Pediatric AIDS • Lymphadenopathy • Hepatosplenomegaly • Nephropathy • Chronic eczema • Oral candidiasis • Weight loss • Failure to thrive • Diarrhea • Encephalopathy
HIV Infection
HIV Management • Antiretroviral therapy • Taken daily • Physician monitoring every 1-2 weeks until stable • Physician monitoring every 2-3 months when stable – CD4 counts, viral loads – CBC, BUN/Cr, electrolytes, UA
957
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
HIV Management - CD4 counts What is CD4 and how is it affected by HIV? • Cluster of differentiation 4 (CD4): glycoprotein expressed on surface of T-4 helper lymphocytes, monocytes, and macrophages • Normal CD4 = >1000 • HIV infection causes decrease in number of T-cells with CD4 receptors • Decreased CD4 count indicates an increase in HIV disease status
HIV Infection
HIV Management - Viral load testing ! Quantitative plasma HIV RNA level –Lower limit 50 copies/mL ! Level undetectable – patient is still infectious
958
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Medications for HIV Nucleoside RT inhibitors (“nukes”) • Interrupt early stage of virus copying
itself • Prevent RNA to DNA conversion • Target newly infected cells • Zidovudine, Didanosine, Stavudine
HIV Infection
Medications for HIV Non-nucleoside RT inhibitors (“non-nukes”) • • • • •
Interrupt early stage of virus copying itself Bind to viral RT Disrupt RNA to DNA conversion Target newly infected cells Nevirapine, Delavirdin
959
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Medications for HIV Side effects of RT inhibitor medications • Decreased RBC, WBC • Pancreatic inflammation
HIV Infection
Medications for HIV Protease inhibitors • Block protease needed for viral formation and growth • Targets new and older infected cells • Saquinavir, Ritonavir, Kaletra • Side effects • Nausea, diarrhea, GI symptoms • May interfere with other drugs
960
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Medications for HIV Fusion inhibitors • Blocks virus’s ability to enter and infect
human immune cells • Used in combination with other HIV treatment • Reduces level of HIV in blood • Fuzeon (T20)
HIV Infection
Medications for HIV HAART – Highly Active Anti-Retroviral Therapy ! Helps addresses HIV resistance ! Involves use of 3 or more different drugs ! Reduces amount of circulating virus to nearly
undetectable levels ! Does not affect oral soft tissue disease in HIV-infected children
961
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Dental Considerations • Determine stage of disease • Current lab parameters – Hematologic – HIVD status • Type of ongoing care • Medications and side effects/drug interactions • Potential sites of infection • Considered ASA III
HIV Infection
HIV to AIDS Conversion Average survival after diagnosis is increasing Challenges still exist • Treatment-resistant viral strains • Late HIV testing • Inadequate access to treatment • Poor treatment compliance
962
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
HIV Oral Lesions Significance of Oral Lesions in pediatric HIV ! Oral lesions common ! Associated with decreased immunity ! May signal advancing disease ! CD4 depletion common when oral lesions present ! Poor cell-mediated immunity ! Humoral dysregulation ! Phagocytic cell defects ! Symptomatic patients have more oral lesions
Herpes Simplex
Aphthous ulcer
Hairy leukoplakia
963
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pseudomembranous Candidiasis Angular chelitis
Linear gingival erythema
Parotid enlargement
964
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
The Management of HIV Oral Lesions Candidiasis (pseudomembraneous, erythematous) • Treatment with antifungal agents – –
Topical: Nystatin, Clotrimazole 2x daily for 14 days Systemic: Fluconazole, systemic given for 5-7 days
Angular cheilitis • Antifungal + topical steroid
Herpes simplex • Systemic antiviral - Acyclovir
HIV Infection
The Management of HIV Oral Lesions Linear gingival erythema • Chlorhexidine
Parotid enlargement • Anti-inflammatory, analgesics, antibiotics, steroids • Saliva replacements, fluoride rinses
Recurrent minor aphthae • Topical steroids
965
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Dental Management/Considerations • • • • • •
Consult with patient’s physician Universal precautions Drug interactions Susceptibility to infection Thrombocytopenia – increased bleeding Delayed exfoliation of primary teeth
HIV Infection
Dental Management/Considerations • More caries than unaffected household peers • Caries increases as CD4 counts decrease • Prevention is critical – Regular recalls – Chlorhexidine daily – Fluoride supplementation as indicated
966
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
HIV Infection
Dental Management/Considerations Rapid HIV testing in dental office • OraQuick Advanced test • Results in 20 minutes • Pre and Post-test counseling
needs to be done
Pediatric Malignancy
967
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
General Considerations • Affects 1 in 7,000 children each year • ALL most common (24%) • CNS Tumors (22%) • 5 year survival > 75%
Pediatric Malignancy
Pediatric vs. Adult Cancer What makes pediatric cancer different? • • • • • • • •
Rare No risk factors to modify No effective screening Early detection does not influence outcome 70% will be long-term survivors Chemotherapy used for almost all patients Intensive therapy – usually in hospital Late effects of therapy noted
968
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Absolute Neutrophil Count: ANC • Indicates ability to fight infections • ANC = WBC x (% seg + % bands) • Neutropenia if ANC < 1,000
Pediatric Malignancy
Dental Issues • • • • • •
Immune system compromise Potential for oral infection Risk of bleeding Cranial or facial radiation Timing of chemotherapy Indwelling catheters
969
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Dental Objectives • Arrest dental disease • Restore oral health • Prevent or manage complications from
medical therapy • Educate patient and caregiver
Pediatric Malignancy
New Diagnosis of Malignancy New Diagnosis of Malignancy: Dental Consult • • • • • • • • • •
Nature of disease Time of diagnosis Modalities of treatment received to date Complications/relapses Hospitalizations Infections Current hematologic status Medications, allergies Review of systems Confirm presence/absence of central line
970
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
New Diagnosis of Malignancy Dental Protocol • • • •
Examination Radiographs as possible Prioritized treatment plan Complete all care prior to start of cancer therapy
Pediatric Malignancy
Example: Medical Treatment Plan of ALL • Remission induction (28 days) • CNS preventive therapy: irradiation and/or intrathecal chemotherapy • Consolidation/intensification: minimize development of drug resistance • Maintenance: chemotherapy 2.5-3 years
971
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Prevention of Oral Disease • • • • • •
Brush teeth and tongue 2-3x/day with soft brush Consider chlorhexidine – helps perio condition Non-cariogenic diet Topical fluorides Stretching exercises (if radiation planned) Frequent recall appointments
Pediatric Malignancy
Dental Treatment Prior to Cancer Therapy • ANC > 1,000 – no need for antibiotic prophylaxis unless infection present • ANC < 1,000 defer elective care • Platelets > 75,000 no additional support except aggressive local measures • Platelets 40,000-75,000 consider platelet transfusion prior to and 24 hrs. after dental care • Platelets < 40,000, defer care
972
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Dental Treatment Prior to Cancer Therapy • Restorative and surgical treatment – under
GA • Pulp therapy for primary teeth • Endo considerations for permanent teeth – Complete 1 week prior to start of cancer treatment OR – Extract and start antibiotics – Asymptomatic endo needs can be deferred
Pediatric Malignancy
Dental Treatment Prior to Cancer Therapy Let patient tolerance and oral hygiene be your guide… • • • • •
Remove fixed orthodontic appliances Band/loop or lingual arch Removable appliances Operculectomy for risky partially erupted molars Exfoliating primary teeth - leave or extract
973
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Oral Complications • Chemotherapy affects oral mucosa • Salivary effects of chemotherapy/radiation
to head and neck – Reduced flow – Thickened • Immunosuppression – Overgrowth of opportunistic organisms
Pediatric Malignancy
Oral Conditions w/ Cancer Therapy • Candidiasis – Nystatin rinse and swallow qid – Mycostatin pastilles qid – Clotrimazole troches – Fluconazole 5 mg/kg
