(AAPD) Comprehensive Review of Pediatric Dentistry (B-Ok - Xyz)

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
December 1, 2008
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Topic/Speaker
DV
Bo
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1 1-14
Growth & Development / Orthodontics 1:44 1 2 1-8
9
Andrew L. Sonis, D.M.D. 1:43 2 3 1-16
4 1-7
Trauma 5 1-14
198 1:38 3
Constance M. Killian, D.M.D. 6 1-7
Dental Materials
309 0:57 3 7 1-12
Steven M. Adair, D.D.S., M.S.
Pulp Therapy
350
2 0:44 4 8 1-9
Steven M. Adair, D.D.S., M.S.
Oral Pathology / Oral Medicine / Syndromes 9 1-14
388 1:46 5
Andrew L. Sonis, D.M.D. 10 1-8
Oral Pathology / Oral Medicine / Syndromes (cont'd)
N/A 1:21 6 11 1-16
Andrew L. Sonis, D.M.D.
Prevention 12 1-11
612 2:03 7
Steven M. Adair, D.D.S., M.S. 13 1-13
Special Needs Patients 14 1-14
699 1:46 8
Constance M. Killian, D.M.D. 15 1-9
Dental Development 16 1-10
819 1:25 8
Steven M. Adair, D.D.S., M.S. 17 1-8
Hospital Dentistry
893 0:36 9 18 1-8
Constance M. Killian, D.M.D.
Special Needs Patients (cont'd)
932 0:53 9 19 1-11
Behavior Management
994 1:19 9 20 1-16
2

PREFACE
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3
Comprehensive Review
Provided by:
American Academy
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
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
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
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

FACULTY
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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
73U&%'A#"4,'.,(*3)U'%#'A"#)%(.'
",5#"/%3#)
! 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
Tooth movement (mm)
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
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#)
! 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
Tooth movement (mm)
Phase 3
Phase 2
Phase 1
85
W&,#"3,5'#A'%##%&'0#-,0,)%
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86
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
Center of Force
Rotation
on the
crown
CR CR
+3",4%3#) ()*'+,U",, #A''

^#"4,
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U08
88
Force
A force (F)
^ is a load applied
to an object that
tends to move
the object.
^
+3",4%3#) ()*'+,U",, #A''

^#"4,
?#*3.<'0#-,0,)%
89
+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
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
Distribution
Nb'U
Nb'U
bG'U
^'L'FGG'U
Duration
Force
Intermittent
Time
92
Duration
Force
Continuous and
decreasing
Time
Duration
Force Continuous and

Constant
Time
93
+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
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Slide 183
als1 photos of dental open bite and skeletal oopen bite

asonis, 5/25/2008
100
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Slide 197
als2 missing laterals

bilateral versus unilateral
consideration of peg lateral
asonis, 5/25/2008
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199
Prevention of Trauma
Who is at high risk for trauma?
Trauma is a part of Anticipatory

Guidance
200
Custom mouthguards
201
Injury Assessment
General Considerations
1. “Primum non nocere”

Do no harm
2. Never treat a stranger
202
Injury Assessment
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
203
History of Current Injury
• Identify adult bringing the child

• What
• When
• Where
• How
• Any treatment done elsewhere for this injury
Emergency Assessment
• Dental trauma is a subset of head

trauma
• Assess awareness/orientation
• Assure a patent airway
• Observe for rhinorrhea or otorrhea
204
• Bruising behind ear -

“Battle’s sign”
• Abnormal vital signs
Rapid Neurologic Exam: Cranial Nerves
III – Oculomotor
• Penlight
• PERRLA
• Abnormalities
205
III, IV, VI: Oculomotor, Trochlear, and
Abducens
• Track movements
• Extraocular movements intact
VII: Facial
• Ask patient to close eyes, smile,
frown
• No asymmetry of movement
206
• Glasgow Coma Scale – see

Appendix
• Eyes
• Best Motor Response
• Best Verbal Response
• Maximum score 15, minimum 3
Glasgow Coma Scale

Finding Rating
A. Eyes
Open spontaneously 4
Open to verbal command 3
Open to pain 2
No response 1
B. Best Motor Response
Obeys verbal command 6
Realizes pain 5
Withdraws from pain 4
Flexion to pain (decorticate) 3
Extension to pain (decerebrate) 2
No response 1
C. Best Verbal Response
Oriented and converses 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Minimal score = 3
Maximum score = 15
207
Intra Cranial Injury
Symptoms from clinical history
• Post-traumatic seizure
• Severe headache
• Loss of consciousness
• Vomiting
• Nausea
• Clinical evidence of skull fracture
What else should make you think ICI?
• Persistent drowsiness
• Amnesia
• Focal neurological signs – “seeing stars”
208
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
After dental treatment, follow

through….
Give post-op instructions for observation

• Patient is persistently sleepy
• Vomiting
• Severe headache
• Abnormal behavior
209
Evaluation and Treatment of Orofacial Trauma

Facial Bones
Extraoral: Hard Tissue - Facial bones
Classification of fractures
Simple
Compound
Comminuted
Favorable
Unfavorable
210

Craniofacial Trauma
Causes
Falls – 64%
Traffic – 22%
Sports – 9%
Violence – 5%
Distribution
Skull vault – 54%
Upper/middle facial third – 37%
Concommitant injuries – 33%

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?
211

Facial Bones
Midface fractures
• Rare in children
• Skull fractures more common
• Causes
• Treatment – nonsurgical best

Facial Bones
Nasal Fracture: most common
midface fracture in children
Signs
• Ecchymosis
• Laceration
• Swelling
• Epistaxis
• Bony irregularities
212

Facial Bones
Signs of Zygomatic Fracture
• Periorbital swelling
• Ecchymosis and hematoma
• Conjunctival hemorrhage
• Palpable step deformity
• Paresthesia
• Limited upward gaze
Frontal view Submentovertex view
213

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
214

Facial Bones
Diagnostic Aids
• Computerized Tomography (CT)
• Radiographs
• AP and Lateral skull
• Waters
• Submental vertex
Management - OMS
215

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

Management of Mandibular Fracture
Management – OMS
• Timing: can defer 24-36 hrs
• Stabilize mandible if deferring treatment
216

Mandibular Fracture
Diagnosis: Subcondylar/Condylar fracture

• Blunt injury to chin
• Bite is “off” or deviated
• Unilateral vs. Bilateral
• Palpate external auditory meatus

Clinical Exam for Possible Subcondylar
Fracture
217

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
218

Management of Mandibular
Fracture
Intracapsular fracture of condyle
• Ankylosis risk in children less than 3 yrs.
• Treatment: mandibular exercises and jaw

stretching
219

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

Fracture of Body of Mandible
• Radiographs
• Management: OMS
• No benefits to prolonged post-operative

antibiotics
220

Fracture of Body of Mandible
Evaluation and Treatment of Orofacial

Trauma
Types of Soft Tissue Injuries
Laceration
Contusions & Abrasion Burn
Puncture
221

Soft Tissue Injuries
Soft Tissue Lacerations
Identify foreign bodies
• ¼ usual exposure for intraoral

xray
• ½ usual exposure for extraoral
xray

Goals of wound management
Avoid infection
Functional and esthetic scar
Repair or Refer
Location of injury
Patient’s ability to heal
222

• Timing of closure
• Wound preparation
• Primary wound closure

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
223

Trauma
Suturing of Soft Tissue Injuries

Soft Tissue Lacerations
Tongue Laceration
• May not require sutures

• Use heavy thread
• Deep bites with needle
• Assure good
approximation
• Bury knots
224

Trauma
Extraora/Intraoral Soft Tissue
Electrical Burns

Electrical Burn: long-term
scarring
225

Electrical Burn: Commisural
Splint
Evaluation!and!Treatment!of!Orofacial Trauma
Extraora/Intraoral Soft!Tissue
226

Intraoral Soft Tissue
• Inspect buccal vestibule
• Inspect floor of mouth
• Evaluate palate for any puncture wounds
227

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
228
229
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
230

• May be first contact with dentist

• Precooperative child
• Long-term concerns for permanent
dentition

Epidemiology
• Maxillary primary incisors
• 2-4 years of age
• Luxation
231

Causes
• Falls
• Automobile accidents
• Child abuse
• Secondary factors

Emergencies
When can treatment be deferred?
What injuries should be seen

ASAP?
232

Clinical Examination
• Address behavior
• Assessment of clinical signs in young

children: objective vs. subjective signs

Remember to look past the obvious……
233

And get the big picture….

Radiographic Examination
• Avoid further injury
• Parental assistance
• Possible immobilization
• Usually record size 2 film
• Extraoral lateral radiographs not helpful in
intrusion
234

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
Diagnostic Findings
Injury Treatment / Follow-up
Clinical Radiographic
Enamel fracture or Take one x-ray Smooth sharp edges with sandpaper disk
Uncomplicated Smooth smaller fractures, place bandage restoration

Crown fracture Evaluate pulp chamber, stage of root with glass ionomer or composite
Enamel + dentin fracture
development, root resorption Clinical exam at 1 week
Clinical and x-ray exam at 3-4 weeks
Pulpotomy, pulpectomy (if possible) or extraction

Take one x-ray
Complicated Enamel + dentin fracture with pulp Clinical exam at 1 week
Evaluate pulp chamber, stage of root
Crown fracture exposure Clinical and x-ray exam at 3-4 weeks, 6
development, root resorption
months, 1 year
Cautious extraction so as not to disturb developing

Crown-root Coronal fragment mobile Take one x-ray - may be able to see permanent tooth while trying to retrieve root
fracture Minimal to moderate displacement gingival extent of fracture fragments; if necessary, leave root fragment to
resorb
If displaced - extract coronal fragment only.

Take one x-ray – determine location of
Coronal fragment usually mobile Leave apical fragment to resorb
fracture
and may be displaced or absent Clinical, x-ray exam annually until successor
(coronal, middle, or apical third)
erupts
Root fracture
If crown firm - monitor only
Clinical exam at 1 week
Coronal fragment may be firm Take one x-ray
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
Tooth-bearing segment is mobile Sutures if needed
Take one x-ray - determine if teeth are in
Alveolar fracture and may be displaced. Step in Clinical exam at 1 week
line of alveolar fracture
arch form may be noted 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

Patient
Gentle toothbrushing after each meal, Clorhexidine swabbed on gingival twice daily, if splinted
instructions
Follow-up as indicated based on type of injury
235
236
237
Primary Dentition: Luxated or Avulsed Teeth

Diagnostic Findings
Injury Treatment / Follow-up
Percussion sensitive Observation
Take one x-ray
Concussion No mobility or sulcular Clinical exam at 1 week
No abnormalities expected
bleeding Clinical and x-ray exam at 6-8 weeks
Tooth mobile but not Take one x-ray

If no occlusal interference - observation
Subluxation displaced No abnormalities expected
Clinical and x-ray exam at 6-8 weeks
Sulcular bleeding Increased PDL space may be noted
Treatment depends on degree of

Tooth displaced laterally, Take one x-ray displacement/occlusal interference: Observation,
Lateral luxation usually in a palatal/lingual May see increased periodontal space at apex extraction
direction of tooth Clinical exam at 2-3 wks
Clinical, xray exam at 6-8 wks, 1 year
Observation for re-eruption

Clinical exam at 1 week,
Take one or two x-ray{s}
Tooth may not be visible. Clinical, xray exam at 3-4 wks
If displaced toward labial bone, tooth appears
Check orientation of crown Clinical exam at 6-8 wks
Intrusion shorter and more opaque
Check for apex through Clinical, xray exam at 6 months, 1 year, then
If displaced toward permanent successor,
labial bone annually until successor erupts
tooth appears longer
Extraction
x-ray annually until successor erupts
Do not replant. Suture if needed

Clinical exam at 1 week
Avulsion Tooth out of socket Take one x-ray - confirm avulsion
Clinical, x-ray exam at 6 months, 1 year,
then annually until successor erupts
Soft diet for 10 - 14 days

Patient
Gentle toothbrushing after each meal, Clorhexidine BID if splinted
instructions
238

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
239

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
240
Primary!Dentition!Trauma
Primary!Tooth!Complications:!
Pulp!Canal!Obliteration
241
242
Intrusion!Injury

Intrusion Injury
Considerations
• 80% of intruded teeth pushed labially

• Majority re-erupt and survive >36mos
• Common findings
• Role of systemic antibiotics
243
Intrusion!Injury!Sequence
Baseline Baseline
4 weeks 12 weeks

Luxated or Avulsed Teeth: Avulsion
244
Age 1 Age 3.5

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
245
Complications!in!Permanent!Successors
What are the possible consequences

to permanent successors?
Complications!in!Permanent!Successors:!
Discoloration/Hypoplasia
246
3.3 yrs 4.5 yrs
247
7 yrs
8.5 yrs
8 yrs of age 8.5 yrs
9 yrs 10 yrs 12 yrs
248
249
250

Parental Discussion Topics
The parents want to know what
will happen as a result of the
trauma.
How do you respond?
251
Permanent Dentition Trauma
Permanent Tooth Trauma

• Age of patient
• Medical status
• Cooperation
• Type of trauma
• Dental development
• Parental desires/concerns
252

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

Treatment
Refer to tables in appendicies: p. 34-

38
• www.iadt-dentaltrauma.org Guidelines for
the management of traumatic dental injuries
Flores, Guidelines I. 2007
Flores, Guidelines II. 2007
253
Permanent Dentition: Tooth and/or Alveolar Fractures

Diagnostic Findings
Injury Treatment / Followup
Uncomplicated Enamel fracture Take x-rays from 3 angulations Smooth with sandpaper disk or bond with
Crown fracture Radiograph of lip or cheek lacerations composite resin as needed
Evaluate pulp chamber, stage of root development
Enamel + dentin fracture Baseline pulp test Rebond fractured segment if intact.
Bandage restoration with glass ionomer or
composite
Clinical,xray exam at 6-8 weeks, 1 year
Complicated Enamel + dentin fracture with pulp Take x-rays from 3 angulations Partial pulpotomy with Ca(OH)2
Crown fracture exposure Radiograph of lip or cheek lacerations Restore with composite
Evaluate pulp chamber, stage of root development 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 Take x-rays from more than one angle to detect Reposition / splint coronal fragment as needed
Pulp may or may not be exposed fracture Longterm: Subgingival fracture site may require
Coronal fragment mobile Pulp test usually positive crown lengthening and/or orthodontic extrusion
Minimal to moderate displacement 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 Take xray from more than one angle Reposition coronal segment, splint 4 weeks with
mobile/displaced Consider occlusal xray for fractures in cervical 1/3 flexible splint; If fracture is in cervical 1/3 splint
Pulp test is usually negative initially – monitor over longer, up to 4 months
Transient crown discoloration time at clinical exams 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 Take x-ray; panograph is helpful in determining Reposition segment and splint 4 weeks.
and may be displaced. fracture lines Sutures if needed
Step in arch form noted Pulp test may or may not be positive 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

Crown Fracture
Crown fracture with/without pulp
exposure
• Injury to enamel, dentin, pulp
• Factors affecting pulpal healing

• Management
254

Crown Fracture:
Uncomplicated Enamel & Dentin Fracture
Crown fracture with/without pulp

exposure – what are the likely
outcomes?
255
256

Crown Fracture:
Complicated Enamel & Dentin Fracture
Crown fracture with pulp exposure

• Within hours and small exposure
• Longer interval and larger exposures
257
258
259
260

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
261
262

To Splint or not to Splint…
• Non-displaced teeth with no mobility
• Fracture in middle third – mobile fragment
• Fracture in cervical third
Antibiotics?
263

Types of healing
• Hard tissue: dentin & cementum form
• Connective tissue: cells from pdl form
• Non-healing: necrosis in coronal

segment

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
264

• Calcium hydroxide as pulp canal
medicament
• Apexification
• Disinfection of root canals
• Weakens dentin walls

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
265

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

Fracture resistance: MTA vs.
Ca(OH)2
Hatibovic-Kofman et al, 2008
266

Luxation Injuries: Concussion
Concussion
• Sensitive to percussion
• No mobility
• No sulcular bleeding
267

Luxation Injuries: Subluxation
• Subluxation
• Sensitive to percussion
• Mobile
• No displacement
268
Permanent!Tooth!Trauma
Luxation Injuries:!Subluxation
269
Injury 6 mos 1yr 9 mos
As time goes by …
3.5 yrs 4.5 yrs
270

Luxation Injuries: Lateral Luxation
• Lateral luxation - displacement in a
direction other than axial
• Pulp supply is ruptured
• PDL becomes compressed
• Sequelae
271
272
Age 8 yrs. Age 20 years

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
273

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
274

Avulsion
Factors affecting Prognosis
• Extraoral time
• Loss of PDL vitality
• Storage media
• Handling of tooth before
replantation
• Patient immune response
275

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

Avulsion
Contraindications to replantation
• Severe cardiac disease
• Seizure disorder
• Severe mental disability
• Compromised healing
• Poor alveolar support
276

Avulsion
Tooth cannot be found
• Verify avulsion
• Assess labial plate of bone
277
After bone grafting

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
278

Avulsion
Replantation Basics
• Obtain informed consent
• Provide local anesthesia
• Curette socket, remove clot
• Replace tooth
• Place flexible splint

Avulsion
Replantation Basics
• Systemic antibiotics
• > 12 years: Doxycycline
• < 12 years: Penicillin V
• Post-op instructions
279

Avulsion
How does root development affect
pulp therapy in avulsed teeth?
• Closed apex
• Open apex
280
1 year 2 years 3 years
6 months
4 years 5 years
281
3 years

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
282

Avulsion
Healing mechanism in avulsion
• 4 days: pulp revascularization begins

• 1 week: gingival attachment re-established
• 2 weeks: PDL at original state

Avulsion
How can PDL and Pulp Problems

affect outcome for avulsed teeth?
Replacement vs. Inflammatory Resorption
283

Avulsion
Closed Apex Outcomes

• Favorable
• Unfavorable

Avulsion
Open Apex Outcomes

• Favorable
• Unfavorable
284

Avulsion
Inflammatory Resorption
• Begins as early as 2-3 weeks
• Radiolucencies: bone and/or cementum
• Endodontic treatment necessary
• Enamel matrix protein derivative

Avulsion
Replacement Resorption
• Begins within 2 weeks
• Tooth gradually replaced by bone
• Transient or permanent
• Enamel protein matrix derivative
(Emdogain) not beneficial
285
8 yrs post avulsion (age 15)

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
286

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
287
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
288
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
289
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
290
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
291
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
292
Child Abuse
Sexual abuse
• Trauma to mouth
• Various infections
Child Abuse
Neglect
Emotional or verbal
293
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
294
295
Child Abuse
Behavioral Indicators
• Child
• Adult
296
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
297
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
298
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:
299
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:
300
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.
301
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.
302
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
303
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.
304

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309
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
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 Patient Age at MST

Placement
Holland 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
• Wide range of failure rates reported (0-

58%)
• 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
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
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
• 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
• 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
• 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
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
• 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 Resin Polyacid modified Resin

cements – modified resin composites - composites
evolved from glass ionomers – “compomers”
search for “glass ionomer
replacement hybrids”
for
silicate cement
319
• 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 w/w% Filler Characteristics

(microns) Filler Type
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 nanosilica, highly esthetic

75-100 nm clusters zrconium/silica
320
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
• 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
Gap formation Layering technique
From Ruiz & Mitra 2006
322
• 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
• 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

for
silicate cement
324
• Type I: luting cements

• Type II: restorative
materials
• II.1 esthetic
• II.2 reinforced
• Type III: lining

materials and fissure
sealants
Sealant Cavity liner

Luting cement
Dentinal adhesive
Crown
cementation Sandwich technique
Orthodontic band or dentin
cementation “replacement”
Orthodontic Tooth restoration,
bracket adhesive including ITR (ART)
325
• 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
• 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
• 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
Materials Continuum

for
silicate cement
• 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
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
• 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

for
silicate cement
331
• 80% GIC + 20% LC

composite resin
• Powder similar to
conventional GIC
Fuji II LC
• Liquid is HEMA, water,
and a polyacid;
significant acid-base
reaction
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
• Strength and solubility

intermediate to GIC and
composites
• Less prone to hydration
problems than GIC
• F release equal to GIC; Vitrebond Plus
can be recharged
• Ease of use intermediate
to GIC and composites;
requires mixing
• Esthetics intermediate to
GIC and composites
• Bond to tooth structure >
GIC
• Less microleakage than
GIC
• Coefficient of thermal
expansion lower than GIC
333
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
• 15-60 sec etch with 37%

phosphoric acid
• Resin tag formation - 10-
75 "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
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
Courtesy of Dr. Jorge Perdigao
primers
336
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
• Sclerotic dentin denser in mineral content
• Reduces penetration of bonding agent
• Additional/extended etching on caries-

affected 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
• 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
339
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
• Self-etch systems modify

but do not remove the
smear layer
• May result in less post-
operative 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
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
• 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
• 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
• 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
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
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
Cast metal frameworks
Magnets were attached with cold cure resin