974
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Oral Conditions w/ Cancer Therapy • Xerostomia – Stimulate flow with xylitol gum – Replace secretions with ice water, ice chips, carboxymethylcellulose solution – Humidify sleeping area – Avoid caffeine – Lip lubricants
Pediatric Malignancy
Oral Conditions w/ Cancer Therapy • Apthous ulcerations – Triamcinolone in orabase (topical steroid) • Herpetic ulcers – Benadryl + Kaopectate elixir – Viscous xylocaine 2% – Acyclovir • Traumatic ulcers – Triamcinolone in orabase
975
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Herpes Simplex Aphthous ulceration
Pediatric Malignancy
Oral Conditions w/ Cancer Therapy Stomatitis • Identify cause to determine best
therapy • PO or IV fluids • Systemic analgesics • Topical anesthetics
976
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Oral Conditions w/ Cancer Therapy Bleeding • Low platelets • Poor liver function • Decreased vascular integrity • Poor oral hygiene • Intraoral bleed may precede intracranial
bleeding – call for medical consult
Pediatric Malignancy
Graft Versus Host Disease (GVHD)
Post-Bone Marrow Transplantation • Usually occurs in first 100 days • Diagnosis of acute oral GVHD
Presence of systemic disease – Exclusion of other sources for lesions – Erythema – tongue, floor of mouth, gingival, labial mucosa – Lesions appear, worsen, or persist beyond day 21 – Prevention of systemic GVHD decreases oral lesions –
977
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Pediatric Malignancy
Long-term Systemic Effects • • • • • • • •
CNS, psychosocial Endocrine Reproductive Secondary neoplasms Cardiac dysfunction Hepatic dysfunction Cataracts Dental
Pediatric Malignancy
Long-term Dental Effects Severity affected by: • Age of patient at time • Stage of tooth development at time • Type and dose of antineoplastic agent • Radiation causes most damage
978
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Long Term Dental Effects • Salivary secretions decreased • Increased caries risk • Dental malformations • Risk of ORN questionable
Panograph Age 15
Panograph Age 8
979
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Long Term Dental Effects Craniofacial effects
• Malocclusion • Ectopic eruption • Facial deformities, skeletal hypoplasia • Trismus
980
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Malignancy
Long Term Dental Effects Orthodontic treatment considerations Light forces ! Shorten treatment time ! Choose simplest method for treatment ! Consider no treatment for mandible ! Use appliances to minimize root resorption !
Solid Organ Transplantation
981
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Solid Organ Transplantation
Demographics 1996-2005: Pediatric organ transplant recipients increased by 23% •
Forms of Solid Organ Transplantation • • • • •
Renal Hepatic Cardiac Pulmonary Pancreatic
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Solid Organ Transplantation Common Features • • • •
Patient is on waiting list Management of patient in debilitated state Transplantation requires match of blood type, HLA factors Lifelong immunosuppression therapy
Solid Organ Transplantation What is the oral-systemic relationship? • • • •
Certain inflammatory cytokines (IL-1#,IL-6) are elevated in inflamed gingiva IL-6 can identify individuals at risk for organ rejection Higher serum IL-6 in individuals with chronic periodontitis compared to those without Serious implications for transplant
983
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Solid Organ Transplantation Pre-Transplant Dental Considerations • Medical consult • Conduct thorough periodontal/dental exam • Record radiographs as possible • Develop treatment plan • Meticulous home care instruction • Treatment carried out • Chlorhexidine rinse pre-op • SBE prophylaxis as indicated • Post-op antibiotics as needed
Solid Organ Transplantation Post-Transplant Dental Considerations • • • • • • •
Medical consult Reinforce oral hygiene program for patient Monitor and treat opportunistic infections – Candida Caution with antibiotics – nephrotoxicity Treat xerostomia Increased risk for caries – post renal transplant Increased risk of “de novo” dysplasias & malignancies • Epithelial dysplasia • Non-Hodgkins lymphoma • Squamous cell & Basal cell carcinomas
984
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Organ Transplantation
Immunosuppression Medications Medications Post Organ Transplant Name
Mechanism
Side Effects
Cyclosporine Neoral Sandimmune
Inhibits production and release of interleukin II
Gingival hypertrophy Hypertension Nephrotoxicity Tremor
Tacrolimus Prograf
Suppress T-cell humoral immunity
Hypertension Anemia Pruritus Nephrotoxicity
Azathioprine AZA Imuran
Antagonizes purine metabolism
Thrombocytopenia Leukopenia Anemia
Steroids Prednisone Solu-medrol
Decreases inflammation Decreases lymphatic system activity
Insomnia Nervousness Increased appetite
Organ Transplantation
Immunosuppression Medications Immunosuppression medications • Cyclosporine – use has decreased • Tacrolimus (Prograf) • Azathioprine (AZA) • Steroids • Calcium channel blockers (Nifedipine)
985
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Organ Transplantation
Immunosuppression Medications Cyclosporine-induced Gingival Overgrowth
Organ Transplantation
Immunosuppression Medications: Gingival Overgrowth • Cyclosporine: 30%
" Gingival effects may reverse if medication is stopped or dose is reduced • Tacrolimus (Prograf) – less gingival overgrowth than
Cyclosporine • Nifedipine: 15% (potentiates effects of Cyclosporine)
" Gingival enlargement can be controlled w/meticulous oral care
986
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Organ Transplantation
Immunosuppression Medications Pathophysiology of gingival overgrowth with Cyclosporine and Nifedipine • Cyclosporine increases fibroblast production of collagen and protein • Nifedipine – inhibits apoptosis of cells, and inhibits macrophage-induced death of fibroblasts (potentiates cyclosporin)
Other Conditions – See Manual Pediatric Kidney Disease Pediatric Liver Disease Hearing Loss Visual Impairment Obstructive Sleep Apnea Muscular Dystrophies Spina Bifida Patients with Gastric Feeding Tube Eating Disorders Pediatric Depressive Disorders Adolescent Pregnancy
987
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Special Needs Patients: A case
!
I would first want to find out about her overall health. I would review the medical history with her parent before proceeding with any dental examination
You are told that her medical history is significant for 22q11.2 deletion syndrome. She has developmental delay, history of cardiac surgery to repair Tetrology of Fallot, cleft palate repair, and immunological problems (all part of 22q11.2 deletion syndrome). What is your next step?
988
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
• I would want to consult with her physician. Particularly
I’m concerned about the need for SBE prophylaxis, since she has had surgery to repair Tetrology of Fallot. • Other concerns would be her immune status, her ability to cooperate for any dental treatment (since she has some developmental delay), and her growth and development in terms of orthodontics. • I would also want to find out if she is under the care of a cleft palate team. • My first step would be to call/write her physician.
Her physican advises that she does need antibiotic prophylaxis, and otherwise should be seen as a well-child. She does see a cleft team annually, and has been evaluated by the orthodontist on the team. What is your next step? • I would want to go over her past dental history, and find out if she has had any restorative dental care, and how that went. • Then I would want to do a clinical examination, and consider ordering radiographs. (I would check first with the orthodontist to see if they had recorded any.)
989
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Discuss your findings. What other diagnostic records would you need to provide comprehensive care for this patient? • Looking at the patient, she’s in the late mixed dentition, I can see enamel hypoplasia affecting her permanent teeth, and she looks to be crowded. Tooth #7 is erupting in crossbite. She also has a very prominent maxillary labial frenum, and you can see the scar from her cleft palate surgery. • Based on her age and dental development, I would recommend a panoramic radiograph, bitewings to detect for caries, and possibly study models to assess the crowding. • Based on the right lateral being small, it may eventually need some restorative treatment.