Some dental anatomy placed in maxillary posterior acrylic
Mandibular acrylic left as monoplane
348
349
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350
Pulp Therapy in Primary

and Young Permanent
Teeth

Histologic Components of Primary

Pulp
• Lymph vessels • Lymphocytes
• Blood vessels
• Odontoblasts
• Nerve tissue
• Collagenous fibers • Odonto-/osteoclasts
• Fibroblasts • Histologically
• Defense cells similar to young
• macrophages, permanent pulp –
neutrophils
cell rich, vascular
351
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
Assessment of Pain
Types of Pain Pulp Status
Spontaneous
Nocturnal Irreversible: Non-vital treatment
Constant
Thermal
Chemical Reversible: Vital treatment
Intermittent
Further Clinical Assessment

• Extent of lesion • Sensitivity to
• location, color percussion
• reliable in primary teeth
• Mobility
• Pulp exposure
• R/O root resorption
• hemorrhagic v necrotic
• Soft tissue swelling • Pulp testing
• electrical
• Lymphadenopathy
• thermal
• percussion
353
Reliability of Pulp Testing

Teeth: Primary Young Mature
permanent 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
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
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
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
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
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
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
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
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
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
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
Pulpotomy Contraindications
• History of unprovoked • Periapical or
pain (?) bifurcation
• Presence of fistula or radiolucency
swelling • Pathologic
• Evidence of necrotic resorption
pulp • Dystrophic
• Uncontrolled pulpal calcification
hemorrhage • 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
Categories of Medicaments
• Fixatives • Coagulants
• FMC, glutaraldehyde • epi, ferric sulfate, aluminum
• Mineralizing and/or chloride
bacteriostatic agents • Antibiotics/Antimicrobials
• Ca(OH)2 • erythromycin, others
• Palliative sealers • Tissue healing agents
• ZOE • collagen, BMP
• Obturators • Glucocorticoids
• mineral trioxide • corticosteroids
aggregate
Medicament Combinations
• Vitapex
• iodoform, Ca(OH)2
• Maisto’s paste
• iodoform, parachlorophenol,
camphor/menthol
• Ledermix
• dimethylchlorotetracycline
• triamcinolone
366
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
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
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
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
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
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
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
Electrosurgical Pulpotomy
Advantages Disadvantages
quick heat leads to tissue destruction
self-limiting persistent inflammation
hemostasis energy cannot be isolated to surface
good visibility root resorption
no systemic effect pulp inflammation
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
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
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 non-
significant 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
Agents for Permanent Tooth

Pulpotomy
• Ca(OH)2 most widely used
• Formocresol
• limited circumstances
• short-term preservation of permanent molar
• Glutaraldehyde
• 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
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
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
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
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
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
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
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
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
• Assumption: Teeth
• apical portion of pulp may still be vital
• Goal:
• encourage this vital tissue to migrate coronally
• Procedure:
• disinfect root canal
• place triple antibiotic paste (ciprofloxacin,
metronidazole, cefaclor)
385
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
Teeth
386
Teeth
Expect continued root lengthening and thickening

Pulp responsive to cold stimulus
387
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388
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
Developmental
variations of normal
oral structures
Epstein’s Pearls
&Epithelial
inclusion cyst
&Palatal midline
390
Bohn’s Nodules
&Buccal and
lingual aspect
of alveolus
&Ectopic
mucous glands
Dental Lamina Cysts
&Crest of the
alveolus
&Remnants of
dental lamina
391
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
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
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 tooth-
bearing 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
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
Bifid Uvula
&Minor
expression of
cleft palate
&Must r/o sub
mucous cleft
&May require
surgical
correction
Macroglossia
396
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
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
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
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
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
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
402
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)
403
Neurofibroma
& Rare in childhood

& Tongue and buccal
mucosa commonly
affected
& Maybe solitary or
multiple
(neurofibromatosis)
Neurofibromatosis
& A.D. ( ~50%
spontaneous
mutations)
& Peripheral form most
common ~90%
& ~70% have oral
involvement
& Café-au-lait spots,
subcutaneous
neurofibromas, Lisch
nodules
404
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
Granular-cell Tumor
& Uncommon benign
lesion
& Tongue most
common site (25%)
& Typically solitary,
asymptomatic, well-
defined, sessile
lesion
Tongue Foreign Body
Fractured palatal
cusp
406
Exophytic Lesions in BMT
Diffuse Swelling of the Tongue
&Congenital
&Inflammatory
&Traumatic
&Others
407
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
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
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
Dental conditions associated with Down

syndrome
& Relative & Increased

macroglossia periodontal disease
& Microdontia & Delayed eruption
& Oligodontia and over-retained
& Class III teeth
malocclusion & Atypical root
& Open-mouth posture morphology
& Fissured tongue & Abnormal palate
& Decreased caries
rate (historical) & Enamel hypoplasia
Hypothyroidism (Cretinism)
& Short stature
& Delayed eruption
& Enamel hypoplasia
& Generalized edema
& Tx: replacement
therapy
411
Hypothyroidism (Cretinism)
& Short stature
& 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
Cystic Hygroma
& Large diffuse
lymphangioma
& Extends from tongue
into neck
& May cause
dysphagia or
respiratory
embarrassment
& Tx: plastic surgery
Cystic Hygroma
413
Cystic Hygroma
Cystic Hygroma
414
Cystic Hygroma
Inflammatory Causes of Diffuse

Tongue Swelling
& Infection
& Allergic
reaction/irritation
& Ludwig’s angina (rare
in children)
415
Multiple Endocrine Neoplasm,

type 2B
&Oral mucosal
neuromas
&Medullary cell
carcinoma of the
thyroid
&Pheochromocytoma
Multiple Endocrine Neoplasm
416
Angioedema
& Allergic form maybe
precipitated by drugs,
foods, etc.
& Hereditary form A.D.
& Most are idiopathic
& Tx:
& Allergic form-
antihistamines
& 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
Indications for Tongue Reduction

&Airway difficulty
&Speech difficulty
&Dentoalveolar protrusion
&Esthetics
&Drooling
&Recurrence of openbite/bimaxillary
protrusion/spacing
Surgical tongue reduction
418
Common Causes of a Sore

Tongue
&Ulceration
&Geographic
tongue
&Median rhomboid
glossitis
&Foliate papillitis

Tongue
&Ulceration
&Geographic
tongue
&Median rhomboid
glossitis
&Foliate papillitis
419

Tongue
&Ulceration
&Geographic
tongue
&Median rhomboid
glossitis
&Foliate papillitis
Glossitis
& Generalized
erythema and
depapillation
& Anemia
& Candidiasis
& Vitamin B deficiency
& Radiotherapy
& Depression
& Diabetes
& Hypothyroidism
420
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
Sublingual Dermoid Cyst
422
Cheeks/Buccal Mucosa
423
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
Candidiasis (Erythematous form)
Candidiasis
(hyperplastic form)
425
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
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
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 (30-
40%) Systemic form
& Tx: steroids
Lupus Erythematous
428
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
Burns (thermal, chemical)

& Common
& White appearance
due to necrotic
tissue
& Associated with a
number of
chemicals, i.e., ASA,
formocresol,
phosphoric acid, Chemical Burn
phenol, etc.
Thermal Burn
“Pizza Palate”
430
Lip Lesions
Causes of Angular Stomatitis
& Candidiasis
& Common finding in
HIV infection
& Staphylococcal,
streptococcal, or
mixed infections
& Nutritional
deficiencies
& Crohn’s disease
& Anemia
431
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
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
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
Herpes simplex
&Herpes labialis
& Reactivation of
HSV
& Recurrent
& Antiviral agents of
limited value
Herpes labialis
1 week f/u
435
Penciclovir (Denavir)
Denavir Promo
436
Burns
& Maybe electric, thermal,

chemical
& Treatment directed at
preventing contraction
of orafice
Varicella/Zoster
& Varicella zoster virus & Infectious 24 hrs.
(chicken pox) before to 6-7 days
after vesicles appear
& Crops of pruritic
vesicles on skin and & Incubation period
may last up to 20
mucous membranes days
& Vesicles may & Resolves in 7-10
precede fever days
& Begins on trunk and & Tx: palliative and
spreads to supportive
limbs/face
437
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
Erythema Multiforme (Stevens-

Johnson 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
Dystrophic EB-dominant form
Dystrophic EB- dominant form
440
Dystrophic EB-recessive form
Impetigo
&Most commonly
caused by:
& staphylococcus
aureus
& beta hemolytic
strep
&Tx:
& Localized: topical
antibiotics
& Widespread:
systemic
antibiotics
441
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
& Melkersson-
Rosenthal syndrome
& Lymphangioma
& Hemangioma
442
Hemangioma
7 months 5 years 12 years
Vascular malformation
S/p laser surgery
443
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
& Psychogenic
& Drugs
444
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
Capillary Malformation:Port Wine

Stain
Capillary Malformation:Port Wine

Stain
446
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
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
Congenital Epulis
Congenital Epulis
449
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
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
452
453
Dwarfism
454
Seven major cateogories of

causes of short stature
1. Genetic
2. Constitutional delay
3. Chronic disease
4. Chromosomal/syndromic
5. Endocrine
6. Psychosocial
7. 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
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 & Infiltrative diseases

& Pituitary & Granulomatous
diseases
& Parasellar
& Infection
& Suprasellar
(hypothalamic) & Miscellaneous
& Radiation
& Pituitary apoplexy
456
Mucopolysaccharidoses
Nutritional
457
Chrondroectodermal Dysplasia
(Ellis van Crevald syndrome)
&Dwarfism
&Polydactaly
&Ectodermal
dysplasia(hidrotic)
affecting nails and
teeth
&Multiple frenae
&Cardiac defects:
50%
Chondroectodermal Dysplasia
Nail dystrophy/ polydactaly

Spade-shaped hand
458
Chondroectodermal Dysplasia
Hallerman-Streiff syndrome
(Oculo-mandibulo-dyscephaly)
& Dyscephaly
& Hypotrichosis
& Microphthalmia
& Cataracts
& Beaked nose
& Micrognathia
& Short stature
& May have
supernumerary
teeth/natal teeth
459
Syndromes Characterized by
Senile-like Appearance
&Progeria
&Werner syndrome
&Cockayne
syndrome
&Rothmund-
Thomson
syndrome
Hypothyroidism
& Large posterior
fontanel
& Macroglossia
& Hypothermia
& Lethargy
& Hypotonia
& Bradycardia
& Delayed growth and
skeletal maturation
460
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 IB-
dentinogenesis 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
Osteogenesis Imperfecta
Osteogenesis
Imperfecta
Blue Sclera
462
Osteogenesis
Imperfecta
Dentinogenesis Imperfecta
Self-Mutilation
&Common in
children with
MR/psychological
problems/autism
&Usually due to
repeated trauma
463
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
Congenital Indifference to Pain
Lesch Nyhan syndrome
& X-linked recessive

& MR
& Spastic CP
& Choreoathetosis
& Bizarre self-mutilating
behavior
& Absence of hypoxanthine-
guanine-
phosphoribosyltransferase
465
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
Systemic Factors influencing

Gingivitis - Endocrine System
& Puberty-associated, menstrual cycle-
associated, 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
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
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
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
LAP Diagnosis
& Medical history
& Familial pattern
& Ethinicity
& DNA probing
LAP Diagnosis
& Medical history
& Familial pattern
& Ethinicity
& DNA probing
471
LAP Diagnosis
& Medical history
& Familial pattern
& Ethinicity
& DNA probing
Treatment: Surgical and non-

surgical 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
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 non-
motile, facultative, anaerobic gram (-) rods
& Suppressed neutrophil chemotaxis
473
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
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
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
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
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
Infectious
& Dental abscess
& Osteomyelitis
& Periodontitis
Miscellaneous
& Acrodynia
& Odontodysplasia
& Vitamin C deficiency
& Leukocyte adhesion deficiency-1
479
Differential Diagnosis
& Hypophosphatasia
& TNSALP
& Urinary phosphoethanolamine
& Papillon-LeFévre syndrome
& Examine palmar/plantar surfaces for
hyperkeratosis
& Periodontitis
& DNA probing
Congenital Causes of
& Hereditary hemorrhagic
telangiectasia
& AD
& Mucosal and
cutaneous
telangiectases
& May result in repeated
bleeding episodes
& Sturge Weber
syndrome
480
Hereditary Hemorrhagic
Telangiectasia
Palatal telangiectases
Acquired Causes of
& Trauma
& Physical, chemical,
radiation, thermal
& Drugs:
chlorhexidene,
cinnamonaldehyde
& Infectious:
candidiasis
& Desquamative
gingivitis
& Leukemia
481
Causes of Gingival Bleeding

& Localized disease & Systemic disease
& Periodontal disease & Clotting defects
& Chronic gingivitis & Hepatobiliary disease
& Chronic periodontitis & Hemophilias
& Von Willebrand’s disease
& ANUG
& Vitamin K deficiency
& HIV gingivitis
& Lymphoproliferative
& HIV periodontitis disorders
& ITP
& Hereditary hemorrhagic
telangiectasia
& Ehlers-Danlos syndrome
& Scurvy
Causes of Gingival Bleeding

(cont.)
&Drugs
& Anticoagulants
& NSAID
&ASA
&Non-ASA
& Cytotoxics
& Sodium valproate
482
Generalized Gingival
Enlargement: Congenital
&Gingival
fibromatosis
&Mucopoly-
saccharidoses
Generalized Gingival
Enlargement: Acquired
& AML
& Aplastic anemia
& Drugs
& Phenytoin
& Cyclosporin
& Calcium-channel
blockers
& Sodium valproate
(rare)
& Tranexamic acid (rare)
& Scurvy
483
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
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 Pyogenic granuloma
& Neoplasms Peripheral Giant Cell
Epulis
485
Peripheral Ossifying Fibroma
Initial presentation Relapse 2y later
Fibro-osseous lesions
486
Fibro-osseous lesions
Facial Swelling/Enlargement-Hard
Tissue: Congenital
&Albright’s
syndrome
&Cherubism
&Hemihypertrophy
487
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
Cherubism
& A.D.
& Bilateral fullness of
cheeks
& Hypertelorism
& Irregularly spaced 1º
dentition
& Giant cell histology
& X-ray: multilocular
radioluncencies
Cherubism
Multilocular Giant cell

radioluncencies histology
489
Facial Swelling/Enlargement-Hard tissue :

Acquired/Inherited
&Fibrous
Dysplasia
&Sickle cell
anemia
&Thalassemia
&Neoplasms Monostotic Fibrous Dysplasia
Sickle Cell Anemia
Hair on end
490
Neoplasm: Neuroblastoma
“racoon eyes”
Periorbital ecchymosis
Obstruction of palpebral
vessels
Facial Swelling: Inflammatory
&Oral
infections
&Cutaneous
infections
&Insect bites
Poison Ivy
491
Facial Swelling: Inflammatory
Odontogenic Infection
Facial Swelling: Traumatic
&P/O
edema/hematoma
&Traumatic
edema/hematoma
&Surgical emphysema
492
Facial Swelling: Immunologic
&Allergic
angioedema
&HANE
Facial Swelling: Immunologic
&Allergic
angioedema
&HANE
493
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
& Vascular malformations
& Vascular tumors
& Melkersson-Rosenthal syndrome
& Crohn’s disease
494
Nasolabial Cyst
Nasolabial Cyst
495
Facial Swelling: Major Salivary

Glands: Inflammatory
& Mumps
& Recurrent parotitis
& Sjögren’s syndrome
& Ascending
sialadenitis
& Recurrent
sialadenitis
& Sarcoidosis
& Actinomycosis

Glands: Neoplasm
Pleomorphic adenoma
496

Glands: Others
& Duct obstruction

& Sialosis
& Parotid
& Submandibular
& Mikulicz disease
& Amyloidosis
& HIV disease

Glands: Others
& Duct obstruction

& Sialosis
& Parotid
& Submandibular
& Mikulicz disease
& Amyloidosis
& HIV disease
497

Glands: Others
& Duct obstruction

& Sialosis
& Parotid
& Submandibular
& Mikulicz disease
& Amyloidosis
& HIV disease

Glands: Others
& Duct obstruction

& Sialosis
& Parotid
& Submandibular
& Mikulicz disease
& Amyloidosis
& HIV disease
498
HIV Disease
&Bilateral
parotid
enlargement
Facial Swelling: Major Salivary Glands:

Drug associated
& Chlorhexidene
& Phenylbutazone
& Iodine compounds
& Thiouracil
& Catecholamines
& Sulphonamides
& Phenothiazines
& Methyldopa
499
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
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
Recurrent Aphthous Ulcers

&Etiology unknown & Minor: most common
& Shallow, round ulcer
&Predisposing & Erythematous halo
factors, I.e. stress & 7-10 day duration
& Major: less common
&Involves & Deep, large ulcers
“unbound” & 3-6 week duration
mucosa & Herpetiform: rare
& Clusters of small ulcers
&Tx: palliative & 1-2 week duration
Apthous Ulcers: treatment

modalities
502
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
Systemic Disease: Cutaneous

& Erosive lichen planus
& Pemphigus vulgaris
& Mucous
membrane/bullous
pemphigoid
& 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
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
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
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
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.)
& Atypical mycobacterium & Histoplasmosis

infection & Coccididioidomycosis
& Syphilis & Blastomycosis
& Aspergillosis & HIV
& Cryptocococcosis & Gram-negative infection
& Leishmaniasis
& Tularemia
& Lepromatous leprosy
& Paracoccidiodomycosis
508
Systemic Disease: Drugs
&Cytotoxics
&Methotrexate
&5-FU
Systemic Disease: Others
& Wegener’s
granulomatosis
& Midline lethal
granuloma
& Histiocytosis
& Noma
Noma
509
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
Generalized Pigmentation
Vitiligo
Racial
&No direct
correlation
between skin
color and oral
pigmentation
&Typically seen
only on gingiva
511
Food/Drugs
&Carotenemia
&Antimalerial
drugs
&Minocycline
&Doxorubicin
Carotenemia
Food/Drugs
&Carotenemia
&Antimalerial
drugs
&Minocycline
&Doxorubicin
Minocycline
512
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
Localized Pigmentation
& Ecchymoses & Neurofibromatosis
& Ephelis & Neuroectodermal
& Melanoma tumor
& Melanoacanthoma & Tattoos
& Melanotic macule & Epithelioid
& Nevus angiomatosis
& Peutz-Jeghers & Smoker’s melanosis
syndrome & Acanthosis nigricans
& Kaposi’s sarcoma
Localized Pigmentation
& Ecchymoses & Neurofibromatosis
& Ephelis & Neuroectodermal
& Melanoma tumor
& Melanoacanthoma & Tattoos
& Melanotic macule & Epithelioid
& Nevus angiomatosis
& Peutz-Jeghers & Smoker’s melanosis
syndrome & Acanthosis nigricans
514
Peutz-Jeghers Syndrome
&A.D.
&Perioral and intraoral pigmentation
&Intestinal polyposis
&Tx: intestinal polyps may
occasionally require surgical
intervention
Peutz-Jeghers Syndrome
515
Soft Tissue Neck Mass/Swelling
Cervical Lymph Nodes:

Inflammatory
&Lymphadenitis
&Glandular fever syndromes
&Mycotic infections
&Other infections
516
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
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
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
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
Cleft Palate
Pierre-Robin Sequence
&Glossoptosis
&Micrognathia
&Cleft palate
&15-25% cardiac
defect
521
Cleidocranial Dysplasia
& Brachycephaly & Clavicular defect
& Frontal and parietal & Delayed or failure of
bossing exfoliation of 1º teeth
& Depressed nasal bridge & Delayed eruption of 2º
& Delayed closure of teeth
sutures and fontanels
& Highly arched palate
& Wormian bones
often with submucous
& Supernumerary teeth
or complete cleft
& Roots lack layer of
cellular cementum
522
Wormian Multiple unerupted

bones 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
524
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
Orofaciodigital Syndrome
“Copper-beaten Skull”
&Craniosynostosis
& Apert’s
syndrome
& Crouzon’s
syndrome
& Pfeiffer’s
syndrome
526
Apert’s Syndrome
& Syndactaly
& Shallow orbits, ocular
hypertelorism
& Parrot nose
& 30% cleft palate
& Crowded dentition
& V-shaped maxilla
& Class III with openbite
Apert’s Syndrome
Syndactaly
527
Crouzon’s Syndrome
& Brachycephaly
& Maxillary hypoplasia
& Ocular hypertelorism
& Parrot nose
& Crowded dentition
& V-shaped maxillary
arch
& Exopthalamus
528
529
Palatal Swelling/Lump:
Developmental
&Unerupted tooth
&Torus palatinus
&Cysts
Inflammatory
&Abscess
&Cyst
&Papillary
hyperplasia
&Sarcoidosis
530
Neoplasm
& Minor salivary gland

tumor
& Fibroma
& Papilloma
& Neuroma
& Neurofibroma
Kaposi’s sarcoma
Halitosis
& Oral sepsis
& Food impaction
& Chronic
dental/periodontal
sepsis
& ANUG
& Dry socket
& Pericoronitis
& Xerostomia
& Oral ulceration
531
Halitosis: Nasopharyngeal
Disease
& Foreign body