990
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Assume that there is no caries. What is your diagnosis for this patient? • 22q11.2 deletion syndrome, with need for antibiotic prophylaxis for dental treatment, repaired cleft palate • Slightly advanced dental development • I can’t tell her molar/canine Angle classification from the photos, but she has a crowded malocclusion, with deep bite, midline deviation, and crossbite of #7. • Enamel hypoplasia affecting a number of permanent teeth • Atypical anatomy #7
Discuss your overall management of this patient. • Based on her medical condition, she would be considered high caries risk. So I would work on a strong preventive plan, use of topical and systemic fluoride, oral hygiene (with parental supervision), more frequent recare exams, and dietary discussion. • I would discuss with her mom that she will be needing orthodontic care and I’d consult with her orthodontist.
991
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How would you manage the orthodontic care of this patient? • I would work with the orthodontist on the cleft palate team, and recommend some interceptive procedures as the patient can tolerate them. • She would initially be indicated for space analysis. If she were not able to tolerate any active interceptive therapy, perhaps placement of a mandibular lingual arch to preserve E space would be a good choice. • I would advise the parents that it will be a team effort, especially keeping up with the preventive treatment during orthodontics.
How would you manage the preventive care for this patient? • I would find out if she has any exposure to systemic fluoride, and would make use of topical and systemic fluoride, oral hygiene (with parental supervision), more frequent recare exams, and have a dietary discussion to reinforce healthy snack and eating habits. • She is high caries risk, and in order to maintain her oral health, it will be critical to focus on preventive efforts.
992
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
The patient’s mother is concerned about the appearance of her front teeth and asks what can be done for them – her family dentist recommended porcelain veneers. How do you respond? • I would tell the mother that the child is not indicated for veneers at this point because the teeth are not yet fully erupted, there would be too much loss of healthy tooth structure, and she can have a great result with some composite resin bonding on these teeth. • Additionally, they may wish to wait until after we know if she will have orthodontic appliances placed on these teeth. Perhaps it would be best to wait until after ortho to restore these teeth.
During her examination she gets upset and refuses to open her mouth and becomes resistant and physically difficult to manage. Her mother insists you finish the examination. How do you manage the child’s behavior? • First, I would see if it may be best to reschedule for another time. If that wasn’t possible, I’d use communicative behavior management – voice control, distraction (I assume tell-show-do wasn’t working). • If that were unsuccessful, and she absolutely had to have the examination, I would consider protective stabilization. I would show it to her mom, discuss it’s use, and obtain her consent before using it. If the child was still hysterical, I would immediately cease the procedure and recommend we try another day.
993
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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994
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Constance M. Killian, D.M.D.
Outline Child Development and Behavior Management of Behavior
995
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Behavior Basics • Most children develop in the normal range • Behavior has meaning • Development is a series of gains and plateaus • Temperament • Interventions must be built on strengths, not deficits
Child Development and Behavior
Temperament Temperament is the “hard-wiring”
996
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Child Development and Behavior
Temperament Temperament descriptions • Easy • Difficult • Slow to warm up • Mix
Child Development and Behavior
Temperament Temperament can be a predictor of behavioral concerns and problems
997
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Temperament Development is also influenced by temperament
Child Development and Behavior
Temperament Temperament helps characterize child’s individuality
“Goodness of fit” • match of temperament between parent and child • helps predict adaptability • “fit” of temperament to a given situation
998
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Temperament Resiliency • Positive demeanor and attitude leads to success • Better predictor than biomedical or sociological
variables
Child Development and Behavior
Attachment Attachment: the emotional bond felt by humans toward special people in their lives • • • •
Occurs during latter part of first year of life Attachment figure is a central to social development Once secure base is established, child is confident in exploring Lack of attachment may relate to behavior difficulties
999
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Child Development and Behavior
Attachment Levels of attachment • •
Secure attachment Insecure attachment
Child Development and Behavior
Temperament-Attachment Relationship • Differences in behavior related to differences in temperament • Children with disruptive behavior usually display attachment disorders and….. vice versa
1000
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Theories of Child Development Maturational Theory: Hall & Gesell • Development is internally-driven • Basis for the developmental milestones
and age norms • Very little depends on parenting • Development depends on maturation
Child Development and Behavior
Theories of Child Development Psychosexual Theory: (Freud) • Emotional life influences behavior and development • Emotions, dreams, feelings, frustrations matter • Interactions between parent and child influence
personality, resiliency, behavior, and adjustment • Children have an active mental life before speech • Emotional past can help assess current behavior
1001
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Theories of Child Development Behaviorism Theory: (Pavlov, Watson, Skinner) • Environment-source of behavioral change • Patterns of reinforcement • Conditioning • Stimulus-response • Reward and punishment
Child Development and Behavior
Theories of Child Development Social Learning Theory: outgrowth of behaviorism
• Social context provides feedback on behavior • Integration of internal processes and environment • Development is a series of upward spirals • Social experiences provide feedback for future
development
1002
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
1003
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Application of Behavioral Techniques • Link between behavior and consequence • Consistency • Timing • Rewards better than punishment
Child Development and Behavior
Application of Behavioral Techniques Piagetian Principles: Jean Piaget • Children think differently than adults • Cognitive development proceeds in distinct
stages – based on age • Children learn through interaction with environment • Child is an active learner not a passive responder
1004
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Piagetian Stages of Cognitive Development Piagetian Stages of Cognitive Development Stage
Age (years)
Way of Understanding
Sensorimotor
birth - 2
Direct sensations
Preoperational
2-6
Own perceptions
Concrete operations
6 - 11
Reason using stable rule system
Formal operations
> 12
Abstract thought, can reason about ideas
Child Development and Behavior
Language Development What is the role of language in dentistry? • Interaction with child • Communicative behavior guidance • Detection problems in language development
1005
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Language Development How does language develop? • Sound recognition • Comprehension = understanding • Production of sounds/words • Accelerates rapidly during second year of life • Early Language Milestone Scale
Child Development and Behavior
Language Development What is the connection between language and cognitive development? • Language delay related to verbal-based
learning disabilities • Atypical language development related to global developmental delay
1006
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Language Development Language/Speech Delay • More subtle than motor development delay • Epidemiology • Causes – – – – – – –
Mental retardation – >50% Hearing loss Maturation delay Bilingualism Psychosocial deprivation Autism Cerebral Palsy
1007
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Behavioral Theory and Dentistry • Behavior in the dental setting is related to overall behavior • Understanding the theories of behavior helps us to understand • Child/parent interaction • Child temperament and attachment issues • Behavioral disorders
Child Development and Behavior
Behavioral Theory and Dentistry Is there a relationship between temperament and ECC? How does temperament impact child dental fear? • Shy children are at greater risk • Children with difficulty regulating emotion are at greater
risk
1008
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Behavioral Theory and Dentistry Temperament and behavior • Approachability • Tendency to withdraw • Intense and active temperament
Child Development and Behavior
Effortful Control What is “Effortful Control”? • Modification of one’s own behavior • Can be exercised by 12 months of age • “Self-soother”
1009
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Development of SelfRegulation Child factors • Cognitive ability • Temperament
Parental factors • Approach to discipline • Overprotection • Limits for child • Self-control • Familial relationships
Child Development and Behavior
Fear/Anxiety in Children Fear: a feeling of impending danger
1010
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Fear/Anxiety in Children Ages 1-2 • • • • •
Large movements Loud sounds Changes in location of familiar things Strangers Separation
Ages 3-4 • • • • •
Animals Imaginary creatures Dark Being alone Physical harm
Child Development and Behavior
Fear/Anxiety in Children Age 5 •
Decrease in fears
Ages 6-8 • • •
Failure in school Ridicule Death of a loved one
37
1011
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Phobias Causes of Phobias •
Negative conditioning
•
Instruction/information
•
Observational conditioning
Child Development and Behavior
Dental Fear What can we learn from medical models?
1012
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Dental Fear and Medical Models Coping plays a critical role Distraction Effortful control Role of parent in promoting coping vs. distress • Hypnosis • Desensitization • Modeling/behavioral rehearsal • • • •
Child Development and Behavior
Dental Fear Dental fear in children • Children with negative behaviors during dental
treatment were more likely to have dental fears
• Not all children with fear are dental behavior
management problems
• Latent-inhibition: The effect of non-invasive visits
1013
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Dental Fear Child’s perception of the dental visit is related to dental fear • Dentist’s empathy (or lack thereof) • Parental dental fear • Subjective experiences of pain/trauma • Child’s overall fearfulness
Child Development and Behavior
Dental Fear How do gender and age relate to dental fear? • Older girls have more dental fear • Older boys underplay their concerns • Adolescents may be more difficult
1014
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Dental Fear What is the role of pain in dental fear? • Subjective experiences more predictive than objective dental pathology • Pain is a multifactorial perception • Child’s perception of the dentist- most important • Maternal anxiety plays a lesser role
Child Development and Behavior
Dealing with Dental Anxiety Prepare and be prepared • Provide information to parent in advance • Health history form •
Temperament
•
History of negative medical/dental experiences
•
Parental expectations
1015
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Dealing with Dental Anxiety Educate parents about predictable anxiety • Dentist = Barbers= Santa Claus, etc. • Things going in the mouth • Sensory stimulation
Child Development and Behavior
Assessment of Child’s Behavior Facial image scale
Child!Fear!Survey!– reproduced!in!references
1016
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Assessment of Child’s Behavior Assessing the child’s behavior in the dental office: Objective observations • Parental responses to questions on
health history
Child Development and Behavior
Assessment of Child’s Behavior Objective observations • Parental interactions with child in office • Negative child behaviors • Internalizing • Externalizing • Uncooperative
1017
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Child Development and Behavior
Parental Perceptions Parental perception of child • Mothers see more negative behavior in other
children
• Mothers classified less of their own children’s
behavior as negative than did an independent observer
• Mothers generally underrate all negative
behaviors
Child Development and Behavior
Parental Expectations Parental expectations and measures of satisfaction • Good communication with dentist • Level of knowledge of dentist • Child will have a positive encounter • Parental presence in treatment area
1018
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management
General Considerations Behavior Management involves an ongoing interaction of three individuals:
Child – Parent – Dentist
Behavior Management
General Considerations Concepts in Behavior Guidance • • • •
Behavior Guidance is an art based on science Communication: the key to success Role of staff and dentist Unintended negative impressions
1019
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management
Non-verbal Communication 3 essential messages • “I see you as an individual and will respond to your needs
as such” • “I am thoroughly knowledgeable and highly skilled” • “I am able to help you and will do nothing to hurt you
needlessly”
Behavior Management
Factors in Behavior Management Decisions What if behavior is challenging? • Risk vs. benefit • Need for treatment – urgency • Consequences of deferred treatment • Interaction between dentist/parent/child
1020
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management
Goals Establish a dental home • Establish communication • Be knowledgeable about oral conditions • Alleviate fear • Deliver quality dental care • Build trust • Promote a positive attitude toward dental care
Behavior Management
Treatment Approach • Assess patient • Behavioral • Physical • Assess parental attitudes/concerns • Create problem list • Create treatment plan with options • Discuss with parent – reach consensus
1021
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management
Treatment Approach • Be an educator • Be willing to recommend a second opinion • Obtain informed consent • Carry out treatment • Assess outcome and plan for future care
Behavior Management
Factors Affecting Behavior Guidance Beliefs about changing parenting styles • Belief that patient behavior is worse now • Belief that patient behavior is related to more
negative parenting style • Parents less likely to instill respect for others
1022
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management
Factors Affecting Behavior Guidance Attitudes of dentists • Pediatric dentists using behavior guidance
techniques that are less assertive • Teaching of HOM decreased by 50% from 19891999 • Parental presence in operatory is preferred by majority of dentists • Male dentists – perceive greater conflict between parental and dentist expectations
Behavior Management
Factors Affecting Behavior Guidance
What about increased awareness of mental health issues?
1023
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management
Factors Affecting Behavior Guidance • Changing families • Diverse, multicultural nature of societies
Behavior Management
Factors Affecting Behavior Guidance What we do and how it is perceived…… • Care • Comfort • Unacceptability of certain behavior guidance
techniques
1024
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Communicative • Distraction • Tell-Show-Do • Nonverbal • Positive Reinforcement • Voice Control
Parental Presence/Absence Nitrous oxide/Oxygen analgesia
Behavior Management Techniques
Advanced Behavior Management • Protective stabilization • Sedation • General Anesthesia
1025
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Deferred Treatment Risks/Benefits must be explained ART (Interim Therapeutic Restoration) and Regimented application of fluoride varnish
Behavior Management Techniques
Informed Consent • Required for all but communicative
techniques
• Parent should be involved • Consider the child’s ability to assent • Components of Informed Consent
1026
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Informed Consent • Describe adjunctive aids • Mouthprop • Rubber dam • Methods of providing informed consent • Understanding leads to acceptance • Dentist oral explanation – best • Written explanation – poorest • Videotape demonstrations – inadequate
Behavior Management Techniques
Basic Behavior Guidance Communication Concepts in Behavior Guidance • Use directive communication vs. asking child to help • Be creative in communicating with children • Identify the particular fear, then specifically address it • Show tools and give explanation
1027
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Distraction • • • • •
Attention directed away from procedure Affects pain perception Requires cognitive ability Inexpensive, creative, effective Review of 26 studies on distraction
Behavior Management Techniques
Basic Behavior Guidance Contingent distraction: “You can watch the videogame as long as you are cooperative” • Effective in three- to nine-year-olds • Inexpensive • Non-invasive
1028
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Dental applications • Gear distraction to child’s age • Videogames/movies/handheld games • Music with earphones • Storytelling • Animal game
Behavior Management Techniques
Basic Behavior Guidance Tell-Show-Do • Can be used for any child • Effective
1029
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Tell-Show-Do
Behavior Management Techniques
Basic Behavior Guidance Nonverbal Communication Positive Reinforcement • Smile • “Thumbs up” sign • Pat on the back
1030
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Positive Reinforcement • Rewards desired behavior • Best when immediate • Requires consistency • Realization that the desired behavior achieved
may be less than totally desired, but is still positive
Behavior Management Techniques
Basic Behavior Guidance Voice Control • Controlled alteration of voice to direct behavior • Volume • Tone • Pace • Highly effective in reducing disruptive behavior • No undesirable emotional effects noted • Considered unacceptable by parents
1031
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance
Voice Control • Alternative methods of voice control:
Cooperation as a choice
Behavior Management Techniques
Basic Behavior Guidance Parental Presence/Absence • Parent must support recommendation
for presence/absence
• Parenting style may have a greater
influence than presence
• Parental preparation
1032
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Parental Presence/Absence • Build parental trust and confidence over time • Be flexible
Behavior Management Techniques
Basic Behavior Guidance Challenges to Basic Behavior Guidance • Developmental/physical disability • Medical conditions • Fear transmitted by parent/peers • Previous negative medical/dental experiences • Dysfunctional parenting
1033
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Case: Basic Behavior Management Gone Awry…… 4-1/2 yr. old child brought for second opinion about “decay on her front tooth”. Previous dentist noted caries and recommended sedation to restore the tooth. Parents were hesitant about sedating the child and wanted another opinion.