& Sinusitis
& Tonsillitis
& Neoplasm
Halitosis: Nasopharyngeal
Disease
& Foreign body

& Sinusitis
& Tonsillitis
& Neoplasm
532
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
Radiographic Key
Concepts
See what’s under the surface…
Radiographic Description and

Interpetation
1. Shape
2. Size
3. Anatomic location
4. Degree of lucency or opacity
5. Recognizable structure(s)
6. Single or multiple
7. Unilocular or multilocular
8. Quality of border
9. Cortical involvement
10. Lamina dura
11. PDL
12. Root resorption
VCU School of Dentistry, Dept. of Oral Pathology
534
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
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
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
538
539
540
Odontogenic Keratocyst
& Most often found in
mandible
& Bone expansion
uncommon
& Pain, discharge, or
paresthesia uncommon
& Tx: “vigorous”
enucleation
& Recurrence not
uncommon
541
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
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
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
• 16yo M
• Incidental finding of
radiolucent lesion in
posterior mandible
• Healthy
545
546
547
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
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
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
550
Median Palatal Cyst
Unilocular when
small/multilocular when large
& Central giant cell granuloma
& Aneurysmal bone cyst
& Central hemangioma
& Odontogenic myxoma
& Cherubism
551
Central Giant Cell Granuloma

& Painless swelling
sometimes causing
displacement of
teeth
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
553
554
555
556
Aneurysmal bone cyst

& Eccentric ballooning of
mandible
& 50% associated with
pain
& Associated with
concurrent lesion
Aneurysmal bone cyst

& Eccentric ballooning of
mandible
pain
& Associated with
concurrent lesion
557
HS
6 yo female
558
559
Central hemangioma
& Vague margins
& Gingival bleeding, bruit,
pulsation
& Tooth mobility
& Potentially life
threatening
560
Odontogenic myxoma
& Faint radiopaque
striations
& Moderate recurrance
rate
A.L.
561
562
563
564
Cherubism
& Bilateral
& “Burns out” over time
565
A.B.
& Painless midface
swelling
& 4yo F
& Healthy
2005
2005
566
567
2005
2007
2005 2007
568
Mixed radiolucent-radiopaque
& 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
odontoma
569
Adenomatoid Odontogenic
Tumor
& 90% appear before 30 y
& 60% form in anterior
maxilla
unerupted tooth (canine)
& Radiographic: may
contain faint radiopaque
foci
Adenomatoid Odontogenic
Tumor
& 90% appear before 30 y
& 60% form in anterior
maxilla
unerupted tooth (canine)
& Radiographic: may
contain faint radiopaque
foci
570
Ameloblastic Fibro-odontoma
& Most often found in children
& Typically asymptomatic and discovered
radiographically
& Most frequently associated woth unerupted
tooth
571
572
Periapical or Central Location

& Central ossifying fibroma
& Juvenile ossifying fibroma
573
Central ossifying fibroma

& Maybe unilocular or multilocular
& Progresses from radiolucent to radiopaque
Juvenile ossifying fibroma

& Multilocular
& Maxilla>mandible
& Aggressive
574
DR 8yo male
575
576
577
Radiopaque
& Odontoma
& Periapical or central location
& Fibrous dysplasia
& Cementoblastoma
& Osteoblastoma
& Peripheral location
& Torus/exostosis
& Osteoma
578
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

location
Fibrous dysplasia
& Maybe multifocal
region
to radiopaque
with time

location
Fibrous dysplasia
& Maybe multifocal
region
to radiopaque
with time
580
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
582
583
584
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
Osteoblastoma
& 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
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
Gardner’s Syndrome
Inflammatory lesions
& Common & Drainage, sinus tract
& Tender or painful to formation
palpation & Cause is often apparent
& Rapid enlargement (days to & Mobile, non-vital tooth
weeks) & Systemic involvement
& Diffuse or localized occurs with advanced
enlargement infection
& Red, tender, swollen & Trismus, occasional
mucosa paresthesia
& Fluctuates in size & Regression with treatment
of source
588
Localized lesions
& Periapical location
& Radiopaque
& Focal sclerosing osteomyelitis
& Radiolucent
& Periapical abscess
& Periapical granuloma
& Periapical cyst
Focal sclerosing osteomyelitis

& Chronic pulpal disease
& Non-expansile
& Well-defined margins
589
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
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
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
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
593
Chronic osteomyelitis with

proliferative perostitis
Proliferative
& Chronic dental infection periostitis
& Diffuse, expansile
& Indistinct margins
& Mottled bone pattern
& “Onion skin”
appearance
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
Aggressive and Malignant

Lesions
& Uncommon or rare & Vital, mobile teeth
& Maybe tender or painful & Extrusion of teeth
& Moderate to rapid growth & Progressive increase in size
(days to weeks to years) & No apparent cause or
& Diffuse enlargement source
& May have multifocal & Systemic involvement
distribution common
& Mucosa red, ulcerated & Frequent
& Lymph nodes firm and fixed 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
Neuroectodermal tumor of
infancy
& Anterior maxilla
& Expansile
& May displace
developing teeth/tooth
buds
& Pigmented surface
& Recurrence moderate
to high
Desmoplastic fibroma of bone

& Maybe multilocular
& Expansile
& “Floating” toothbuds
& Soft tissue extension
& High recurrence rate
596
Localized histiocytosis
(eosinophilic granuloma)
& Maybe multifocal & “Floating” teeth
& Punched radiolucencies & Often soft tissue
& Usually non-expansile involvement
Central sarcomas of bone

& Body of mandible
& Paresthesia
& Unilocular or
multilocular
& Cortical perforation
597
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
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
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
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
602
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
Leukemia (AML)
& Widespread
involvement
& Occasional gingival
enlargement due to
leukemic infiltrates
& Loss of lamina dura
& Diffuse, poorly defined
radiolucency
& Occasional periosteal
bone formation
604
605
Differential Diagnosis
& Leukemic infiltrate

& Ewing’s Sarcoma
& Primary malignancy (NH Lymphoma)
& Langerhans Cell Histiocytosis (E.G.)
& Giant Cell Granuloma/Tumor
606
Metastic disease
& Poorly defined
radiolucency
& Soft tissue extention
common
& paresthesia
607
Metastic disease
& Poorly defined
radiolucency
& Soft tissue extention
common
& paresthesia
608

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Etiology, Epidemiology, and

Prevention of Dental Disease in
Children
Current Concepts and Recent Evidence
Dr. Steve Adair

Definition
Dental caries is a dietary carbohydrate-
modified 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
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 “Miller time”
considered responsible for
breakdown of tooth
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
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
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, non-
desquamating surface
• Window of infectivity relies on virgin
tooth surfaces for initial colonization
• Second window may open when
permanent dentition erupts
616
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
25% S mutans 75%
S mitis S sanguis
1 8 11 19 26 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
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
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
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
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
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
Etiology - Diet
! Hopewood House (Australia) 1947 - 52
! diets devoid of sugar and white flour
! extremely low dental caries prevalence
! Vipeholm (Sweden) 1945 – 52

! 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
Sucrose
• Glucose + fructose
metabolized by biofilm bacteria
fructan
glucan +
Glucan
From
• Water soluble sucrose only
• 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
Fructan
From fructose
only
• Produced extracellularly
• Water soluble
• May be used by MS as
energy source
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
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
Biofilm pH after Sucrose Ingestion
7.0 Stephan curve

Remineralization
6.0
pH
Demineralization
5.0
4.0
1 10 30 45 60
Minutes
Stephan Curves
6.5
Caries Resistant
6
Caries Susceptible
5.5
5
0 5 10 15 20 25 30
627
Other Dietary Factors
7.0
Frequency of ingestion
6.0
pH
5.0
4.0 Refined CHO ingestions
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
Protective Food Factors
similar to milk, fat flavonoids,

Ca, PO4, casein, salivary stimulation, CPP-ACP antibacterial actions
proteose peptones
gustatory stimulus, fat 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
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
Etiology – Host Factors

! Tooth factors
! quality of enamel
! presence/depth of pits and fissures
! hypoplasia
! fluoride exposure
! Saliva
! 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
Saliva
! Flow rate reduced by:
! medications (antihistamines, antiasthmatics,
antidepressants, others)
! disease (degenerative, metaplastic)
! dehydration
! radiation
! age
! Increased by:
! gustatory stimulants (sugar-free candy)
! masticatory stimulants (s-f chewing gum)
Caries Factors
Dietary intake
Oral flora – of
principally MS refined CHO
Caries
Host factors
632
The Caries Balance

Protective Factors
• Saliva flow and components
Pathological Factors • Fluoride - remineralization
Acid-producing bacteria • Antibacterials:-
• Frequent eating/drinking of chlorhexidine, xylitol, new?
fermentable carbohydrates
•Sub-normal saliva flow and
function
Caries No Caries
Courtesy of Dr. John Featherstone, UCSF
Modifying Effects
Stress
Genetics
Diet
Oral flora
Caries Race / ethnicity
Culture
General health Healthcare delivery system

Host factors
Behavior/education
Socioeconomic status
633
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
Epidemiology of Caries
• 1970s - present
• NIDR documented decline in caries
prevalence
Mean DMFT
Age 1963-70 1971-74 1979-80 1986-87
6-11 1.4 1.7 1.1 0.71

12-17 6.2 6.2 4.6 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
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

dmf/DMF
every year of life
Birth age
Caries is “steady-state” disease
636
The Caries Process
root surfaces
• Epidemiology
permanent
crowns
dmfs/
DMFS primary
Birth age
Expression is variable over time
Histopathology of Caries
• Demineralization - remineralization
dynamic process, constant,
not on/off
637
Zones of early lesion
surface (5-10% mineral loss)
body – 60% loss
translucent zone – 5-10% loss
normal enamel
White spot lesion
Radiographic Histologic
638
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
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)
• 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
• 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
Historical approach:
Diagnosis
Cavities No cavities
Treatment
Maintenance (“Recall”)
Health
641
Diagnosis
Caries+ Caries-
Cavity+ Cavity- Cavity+ Cavity-
Treat Caries
Treat Cavity
Maintenance
Health
Classification:
Findings Status Group
Caries+ Cavity+ Manifest disease
Caries+ Cavity- Premanifest disease
Caries- Cavity+ Postmanifest/arrested
Caries- Cavity- Inactive disease
642
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

Caries removal –
no local anesthesia
Lesions in
young patient

Caries removal –
no local anesthesia
Lesions in Lesions restored

young patient
644
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
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
Anticipatory Guidance
• Developmentally paced information

• Provides practical, developmentally-
appropriate 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
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
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 OHRQoL
o impact of the disease on the
family (Malden et al 2007)
649
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
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
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
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
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