1034
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance Lessons learned: Patient-directed treatment plans are usually doomed for failure. Same goes for Parent-directed treatment plans. When there are two pages of progress notes for 2 appointments, it’s not going well. The child’s dental experience isn’t isolated – the home environment and parental philosophy looms large.
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide N2O/O2 is considered a form of basic behavior management Features • Inhalational • Mechanism • Effects
1035
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Advantages • Rapid onset and recovery time • Ease of titration • Excellent safety record • Can be used with communicative behavior
management techniques
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Disadvantages • Weak agent • Depends on patient acceptance • Patient must be able to breath through nose • Occupational hazards • Potentiates effects of other sedatives • May cause nausea or excitement • Diffusion hypoxia may occur
1036
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Indications • • • •
Fearful or anxious patient Patient with exaggerated gag reflex Cooperative patient needing much dental treatment Patient with difficulty achieving local anesthesia
Contraindications • First trimester of pregnancy • Chronic obstructive pulmonary disease
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Medical consultation indicated • Acute otitis media, recently placed tympanic
membrane grafts • Severe asthma • Sickle cell disease • Bleomycin sulfate therapy (anti-neoplastic antibiotic)
1037
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Pre-procedural considerations • Review medical history • Documentation • Rationale • Any pretreatment dietary instructions • Informed Consent
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Equipment • • • • •
Nasal hood Failsafe mechanism Scavenging system Emergency cart Positive pressure oxygen delivery system
1038
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Personnel and training • Appropriate license or permit • Appropriate training and certification in CPR • Office emergency protocol
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Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Administration • • • • • •
Flow rate of 5-6L/min 100% oxygen for first 1-2 minutes Titrate nitrous oxide to maximum of 50% Continue with communicative techniques Monitor appropriately Use 100% oxygen for 3-5 minutes at end of procedure
Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Administration • Nausea increased by • •
Longer administration of nitrous oxide Upward/downward/upward changes in level
• If child appears restless • •
May be ready to vomit May be entering into deeper level of sedation
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Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide Documentation • • • •
Percent nitrous oxide used Duration of procedure Post-treatment oxygenation Patient response to nitrous oxide
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Behavior Management Techniques
Basic Behavior Guidance - Nitrous Oxide What is the sedative role of Nitrous Oxide? Use of nitrous oxide >60% may cause moderate to deep sedation Nitrous oxide used with other pharmacologic agents increases their sedative effects
Advanced Behavior Management
Protective Stabilization Goals • Reduce untoward movement • Protect from injury • Facilitate dental care delivery
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Advanced Behavior Management
Protective Stabilization Indications • Limited treatment • Immediate assessment needed
Contraindications • • • •
Physical condition which prevents safe stabilization Previous psychological trauma Cooperative non-sedated patients Non-sedated uncooperative patients with extensive dental needs
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Advanced Behavior Management
Protective Stabilization Precautions • Monitor tightness and duration • Caution not to compromise circulation or
respiration • Stabilization must be ceased in a hysterical patient
Advanced Behavior Management
Protective Stabilization How do parents view protective stabilization? Positive verbal presentation of papoose board increases parental acceptance of technique Kupietzky & Ram, 2005
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Advanced Behavior Management
Protective Stabilization Memories and Protective Stabilization • Children do not remember early use of
restraint
• Children have greater negative recall of
medical interventions than of dental interventions
• Memory is affected by parallel phenomena
Advanced Behavior Management
Protective Stabilization Documentation • Consent • Type of stabilization used and why • Length of time stabilization used • Effectiveness of stabilization
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Advanced Behavior Management
Sedation No dentist should provide sedation unless formally trained and in possession of a state permit consistent with the type of sedation being administered.
Advanced Behavior Management
Sedation Goals of sedation • Guard patient’s safety and welfare • Minimize physical discomfort and pain • Control anxiety, minimize psychological trauma,
maximize amnesia • Control behavior and movement • Return patient to state for safe discharge
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Advanced Behavior Management
Sedation Indications • Young patient, pre-cooperative • Uncooperative patient • Certain medical, mental, or physical disabilities • Extensive treatment needs • Protection of developing psyche
Advanced Behavior Management
Indications for Sedation Age Behavior
Age Special Health Care Needs
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Advanced Behavior Management
Sedation Factors influencing the sedation outcome • Age • Cognitive • Child’s behavior/temperament
Advanced Behavior Management
Sedation How does the patient’s development affect sedation?
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Advanced Behavior Management
Sedation Remember…. Sedation is not a static level or state, but is a continuum
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Advanced Behavior Management
Sedation Concept of rescue Recognize the levels of sedation • Have skills to provide cardiopulmonary support • Have skills to rescue the patient •
Advanced Behavior Management
Sedation Levels of sedation • Defined by responsiveness and physiologic
changes • Patient can move from one level to another without warning • Monitoring requirements increase as level of sedation increases
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Advanced Behavior Management
Sedation Levels of Sedation Minimal
Moderate
Deep
Goal
• Decrease anxiety • Facilitate coping
• Decrease anxiety • Facilitate coping
Patient Responsiveness
• Responds normally to verbal commands • Interactive • Aware of but less responsive to clinical stimuli
• More calm • Uneasily aroused • Responds to verbal commands • Non-interactive • Aware of but less responsive • Unaware of and minimally to clinical stimuli responsive to clinical stimuli
Physiologic Changes
• No loss of protective reflexes • No loss of protective reflexes • Normal vital signs • Normal vital signs
Personnel needed
2
• Eliminate anxiety • Override coping skills
• Partial or complete loss of protective reflexes • Stable and minimally or moderately below health status norms
2
3
Advanced Behavior Management
Sedation Monitors during sedation • Dentist observation of patient • Pulse oximeter • Capnograph • Pre-cordial stethoscope • Blood pressure • EKG • Temperature • Bispectral analysis
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Advanced Behavior Management
Sedation Considerations for sedation Know the guidelines Careful patient selection Select drug based on procedure Use lowest dose of drug with highest therapeutic index • Know the drugs • Informed consent • • • •
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Advanced Behavior Management
Sedation Considerations for sedation • Pre-operative instructions • Responsible persons for transport • Monitoring • Emergency preparedness • Documentation
Advanced Behavior Management
Sedation- Patient selection Patient selection: ASA classification • ASA I and II – generally appropriate • ASA III and IV – generally
contraindicated
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Advanced Behavior Management
Sedation – Patient Assessment • Medical History • • • •
Current illness Chronic conditions Medications, including herbal Sleep apnea
• Physical Assessment • • • •
Cardiovascular Respiratory Airway Behavioral
Advanced Behavior Management
Sedation – Patient Assessment Patient Examination • Document behavior and justification for sedation • Extraoral assessment • Intraoral assessment • • •
Soft/hard tissues, airway Gag reflex Tonsil Size
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Mallampati Classification
Advanced Behavior Management
Sedation – Patient Selection Poor candidates for sedations • • • • •
ASA III and IV Sleep apnea Obesity - dose by age, not weight Abnormal airway Chronic medical conditions
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Advanced Behavior Management
Sedation – Patient Selection Why is the child airway more challenging? • Different anatomy • Relatively larger tongue/epiglottis • Mandible less developed • Increased airway resistance
Advanced Behavior Management
Sedation Respiratory System • Ventilation: air movement into/out of lungs • Oxygenation: oxygen delivered to tissues • • • • • •
Requires patent airway Transport across alveoli Hb transport of oxygen Transport via cardiovascular system Metabolic tissue exchange Elimination of carbon dioxide
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Advanced Behavior Management
Sedation Monitoring respiration • • • • • •
Observation of chest movements Precordial stethoscope Heart rate Pulse oximeter Capnograph EKG and defibrillator for deep sedation
Advanced Behavior Management
Sedation in action
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Advanced Behavior Management
Sedation Cardiovascular system in Children • Blood pressure dependent on heart rate • Drop in heart rate leads to hypotension • Monitoring cardiovascular status – Blood pressure – Pulse oximeter – Pulse palpation –closest to heart is best
Advanced Behavior Management
Sedation Pre-Op: Plan for the unexpected • Emergency cart • Check all machines • Calculate and record dosages for reversal agents • Calculate maximum dose of local anesthetic • Review any specific concerns about patient • Discuss plan with auxiliaries
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Advanced Behavior Management
Sedation - Documentation • • • • • • • • •
Rationale/justification Informed consent Pre-sedation instructions, including diet Baseline weight, vital signs Medications used Any immobilization used Monitoring during procedure Effectiveness Discharge condition
Advanced Behavior Management
Sedation How do pediatric dentists assess the effectiveness of a sedation? Management style of the pediatric dentist : Authoritarian vs. Child Advocate
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Advanced Behavior Management
Sedation Discharge criteria • Airway uncompromised • Cardiovascular function stable • Patient awake, protective reflexes intact • Adequate hydration • Patient responsive, talking • Ambulatory with assistance • Responsible adult present
Advanced Behavior Management
Sedation – Routes of Administration Oral • • • • • • •
Most common route Easily accepted - no injections Prolonged onset and recovery Relatively safe if only using one drug Less predictable First pass hepatic metabolism Inability to titrate
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Advanced Behavior Management
Sedation – Routes of Administration Intranasal • Rapid onset • Use atomizer: 1-cc syringe • Inability to titrate • No first-pass metabolism • Indicated for when patient refuses oral meds
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Advanced Behavior Management
Sedation – Routes of Administration Intramuscular • Faster absorption than oral route • Ease of administration • Potential for trauma to injection site • Prolonged onset and recovery • Inability to titrate • Painful • Increased liability costs
Advanced Behavior Management
Sedation – Routes of Administration Intravenous • • • • • • • • • •
Optimum route Rapid onset Drug can be titrated Absorption not a factor Drug can be administered in small amounts over time IV access is available in case of emergency Starting IV may be difficult Venipuncture complications Requires highest level of monitoring Increased liability costs
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Advanced Behavior Management
Sedation – Drugs Commonly Used Chloral hydrate • • • • • • • • •
Nonbarbituate sedative-hypnotic No analgesic/anxiolytic effect Given orally or as suppository Onset 30-60 minutes Duration 5-8 hours Dosage: 25-50mg/kg to 1 gm maximum No reversal agent Unpleasant taste, gastric irritation Precautions
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Advanced Behavior Management
Sedation – Drugs Commonly Used Meperidine (Demerol) • • • • • • • • • • •
Narcotic Analgesic Sedative Oral or parenteral Onset 30 minutes Duration 2-4 hours Dosage: 1-2mg/kg to maximum dose of 50mg Reversal agent Unpleasant taste Precautions CNS, CV, Respiratory depression
Advanced Behavior Management
Sedation – Drugs Commonly Used Hydroxyzine (Vistaril, Atarax) • Antihistamine, anti-emetic • Analgesic • CNS depression • Used with other meds • Onset 15-30 minutes • Duration 2-4 hours • Dosage 1-2mg/kg orally • Effect similar to nitrous oxide • Pleasant taste
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Advanced Behavior Management
Sedation – Drugs Commonly Used Benzodiazepines • • • • •
Anxiolytic, amnesic Muscle relaxant CNS depression Minimal CV, respiratory effects Reversal agent
Advanced Behavior Management
Sedation – Drugs Commonly Used Diazepam (Valium) Onset 45-60 minutes Duration 6-8 hours Dosage (general guide): 1mg/year of age Indications Minimal adverse reactions Contraindication – patients with narrowangle glaucoma • Precautions • • • • • •
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Advanced Behavior Management
Sedation – Drugs Commonly Used Midazolam (Versed) • Onset 5-10 minutes • Duration: 30 minutes • Dosage 0.25 to 1.0mg/kg in children to • • • •
15mg maximum Equally effective for different ages Administer with another liquid Precautions Use with other medications
Advanced Behavior Management
Sedation – Drugs Commonly Used Complications of Midazolam • Paradoxical negativism • Hallucinations/nightmares
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Advanced Behavior Management
Sedation – Drugs Commonly Used Reversal of Benzodiazepines: Flumazenil Pre-op: calculate dosage that would be needed IV or Sublingual: 0.01mg/kg Maximum total dose: 1mg Onset within 1 minute Repeat as needed Follow recovery procedure
• • • • • •
Advanced Behavior Management
Local Anesthetic Lidocaine (xylocaine) • • • • • • • •
CNS depression Minimal CV effects 4mg/kg with or without vasoconstrictor Anesthesia onset – 5 minutes Pre-op: Calculate maximum dose for patient Toxicity with intravascular injection Overdose appears as seizure Potentiates other sedatives
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Advanced Behavior Management
Using Drugs in Combination • Benefits • Potentiation effects
Advanced Behavior Management
Emergencies • Upper airway obstruction • Respiratory depression • Overdose of medications • Seizure • Allergic reaction • Vomiting, aspiration • Syncope • Hypoglycemia
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Advanced Behavior Management
Adverse Events What are the common adverse events in pediatric sedation? • Respiratory arrest – 43% • Respiratory depression – 30% • Cardiac arrest – 8% Cote, April 2000
Advanced Behavior Management
Adverse Events What about NPO Adverse Events? • Review of 1014 patients sedated in ED • NPO guidelines not always followed • 6.7% serious adverse events Agrawal, 2003
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Advanced Behavior Management
Adverse Events Factors contributing to adverse events • • • • • • •
Non-hospital-based facilities (92% vs. 37%) Inadequate resuscitation Inadequate monitoring Inadequate pre-sedation evaluation Medication errors Inadequate recovery procedures Lack of independent observer Cote, 2000
Advanced Behavior Management
Adverse Events Medication Considerations • Use of 3 or more drugs • All routes of administration • Meds should be given with medical supervision • Post-sedation observation longer for certain meds
Cote, 2000
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Advanced Behavior Management
Sedation Post Sedation Period • Critical time – adverse events can occur • Serious adverse events occurred 25 minutes after last
medication given
• Combination regimen subjects at greater risk • Patients may fall asleep in car – adverse events can
occur in car or at home
• Discharge criteria should be met or exceeded
Advanced Behavior Management
Emergency Basics Know emergency procedures Have plan Emergency cart up-to-date and handy Recognize problem Stop treatment EMS numbers available at multiple stations • Patient – P-A-B-C-D • • • • • •
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Advanced Behavior Management
Emergency Preparedness Personnel Training Patient Factors ! Know medical history ! Know sedation specifics ! Pre-operative assessment
Advanced Behavior Management
Emergency Preparedness Follow Guidelines • NPO status • Monitoring • Discharge criteria
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Advanced Behavior Management
Emergency Preparedness Emergency equipment • • • • •
Positive pressure oxygen Rescue drugs Nasal and oral airways – assorted sizes Masks – assorted sizes Training to use all of above
Advanced Behavior Management
Emergency Preparedness Quality assurance
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Speech and Language Milestones Hearing and Understanding Birth-3 Months • Startles to loud sounds. • Quiets or smiles when spoken to. • Seems to recognize your voice and quiets if crying. • Increases or decreases sucking behavior in response to sound. 4-6 Months • Moves eyes in direction of sounds. • Responds to changes in tone of your voice. • Notices toys that make sounds. • Pays attention to music. 7 Months-l Year • Enjoys games like peek-a-boo and pat-a-cake. • Turns and looks in direction of sounds. • Listens when spoken to. • Recognizes words for common items like “cup”, “shoe”, “juice”. • Begins to respond to requests (“Come here”, “Want more?”). 1-2 Years • Points to a few body parts when asked. • Follows simple commands and understands simple questions (“Roll the ball”, “Kiss the baby”, “Where’s your shoe?”). • Listens to simple stories, songs, and rhymes. • Points to pictures in a book when named. 2-3 Years • Understands differences in meaning (“ go-stop”, “in-on”, “big-little”, “up-down”). • Follows two requests (“Get the book and put it on the table”). 3-4 Years • Hears you when call from another room. • Hears television or radio at the same loudness level as other family members. • Understands simple, “who?” “what?” “where?” “why?” questions. 4-5 Years • Pays attention to a short story and answers simple questions about it. • Hears and understands most of what is said at home and in school.