• 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
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
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
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
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

• 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
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
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
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
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
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
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
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

60
(Data compiled from
% dentifrice retained
50 several studies)
40
30
20
10
2 4 7 10 13
Age
665
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
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
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
F Retention from F Mouthrinse
Age Volume of Rinse Mg F

(years) Rinse Time (s) Retained
3 5 mL 30 0.38
5 mL 60 0.41
4 5 mL 30 0.25
5 mL 60 0.35
5 7 mL 30 0.27
10 mL 60 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
Effectiveness of Self-Applied Gels

Application % DMFs
Community Preparation Frequency Reduction
Optimally APF 3x/week (total 225) 19%

fluoridated 3x/week (total 162) 15% (dfs)
Fluoride APF 5x/week (total 245) 75%

deficient NaF 5x/week (total 245) 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
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
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
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
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
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
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
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
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
Milgrom et al 6-Month Data
Log MS CFU/mL
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
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
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
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
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)
! broad spectrum topical iodophor
microbicide
! topical use reduces risk for ECC (Lopez
et al 1999)
! Mouthrinses containing essential
oils (Fine et al 2000; Zhang et al
2004)
! Cetylpyridinium chloride, triclosan,
sanguinaria extracts, hexetidine,
enzymes, metal ions, others
683
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
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
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
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
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
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
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
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
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

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699
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.
700
Special Needs
• May cause limitations in

performing daily self-
maintenance
• 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
Special Needs
Epidemiology
Causes of Disability
• Extreme pre-term birth (< 26 weeks)
• Congenital disorders
• Acquired disorders – accidents, diseases
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
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
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
Special Needs
Be prepared
!Communicate with caregiver
!Plan for emergencies
!Staff training
Special Needs
• Listen and learn
• Be flexible
• Think multi-disciplinary when

treatment planning
705
Special Needs
• 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
706
Special Needs
Your office can be the great equalizer
Special Needs
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
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
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
Asthma and the Airway
Asthma and the Airway
710
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
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
712
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
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
Asthma
Dentofacial findings
• High palate
• Increased anterior face height
• Increased overjet
• Greater incidence of posterior
crossbite
Asthma
• Evidence of steroid use

• Candidiasis
• Tongue enlargement
• Pharyngeal irritation
715
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
716
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
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
718

Incidence of Congenital Heart Disease is 8-10 per
1,000 live births

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
Anatomy of
the Heart

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
720
Anatomy!of!the!
Heart:!Increased!
Pulmonary!Flow
Example:!VSD

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
721
Decreased!
Pulmonary!Flow
Example:!Tetrology of!Fallot
1.!!Pulmonary!stenosis
2.!Right!ventricular!!!
hypertrophy
3.!Overarching!aorta
4.!VSD

Cardiac Defects
Obstructive defects
• Anatomic narrowing: coarctation of aorta,
aortic stenosis, pulmonic stenosis
• Valvular, subvalvular or supravalvular
• Appears as CHF over time
722

Cardiac Defects
• Primary pump failure

• Dilated cardiomyopathy
• Hypertrophic cardiomyopathy : can result

in syncope, sudden death

Cardiac Defects
Hypertrophic Cardiomyopathy
• Thickening of cardiac muscle
• Most often affects ventricular

septum
48
723

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

Management of Cardiac Conditions
• Valve stenosis: corrected by balloon
valvuloplasty
• Condition improves as leaflets of valve are separated
• Valve is able to open
724

Open heart surgery
• ASD/VSD repair – patch closure

• Shunts
• Valve replacement

Valve Replacement: Bioprosthetic valves
• Porcine, bovine, human

• Benefits
– No need for anticoagulants
– Good hemodynamics
725

Valve Replacement: Mechanical valves
• Doesn’t grow with patient

• Need anticoagulants
• Readily available, replacements available
Mechanical and Tissue Heart Valves
726

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

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

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

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
728

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%

Risk of Transient Bacteremia
Antibiotic Prophylaxis against Infective

Endocarditis: 2007 AHA Guidelines
A Change in Emphasis
729

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

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

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

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
732
Genetics and Congenital Disorders

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

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

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

Diagnosis of Genetic
Disorders
Genetic disorder may result from

spontaneous mutation with no familial
inheritance pattern
734

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

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

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

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

Modes of Inheritance
Multifactorial Inheritance: caused by

interaction between genetic and
environmental factors
• Cardiovascular disease
• Diabetes

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
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
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
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

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
Autosomal Dominant Transmission

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

Type 2
Dental Findings
• Primary and permanent dentition affected
• Teeth blue-gray/brown
• Teeth susceptible to severe wear
• Pulpal obliteration/dental abscesses
742
743

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

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
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

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

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

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

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

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

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

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

Cystic Fibrosis
Management of Digestive System

! Pancreatic enzyme supplements
! Vitamins - fat-soluble A,D,E,K
! Iron
! Increase caloric intake to 120-150%
RDA

Cystic Fibrosis
Oral Findings in CF
! Increased enamel defects
! Decreased caries
! Increased calculus
! Salivary pH elevated
! Gingivitis
! Potential for mouthbreathing/malocclusion
750

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
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
X-Linked Recessive Transmission

Dental/Craniofacial features
• Hypodontia to complete
anodontia of primary and
permanent teeth
• Dental agenesis results in

underdevelopment of alveolar
ridges
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
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
The Cascade of Coagulation
Fibrinolysis
How is the clot removed?
• Plasmin dissolves fibrin clot
• Plasmin is regulated by antiplasmin and

plasminogen activator inhibitor
755
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
Anticoagulant Medications
• Aspirin
• NSAID
• Warfarin (Coumadin) – inhibits
production of Vit K-dependent factors
756
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
Patients at Moderate Risk for Bleeding
• Family history
• Abnormal bruising
• Liver disease
• ASA/NSAID use
–Juvenile rheumatoid arthritis
757
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
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
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
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
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
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
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
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
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
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
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
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
Hemophilia
• X-linked recessive inheritance

• 1/3 cases – new mutations
• Hemophilia A – Factor VIII – most
common (85%)
• Hemophilia B – Factor IX (15%)
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%)
764
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
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
Hemophilia - Complications
• Arthropathy
• Bleeding into CNS or
airway
• HIV infection
• Hepatitis
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
Management of coagulation disorders
• Replacement with recombinant factors VIII and IX
Evolution of Factor VIII
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
Management of coagulation
disorders: Antifibinolytics
• Prevent clot dissolution

• Amicar: e-aminocaproic acid
• Cyklokapron: tranexamic acid
Aminocaproic Acid (Amicar)
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
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
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
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
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
Thrombotic Disorders
Management
Acute
• Heparin for several days, followed by
Warfarin for 3-6 months
Long-term
• Anti-coagulant therapy
771
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
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
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
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
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
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
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
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
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
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
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
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
Diabetes
• 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
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
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
Diabetes
Long-Term Complications
Caused by chronic hyperglycemia
• Retinopathy
• Nephropathy
• Neuropathy
• Peripheral vascular disease
• Hypertension
• Atherosclerosis
• Coronary artery disease
Gastro-Esophageal Reflux
Disease
786
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
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
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
790
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
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
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
Seizure Disorders
• 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
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
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
Seizure Disorders
• 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
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
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
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
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
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
Seizure Disorders
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
Medications
Dilantin-induced gingival hyperplasia
802
Seizure Disorders
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
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
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
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
ADHD
Common Behaviors and
Symptoms
Inattentive
ADHD
Symptoms
Hyperactivity
807
ADHD
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
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
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
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
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
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
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
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
ADHD
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
• Increased bruxism
• Involve parent in oral hygiene
• Remember that patient has ADHD
• Update history/progression of ADHD
since last dental visit
816
ADHD
• Look up medications – side effects
• Increased risk of dental trauma

• Poor coordination
• Impulsivity
Developmental Disabilities
817

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819

• Dental lamina
• Bud stage
• Cap stage
• Bell stage
• Advanced bell stage
• Hertwig’s epithelial root sheath
820
• 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
• 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
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
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
• Supplemental “normal”
morphology
Supplemental permanent?
Supplemental primary
incisor
825
•Rudimentary conical
tuberculate
molariform
826
827
828
• Down
• Apert
• Sturge-Weber
• Cleidocranial
• Orofaciodigital
dysplasia syndrome I
• Gardner • Hallerman-Strief
• Cleft lip and
• Crouzon
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
• Problems may arise from
• failure of induction
• abnormality of lamina
• insufficient space
• physical obstruction of lamina
830
Bilateral
831
Missing primaries
No (?) permanent teeth
• Ectodermal dysplasia • Incontinentia pigmenti

• Crouzon • Orofaciodigital
syndrome I
• Achondroplasia
• Hallerman-Strief
• Chondroectodermal
dysplasia • Reiger
• Seckel • Extremely talented/rich

former NBA players
Other ectodermal organs sometimes affected: salivary glands,

skin (sweat glands), hair, nails – not part of ectodermal dysplasia
832
• 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
Barrel-shaped lateral
Peg lateral on right, missing lateral on left
Microdont molars and 3 premolars
Relative generalized
834
• 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
Photos courtesy of
Dr. Lourdes Santos-Pinto
836
• 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
Single pulp canal; extra crown

(depends on clinical appearance)
• Twinning
• complete cleavage of single bud
• mirror image “supernumerary” tooth
838
• 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
• Concrescence
• fusion occurs after root formation complete
• etiology: trauma?, crowding?
• may occur pre- or post-eruption
840
• 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 part of root entire root
841
• 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
• 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
• 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
• 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
• Enamel defects
• amelogenesis type I
• amelogenesis type IV (discussed under
Maturation)
• Dentin defects
• dentinogenesis types I, II, III
846
• 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
848
849
• Heritable defect of predentin matrix

• normal mantle dentin
• amorphic and atubular circumpulpal dentin
• Incidence 1:8000
• Three types as defined by Shields
850
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
• 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
• 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
• Enamel hypoplasia
• systemic
• local
• Enamel pearls
854
• 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
• 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
• 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
• 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
• “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
860
• Vitamin D-resistant • Ehlers-Danlos

rickets syndrome
• Hypoparathyroidism • Epidermolysis
• Pseudohypopara- bullosa
thyroidism • Osteogenesis
• Albright’s hereditary imperfecta
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
Hypophosphatasia
Cleidocranial dysplasia
• Enamel hypomineralization - systemic and

local
• Hypomineralized permanent first molars
• Amelogenesis imperfecta type III
• Enamel fluorosis
862
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
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
• 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
• 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
• Amelogenesis imperfecta type II

• Amelogenesis imperfecta type IV
867
• Normal enamel thickness, but under-

mineralized, 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
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
• 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
• 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
• 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
• 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, user-
fabricated or user-modified trays
873
• 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
• 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
• 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
• 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
• 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
• 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 15-