Talking Birth-3 Months • Makes pleasure sounds (cooing, gooing). • Cries differently for different needs. • Smiles when sees you.
4-6 Months • Babbling sounds more speech-like with many different sounds, including p, b, and m. • Vocalizes excitement and displeasure. • Makes gurgling sounds when left alone and when playing with you. 7 Months-l Year • Babbling has both long and short groups of sounds such as “tata upup bibibibi.” • Uses speech or non-crying sounds to get and keep attention. • Imitates different speech sounds. • Has 1 or 2 words (bye-bye, dada, mama) although they may not be clear. 1-2 Years • Says more words every month • Uses some 1-2 word questions (“Where kitty?”, “Go byebye?”, “What’s that?”). • Puts 2 words together (“more cookie”, “no juice”, “mommy book”). • Uses many different consonant sounds of the beginning of words. 2-3 Years • Has a word for almost everything. • Uses 2-3-word “sentences” to talk about and ask for things. • Speech is understood by familiar listeners most of the time. • Often asks for or directs attention to objects by naming them. 3-4 Years • Talks about activities at school or at friends’ homes. • People outside family usually understand child’s speech. • Uses a lot of sentences that have 4 or more words. • Usually talks easily without repeating syllables or words. 4-5 years • Voice sounds clear like other children’s. • Uses sentences that give lots of details (e.g. “I like to read my books”). • Tells stories that stick to topic. • Communicates easily with other children and adults. • Says most sounds correctly except a few like l, s, r, v, z, ch, sh, th. • Uses the same grammar as the rest of the family.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
AFTER YOUR CHILD’S SEDATION Today your child had dental treatment under conscious sedation. He/she received the following medicines(s) for sedation: Chloral hydrate Diazepam (valium) Meperidine (Demerol) Midazolam (versed) Hydroxyzine (Vistaril) Other _____________________ The name of the doctor who took care of your child is: ____________________________________________ Children respond to sedation in their own way, but the following guidelines will help you know what to expect at home.
GOING HOME 1. Your child will not be able to walk well, so we suggest that you carry your child or use a stroller to the car or around the office. 2. Young children (up to age 3 or 4 or 40 inches tall) must be restrained in a car safety seat. 3. Older children must be restrained with a seat belt, and should be assisted into your home by two people.
ACTIVITY 1. Your child may take a long nap. He/she may sleep from 3 to 8 hours and may be drowsy and irritable for up to 24 hours after sedation. When your child is asleep, you should be able to awaken him/her easily. 2. Your child may be unsteady when walking or crawling and will need support to protect him/her from injury. An ADULT must be with the child at all times until the child has returned to his/her usual state of alertness and coordination. 3. Your child should not perform any potentially dangerous activities, such as riding a bike, playing outside, handling sharp objects, working with tools, or climbing stairs until they are back to their usual alertness and coordination for at least one hour. 4. We advise you to keep your child home from school or daycare after treatment and possibly the next day if your child is still drowsy or unable to walk well. Your child should have returned to his/her usual state of alertness and coordination within 24 hours.
EATING AND DRINKING INSTRUCTIONS Begin by giving clear liquids such as clear juices, water, jello, popsicles, or broth. If your child does not vomit after 30 minutes, you may continue with solid foods. IF YOUR CHILD IS VOMITING AFTER SEDATION OR UNABLE TO EAT AND DRINK: Please contact the doctor at the office or at the following number: __________________.
REASON TO CALL THE DOCTOR 1. 2. 3. 4.
You are unable to arouse your child. Your child is unable to eat or drink. Excessive vomiting or pain. Your child develops a rash.
FOR THESE OR ANY OTHER CONCERNS about your child’s sedation, please contact the doctor.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Appendix A. Recommended Discharge Criteria
1. Cardiovascular function and airway patency are satisfactory and stable. 2. The patient is easily arousable, and protective reflexes are intact. 3. The patient can talk (if age appropriate). 4. The patient can sit up unaided (if age appropriate), 5. For a very young or handicapped child incapable of the usually expected responses, the presedation level of responsiveness or a level as close as possible to the normal level for that child should be achieved. 6. The state of hydration is adequate.
Appendix B. ASA Physical Status Classification Class I Class II Class III Class IV Class V
A normally healthy patient. A patient with mild systemic disease (eg, controlled reactive airway disease). A patient with severe systemic disease (eg, a child who is actively wheezing). A patient with severe systemic disease that is a constant threat to life (eg, a child with status asthmaticus). A moribund patient who is not expected to survive without the operation (eg, a patient with severe cardiomyopathy requiring heart transplantation).
Appendix C. Drugs* That May Be Needed to Rescue a Sedated Patient * The choice of emergency drugs may vary according to individual or procedural needs.
Albuterol for inhalation Ammonia spirits Atropine Diphenhydramine Diazepam Epinephrine (1: 1000, 1: 10 000) Flumazenil Glucose (25% or 50%) Lidocaine (cardiac lidocaine, local infiltration) Lorazepam Methylprednisolone Naloxone Oxygen Fosphenytoin Racemic epinephrine Rocuronium Sodium bicarbonate Succinylcholine
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Appendix D. Emergency Equipment That May Be Needed to Rescue a Sedated Patient ** *
* The choice of emergency equipment may vary according to individual or procedural needs. ** The practitioner is referred to the SOAPME acronym described in the text in preparation for sedating a child for a procedure.