18%
• 90% are true primary
teeth
• Etiology unknown
• Most are poorly formed
• Most may exfoliate early
(?)
879
880
• biting, drooling # decreased appetite

for solid foods
• gum rubbing, sucking
# mild (<102)
temperature elevation
• irritability,
wakefulness # no combination could
predict teething
• ear rubbing, facial # symptoms occurred in
rash <35% of infants
Macknin et al 2000
881
• 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
• 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
• Malfunction of eruption
mechanism causes non-
ankylosed 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
• 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
• Diseases of bone • Diseases of blood

• Diseases of • Physical and
periodontium chemical injuries
• Diseases of • Benign and
metabolism malignant tumors
• Deviations of growth • Dental anomalies
• Type of dentigerous cyst

• Either dentition
• No sex predilection
• Usually asymptomatic
• No treatment usually
required
• R/O hemangioma
886
• 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
Ectopic #3 and #30
Self-correction
Canine resorption
888
• 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
• 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
• Prevalence
• 44-97% in 6-year-olds
• Racial distribution
• higher in African Americans, Mediterranean
whites
• higher in females at younger ages (?)
• Normal development • Physical impediment to

• Excessive skeletal closure
growth • mesiodens, retained primary
teeth
• Pernicious habits • interruption of transseptal
• Deficiency of tooth fibers
material • Artificial
• spaced dentition, missing • RPE
teeth, xs ob and/or oj, others • Milwaukee brace
891
• Usually a combination of orthodontics and

bond-o-dontics
892
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893
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
Who benefits from GA for dental

treatment?
Indicated for the OR?
895
How can pediatric dentists interface

with hospitals?
GA must be seen as part of a

long-term comprehensive treatment
plan
896
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
Decision to Use General

Anesthesia
Extent of treatment needs

Anesthesia
The General Health of the Patient
898

Anesthesia
• Other options available for treatment

• Traditional behavior management
techniques
• Alternative Restorative Technique (ART)

Anesthesia
• Will the patient be able to cooperate for

the needed treatment without GA?
• Ask parent about previous experiences
899

Anesthesia
• What is the patient’s dental history?
• Radiographs?
• Previous treatment?
• Conditions of previous treatment

Anesthesia
• What are the parental expectations?
• What are the parental fears?
• Communication is essential
900

Anesthesia
Indications for GA
• Young age
• Uncooperative/combative behavior
• Developmental disability
• Medical disability
• Extensive dental disease

Anesthesia
Contraindications to GA
• Minimal dental disease
• Certain high-risk medical conditions
901

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
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)

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

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
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
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

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

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
907
• 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
Mallampati Classification

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
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
910
! Previous history of GA and any

complications
! Known difficult airway
! History of premature birth
! MH-susceptible or 1st degree relative with
MH-susceptibility
• 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
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
problems
Congenital syndromes/conditions
• Trisomy-21
• Pierre Robin
• Crouzon
• Treacher Collins
• History of repaired cleft palate
• JRA: decreased cervical mobility
912
Assess health and airway

status
problems
Cardiac conditions
• Congenital heart disease
• Document need for SBE prophylaxis
Neurologic conditions
• Seizure disorder
• V-P shunt present?
• CP
• Myopathy

• Possible causes of airway/anesthesia
problems
• Obesity
• GERD
• Obstructive Sleep Apnea
• Oncological disease
• History of organ transplantation
• Bleeding disorders
• History of pseudocholinesterase
deficiency
913
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
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
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
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 2-
3mg/kg with atropine and midazolam
• IV or Mask induction can begin when the
patient is sedated
917
Monitors
• EKG
• BP
• Pulse Oximeter
• Capnography Device
• Precordial Stethoscope
• Temperature measuring device
• Bispectral Index
Heating/cooling blankets should be available

Neuromuscular blocking agents
• Avoid succinylcholine – may cause fatal
hyperkalemia
• Vecuronium, rocuronium (intermediate-acting)
• Mivacurium (short-acting)
918
Induction of Anesthesia
!By mask
!Sevoflurane
!Intubation – nasotracheal vs.

endotracheal
Intubation
919
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
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
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
Ready to Go
Radiographs in the OR
923
Be
prepared
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
Ongoing Monitoring by Anesthesia
Complications
• Tube problems
• IV disconnected
• Bleeding
• Edema
• Arrythmia
925
• 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
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
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
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
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
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
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932
! Physical or mental
disabilities
! Functional limitations
! Need for enhanced
services
! Persistent dependency
! Expense: long-term care,
medications
! Parent stress higher
Questions to Ask
• Overall family functioning – caretakers
• Level of receptive/expressive function
• Educational situation
• Diet and oral hygiene
• Input for behavior management
933
Build confidence
Engage the child
Promote independence
Provide support and education
934
Assessing Patient Abilities
935
936
Cerebral Palsy
• 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
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
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
Cerebral Palsy
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
Medications
! Baclofen – muscle relaxant
! Botox
Consider chlorhexidine to aid in gingival health
Treatment needs
940
Autism Spectrum Disorders -

ASD
Autism Spectrum Disorders -

ASD
Autism:
Neurodevelopmental disorder in which
social interaction, language, behavior,
and cognitive function are severely
impaired
941
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%

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

Categories of Autism
• Classic autism – most severe
• Asperger Syndrome
• Pervasive Developmental Disorder, not

otherwise specified

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

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

Affected Areas of Brain
• Frontotemporal region
• Synapse dysregulation
• Amygdala and associated limbic regions
• Cerebellum
944

Deficits in Autism
• Ability to recognize and understand mental

states of self and others and use this to
predict behavior
• Executive function
• Central coherence

Effects of Autism on Family
• Increased stress
• Increase in negative outcomes for
siblings
• Loss of employment/income
• Lost leisure time
• Increased familial conflicts
945

Medical Management of ASD
Goals
• Minimize core features of ASD
• Minimize family stress
• Maximize functional independence and
quality of life

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

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

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

Side Effects of Medications for
Autism
Methylphenidate (Ritalin, Concerta) - stimulant

! Tachycardia
! Nervousness
! Anorexia
! Insomnia
! Xerostomia

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

Autism
Risperidone (Risperdal) - antipsychotic

! Potentiates CNS depressants
! Xerostomia
! Dysphagia
! Altered taste
! Stomatitis
! Gingivitis
! Tongue edema
! Facial edema

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

Caries, Oral Hygiene, Diet
• Caries rate: similar or less than healthy population
• Oral hygiene: difficulty accepting brushing/flossing
• Diet: food often used as reward

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

• 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

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
952
953

Oral Findings
• Evidence of erosion
• Evidence of bruxism
• Macrocephaly
• Possible bruising/abrasions on
head
954

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
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
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
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
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
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
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
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
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 Aphthous ulcer

Simplex
Hairy leukoplakia
963
Pseudomembranous Candidiasis
Angular chelitis
Linear gingival erythema
Parotid enlargement
964
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
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
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
• Affects 1 in 7,000 children each year

• ALL most common (24%)
• CNS Tumors (22%)
• 5 year survival > 75%
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
Absolute Neutrophil Count: ANC
• Indicates ability to fight infections
• ANC = WBC x (% seg + % bands)
• Neutropenia if ANC < 1,000
Dental Issues
• Immune system compromise

• Potential for oral infection
• Risk of bleeding
• Cranial or facial radiation
• Timing of chemotherapy
• Indwelling catheters
969
Dental Objectives
• Arrest dental disease

• Restore oral health
• Prevent or manage complications from
medical therapy
• Educate patient and caregiver
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
New Diagnosis of Malignancy
Dental Protocol
• Examination
• Radiographs as possible
• Prioritized treatment plan
• Complete all care prior to start of cancer therapy
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
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
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
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
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
Oral Complications
• Chemotherapy affects oral mucosa
• Salivary effects of chemotherapy/radiation
to head and neck
– Reduced flow
– Thickened
• Immunosuppression
– Overgrowth of opportunistic organisms
Oral Conditions w/ Cancer Therapy
• Candidiasis
– Nystatin rinse and
swallow qid
– Mycostatin pastilles qid
– Clotrimazole troches
– Fluconazole 5 mg/kg
974
• Xerostomia
– Stimulate flow with xylitol gum
– Replace secretions with ice water, ice chips,
carboxymethylcellulose solution
– Humidify sleeping area
– Avoid caffeine
– Lip lubricants
• Apthous ulcerations
– Triamcinolone in orabase (topical steroid)
• Herpetic ulcers
– Benadryl + Kaopectate elixir
– Viscous xylocaine 2%
– Acyclovir
• Traumatic ulcers
– Triamcinolone in orabase
975
Herpes Simplex
Aphthous ulceration
Stomatitis
• Identify cause to determine best
therapy
• PO or IV fluids
• Systemic analgesics
• Topical anesthetics
976
Bleeding
• Low platelets
• Poor liver function
• Decreased vascular integrity
• Poor oral hygiene
• Intraoral bleed may precede intracranial
bleeding – call for medical consult
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
Long-term Systemic Effects
• CNS, psychosocial
• Endocrine
• Reproductive
• Secondary neoplasms
• Cardiac dysfunction
• Hepatic dysfunction
• Cataracts
• Dental
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
Long Term Dental Effects
• Salivary secretions decreased
• Increased caries risk
• Dental malformations
• Risk of ORN questionable
Panograph Age 15
Panograph Age 8
979
Craniofacial effects
• Malocclusion
• Ectopic eruption
• Facial deformities, skeletal
hypoplasia
• Trismus
980
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
Solid Organ Transplantation

Demographics
1996-2005: Pediatric organ transplant
recipients increased by 23%
• <Age 1, increased 19%
• Ages 1-5, increased 18%
Transition from life-threatening disease
to a chronic condition
Forms of Solid Organ

Transplantation
• Renal
• Hepatic
• Cardiac
• Pulmonary
• Pancreatic
982

Common Features
• Patient is on waiting list

• Management of patient in debilitated
state
• Transplantation requires match of
blood type, HLA factors
• Lifelong immunosuppression therapy

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

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

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
Organ Transplantation
Immunosuppression Medications
Medications Post Organ Transplant
Name Mechanism Side Effects
Cyclosporine Inhibits production and release of Gingival hypertrophy

Neoral interleukin II Hypertension
Sandimmune Nephrotoxicity
Tremor
Tacrolimus Suppress T-cell humoral immunity Hypertension