Intravenous Equipment
Assorted IV catheters (eg, 24-, 22-, 20-, 18-, 16-gauge) Tourniquets Alcohol wipes Adhesive tape Assorted syringes (eg, 1-, 3-, 5-, 10-mL) IV tubing Pediatric drip (60 drops/mL) Pediatric burette Adult drip (10 drops/mL) Extension tubing 3-way stopcocks IV fluid Lactated Ringer solution Normal saline solution D50.25 normal saline solution Pediatric IV boards Assorted IV needles (25-, 22-, 20-, and I8-gauge) Intraosseous bone marrow needle Sterile gauze pads
Airway Management Equipment
Face masks (Infant, child, small adult, medium adult, large adult) Breathing bag and valve set Oropharyngeal airways (Infant, child, small adult, medium adult, large adult) Nasopharyngeal airways (Small, medium, large) Laryngeal mask airways (1, 1.5,2,2.5,3,4, and 5) Laryngoscope handles (with extra batteries) Laryngoscope blades (with extra light bulbs) Straight (Miller) No. I, 2, and 3 Curved (Macintosh) No.2 and 3 Endotracheal tubes (2.5, 3.0, 3.5, 4.0, 4.5, 5.0, 5.5, and 6.0 uncuffed and 6.0, 7.0, and 8.0 cuffed) Stylettes (appropriate sizes for endotracheal tubes) Surgical lubricant Suction catheters (appropriate sizes for endotracheal tubes) Yankauer-type suction Nasogastric tubes Nebulizer with medication kits Gloves (sterile and nonsterile, latex free)
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Resource Section
Reference Manual 2005-2006
Management of Medical Emergencies For all emergencies 1. Discontinue dental treatment 2. Call for assistance/someone to bring oxygen and emergency kit 3. Position patient: ensure open and unobstructed airway 4. Monitor vital signs 5. Be prepared to support respiration, support circulation, call for additional help Condition
Signs and symptoms
Treatment
Allergic reaction (mild or delayed)
Hives, itching, edema, erythema of skin, mucosa, conjunctiva
1. Discontinue all sources of Diphenhydramine 1 mg/kg allergy-causing substances Child: 10-25 mg qid 2. Administer diphenhydramine Adult: 25-50 mg qid
Oral
Allergic reaction (sudden onset): anaphylaxis
Urticaria – itching, flushing, hives; rhinitis; wheezing/difficulty breathing; bronchospasm; laryngeal edema; weak pulse; marked fall in blood pressure; loss of consciousness
This is a true, lifethreatening emergency 1. Call for medical help 2. Administer epinephrine 3. Administer oxygen 4. Monitor vital signs
IM or SubQ
Acute asthmatic attack
Shortness of breath, wheezing, coughing, tightness in chest, cyanosis, tachycardia
1. Sit patient upright or in a 1. Try patient’s inhaler or Inhale comfortable position one from emergency kit 2. Administer oxygen 2. Epinephrine 1:1000 IM or SubQ 3. Administer bronchodilator 0.01 mg/kg every 15 min 4. If bronchodilator is ineffective, as needed administer epinephrine
Anesthetic toxicity
Light-headedness, changes in vision and/or speech, changes in mental status, confusion, agitation, tinnitis, tremor, seizure, tachypnea, bradycardia, unconsciousness, cardiac arrest
1. Assess and support airway, breathing, and circulation 2. Administer oxygen 3. Monitor vital signs 4. Transport to emergency center as indicated
Supplemental oxygen
Mask
1. Reassure patient 2. Assess and support airway, breathing, and circulation 3. Administer oxygen 4. Monitor vital signs 5. Transport to emergency center as indicated
Supplemental oxygen
Mask
Anesthetic reaction: Anxiety, tachycardia/palpitations, vasoconstrictor restlessness, headache, tachypnea, chest pain, cardiac arrest
Drug dosage
Epinephrine 1:1000 0.01 mg/kg every 5 min until recovery or until help arrives
Drug delivery
Overdose: benzodiazepine
Somnolence, confusion, diminished 1. Assess and support airway, reflexes, respiratory depression, breathing, and circulation apnea, respiratory arrest, 2. Administer oxygen cardiac arrest 3. Monitor vital signs 4. Establish IV access and reverse with flumazenil 5. Monitor recovery
Flumazenil 0.01 mg/kg IV (not to exceed a total of 1 mg) at a rate not to exceed 0.2 mg/min
Overdose: narcotic
Decreased responsiveness, 1. Assess and support airway, respiratory depression, respiratory breathing, and circulation arrest, cardiac arrest 2. Administer oxygen 3. Monitor vital signs 4. Reverse with naloxone 5. Monitor recovery
Naloxone 0.01 mg/kg (may repeat after 2-3 min)
IV, IM, or SubQ
Seizure
Warning aura; disorientation, blinking, or blank stare; uncontrolled muscle movements; muscle rigidity; unconsciousness; postictal phase: sleepiness; confusion; amnesia; slow recovery
1. Recline and position to prevent injury 2. Ensure open airway and adequate ventilation 3. Monitor vital signs 4. If status is epilepticus, give diazepam
Diazepam Child up to 5 y: 0.2-0.5 mg slowly every 2-5 min with maximum=5 mg Child 5 y and up: 1 mg every 2-5 min with maximum=10 mg
IV
Syncope (fainting)
Feeling of warmth, skin pale and moist, pulse rapid initially then gets slow and weak, dizziness, hypotension, cold extremities, unconsciouness
1. Recline, feet up 2. Loosen clothing that may be binding 3. Ammonia inhaler 4. Administer oxygen 5. Cold towel on back of neck 6. Monitor recovery
Ammonia in vials
Inhale
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239
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Guidelines for Infection Control in Dental Health-Care Settings — 2003
INSIDE: Continuing Education Examination
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
MMWR CONTENTS (52
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Introduction ......................................................................... 1 Background ......................................................................... 2 Previous Recommendations .............................................. 3 Selected Definitions .......................................................... 4 Review of Science Related to Dental Infection Control ......... 6 Personnel Health Elements of an Infection-Control Program .......................................................................... 6 Preventing Transmission of Bloodborne Pathogens ................................................ 10 Hand Hygiene ................................................................ 14 Personal Protective Equipment ........................................ 16 Contact Dermatitis and Latex Hypersensitivity ................. 19 Sterilization and Disinfection of Patient-Care Items ......... 20 Environmental Infection Control ..................................... 25 Dental Unit Waterlines, Biofilm, and Water Quality ......... 28 Special Considerations ...................................................... 30 Dental Handpieces and Other Devices Attached to Air and Waterlines .................................................... 30 Saliva Ejectors ................................................................ 31 Dental Radiology ............................................................ 31 Aseptic Technique for Parenteral Medications ................. 31 Single-Use or Disposable Devices ................................... 32 Preprocedural Mouth Rinses ........................................... 32 Oral Surgical Procedures ................................................ 32 Handling of Biopsy Specimens ........................................ 33 Handling of Extracted Teeth ............................................ 33 Dental Laboratory ........................................................... 33 Laser/Electrosurgery Plumes or Surgical Smoke .............. 34 M. tuberculosis ................................................................. 35 Creutzfeldt-Jakob Disease and Other Prion Diseases ...... 36 Program Evaluation ........................................................ 37 Infection-Control Research Considerations ..................... 38 Recommendations ............................................................. 39 Infection-Control Internet Resources ................................. 48 Acknowledgement ............................................................. 48 References ......................................................................... 48 Appendix A ....................................................................... 62 Appendix B ........................................................................ 65 Appendix C ....................................................................... 66 Continuing Education Activity* ....................................... CE-1
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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#
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
Pediatric Anaphylaxis/Allergic Response
Assess ABCs
Patient alert, responsive with localized alergic reaction
Transport ASAP and contact med control
Establish patent airway 100% oxygen by non-rebreather mask or BVM ETT as indicated
Diphenhydramine 1-2 mg PO
Reassess ABCs Pulse oximeter if available Monitor
Monitor
Epinephrine (1:1000) 0.01 cc/kg SQ (max 0.3 cc) or 0.1 cc/kg ET If hemodynamically unstable, use Epi 1:10000 at 0.1 cc/kg IV Establish IV or IO with NS or LR For BLS, may administer patients own Epi-Pen
Yes
Reassess: is patient hemodynamically stable?
No
Trendelburg position Continue oxygen and support; monitor
Consider fluid bolus at 20 cc/kg NS Repeat prn
For Wheezing, Albuterol 2.5-5.0 mg in 2-3 cc NS by nebulizer prn
Diphenhydramine 1-2 mg/kg IV/IM
1095
Continue tx and support prn during transport
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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1096
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
8FCTJUFT
1097
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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1098
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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1099
Copyright American Academy of Pediatric Dentistry, 2008. All Rights Reserved.
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