Prograf Anemia
Pruritus
Nephrotoxicity
Azathioprine Antagonizes purine metabolism Thrombocytopenia
AZA Leukopenia
Imuran Anemia
Steroids Decreases inflammation Insomnia
Prednisone Decreases lymphatic system activity Nervousness
Solu-medrol Increased appetite
Immunosuppression medications
• Cyclosporine – use has decreased
• Tacrolimus (Prograf)
• Azathioprine (AZA)
• Steroids
• Calcium channel blockers (Nifedipine)
985
Cyclosporine-induced Gingival Overgrowth
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
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
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
• 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
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
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
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
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
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994
Outline
Child Development and Behavior
Management of Behavior
995

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

Temperament
Temperament is the “hard-wiring”
996
Child Development and

Behavior
Temperament
Temperament descriptions
• Easy
• Difficult
• Slow to warm up
• Mix

Temperament
Temperament can be a predictor

of behavioral concerns and
problems
997

Temperament
Development is also influenced

by temperament

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

Behavior
Temperament
Resiliency
• Positive demeanor and attitude leads to success
• Better predictor than biomedical or sociological

variables

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

Attachment
Levels of attachment
• Secure attachment
• Insecure attachment

Temperament-Attachment
Relationship
• Differences in behavior related to differences in

temperament
• Children with disruptive behavior usually display
attachment disorders and….. vice versa
1000

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

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

Theories of Child
Development
Behaviorism Theory: (Pavlov, Watson, Skinner)
• Environment-source of behavioral change
• Patterns of reinforcement
• Conditioning
• Stimulus-response
• Reward and punishment

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
1003

Application of Behavioral
Techniques
• Link between behavior and consequence

• Consistency
• Timing
• Rewards better than punishment

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

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
Abstract thought, can reason about

Formal operations > 12
ideas

Language Development
What is the role of language in dentistry?
• Interaction with child
• Communicative behavior guidance
• Detection problems in language development
1005

Behavior
How does language develop?

• Sound recognition
• Comprehension = understanding
• Production of sounds/words
• Accelerates rapidly during second year of life
• Early Language Milestone Scale

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

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

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

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

Dentistry
Temperament and behavior
• Approachability
• Tendency to withdraw
• Intense and active temperament

Effortful Control
What is “Effortful Control”?
• Modification of one’s own behavior

• Can be exercised by 12 months of age
• “Self-soother”
1009

Development of Self-
Regulation
Child factors
• Cognitive ability
• Temperament
Parental factors
• Approach to discipline
• Overprotection
• Limits for child
• Self-control
• Familial relationships

Fear/Anxiety in Children
Fear: a feeling of impending danger
1010

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

Age 5
• Decrease in fears
Ages 6-8
• Failure in school
• Ridicule
• Death of a loved one
37
1011

Phobias
Causes of Phobias
• Negative conditioning
• Instruction/information
• Observational conditioning

Dental Fear
What can we learn from medical models?
1012

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

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

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

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

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

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

Dealing with Dental Anxiety
Educate parents about predictable anxiety

• Dentist = Barbers= Santa Claus, etc.
• Things going in the mouth
• Sensory stimulation

Assessment of Child’s
Behavior
Facial image scale
Child!Fear!Survey!– reproduced!in!references
1016

Behavior
Assessing the child’s behavior in the

dental office: Objective observations
• Parental responses to questions on
health history

Behavior
Objective observations
• Parental interactions with child in office
• Negative child behaviors

• Internalizing
• Externalizing
• Uncooperative
1017

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

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
Behavior Management
Behavior Management involves an ongoing
interaction of three individuals:
Child – Parent – Dentist
Behavior Management
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
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
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
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
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 1989-
1999
• Parental presence in operatory is preferred by
majority of dentists
• Male dentists – perceive greater conflict
between parental and dentist expectations
Behavior Management
What about increased awareness

of mental health issues?
1023
Behavior Management
• Changing families
• Diverse, multicultural nature of societies
Behavior Management
What we do and how it is perceived……
• Care
• Comfort
• Unacceptability of certain behavior guidance

techniques
1024
Behavior Management Techniques

Basic Behavior Guidance
Communicative
• Distraction
• Tell-Show-Do
• Nonverbal
• Positive Reinforcement
• Voice Control
Parental Presence/Absence
Nitrous oxide/Oxygen analgesia

Advanced Behavior
Management
• Protective stabilization
• Sedation
• General Anesthesia
1025

Deferred Treatment
Risks/Benefits must be explained
ART (Interim Therapeutic

Restoration) and Regimented
application of fluoride varnish

Informed Consent
• Required for all but communicative
techniques
• Parent should be involved
• Consider the child’s ability to assent
• Components of Informed Consent
1026

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

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

Distraction
• Attention directed away from procedure
• Affects pain perception
• Requires cognitive ability
• Inexpensive, creative, effective
• Review of 26 studies on distraction

Contingent distraction:
“You can watch the videogame as long as you are
cooperative”
• Effective in three- to nine-year-olds

• Inexpensive
• Non-invasive
1028

Dental applications
• Gear distraction to child’s age
• Videogames/movies/handheld games
• Music with earphones
• Storytelling
• Animal game

Tell-Show-Do
• Can be used for any child
• Effective
1029
Tell-Show-Do

Nonverbal Communication
Positive Reinforcement
• Smile
• “Thumbs up” sign
• Pat on the back
1030
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

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
Behavior Management
Techniques
Voice Control
• Alternative methods of voice control:

Cooperation as a choice

• Parent must support recommendation
for presence/absence
• Parenting style may have a greater
influence than presence
• Parental preparation
1032
Behavior Management
Techniques
• Build parental trust and confidence over time
• Be flexible

Challenges to Basic Behavior

Guidance
• Developmental/physical disability
• Medical conditions
• Fear transmitted by parent/peers
• Previous negative medical/dental experiences
• Dysfunctional parenting
1033

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

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.

Basic Behavior Guidance - Nitrous Oxide
N2O/O2 is considered a form of basic

behavior management
Features
• Inhalational
• Mechanism
• Effects
1035

Advantages
• Rapid onset and recovery time
• Ease of titration
• Excellent safety record
• Can be used with communicative 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

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

Oxide
Medical consultation indicated

• Acute otitis media, recently placed tympanic
membrane grafts
• Severe asthma
• Sickle cell disease
• Bleomycin sulfate therapy (anti-neoplastic
antibiotic)
1037

Oxide
Pre-procedural considerations
• Review medical history
• Documentation
• Rationale
• Any pretreatment dietary instructions
• Informed Consent

Oxide
Equipment
• Nasal hood
• Failsafe mechanism
• Scavenging system
• Emergency cart
• Positive pressure oxygen delivery system
1038

Oxide
Personnel and training

• Appropriate license or permit
• Appropriate training and certification in CPR
• Office emergency protocol
1039

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

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
1040

Oxide
Documentation
• Percent nitrous oxide used
• Duration of procedure
• Post-treatment oxygenation
• Patient response to nitrous oxide
1041

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
1042

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
1043
1044
1045

Precautions
• Monitor tightness and duration
• Caution not to compromise circulation or
respiration
• Stabilization must be ceased in a hysterical
patient

How do parents view protective

stabilization?
Positive verbal presentation of papoose board

increases parental acceptance of technique
Kupietzky & Ram, 2005
1046

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

Documentation
• Consent
• Type of stabilization used and why
• Length of time stabilization used
• Effectiveness of stabilization
1047

Sedation
No dentist should provide sedation

unless formally trained and in
possession of a state permit consistent
with the type of sedation being
administered.

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
1048

Sedation
Indications
• Young patient, pre-cooperative
• Uncooperative patient
• Certain medical, mental, or physical disabilities
• Extensive treatment needs
• Protection of developing psyche

Indications for Sedation
Age
Behavior
Age
Special Health Care Needs
1049

Sedation
Factors influencing the sedation

outcome
• Age
• Cognitive
• Child’s behavior/temperament

Sedation
How does the patient’s development

affect sedation?
1050

Sedation
Remember….
Sedation is not a static level or state,

but is a continuum
1051

Sedation
Concept of rescue
• Recognize the levels of sedation
• Have skills to provide
cardiopulmonary support
• Have skills to rescue the patient

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
1052

Sedation
Levels of Sedation
Minimal Moderate Deep
• Decrease anxiety • Decrease anxiety • Eliminate anxiety

Goal
• Facilitate coping • Facilitate coping • Override coping skills
• Responds normally to verbal

• More calm • Uneasily aroused
commands
Patient • Responds to verbal commands • Non-interactive
• Interactive
Responsiveness • Aware of but less responsive • Unaware of and minimally
• Aware of but less responsive
to clinical stimuli responsive to clinical stimuli
to clinical stimuli
• Partial or complete loss

of protective reflexes
Physiologic • No loss of protective reflexes • No loss of protective reflexes
• Stable and minimally or
Changes • Normal vital signs • Normal vital signs
moderately below health
status norms
Personnel needed 2 2 3

Sedation
Monitors during sedation
• Dentist observation of patient
• Pulse oximeter
• Capnograph
• Pre-cordial stethoscope
• Blood pressure
• EKG
• Temperature
• Bispectral analysis
1053

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
1054

Sedation
Considerations for sedation
• Pre-operative instructions
• Responsible persons for
transport
• Monitoring
• Emergency preparedness
• Documentation

Sedation- Patient selection
Patient selection: ASA classification

• ASA I and II – generally appropriate
• ASA III and IV – generally
contraindicated
1055

Sedation – Patient
Assessment
• Medical History
• Current illness
• Chronic conditions
• Medications, including herbal
• Sleep apnea
• Physical Assessment
• Cardiovascular
• Respiratory
• Airway
• Behavioral 129

Sedation – Patient
Assessment
Patient Examination
• Document behavior and justification for
sedation
• Extraoral assessment
• Intraoral assessment
• Soft/hard tissues, airway
• Gag reflex
• Tonsil Size
1056
Mallampati Classification

Sedation – Patient Selection
Poor candidates for sedations
• ASA III and IV
• Sleep apnea
• Obesity - dose by age, not weight
• Abnormal airway
• Chronic medical conditions
1057

Sedation – Patient Selection
Why is the child airway more challenging?

• Different anatomy
• Relatively larger tongue/epiglottis
• Mandible less developed
• Increased airway resistance

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
1058

Sedation
Monitoring respiration
• Observation of chest movements
• Precordial stethoscope
• Heart rate
• Pulse oximeter
• Capnograph
• EKG and defibrillator for deep sedation

Sedation in action
1059

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

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
1060

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

Sedation
How do pediatric dentists assess the
effectiveness of a sedation?
Management style of the pediatric dentist :

Authoritarian vs. Child Advocate
1061

Sedation
Discharge criteria
• Airway uncompromised
• Cardiovascular function stable
• Patient awake, protective reflexes intact
• Adequate hydration
• Patient responsive, talking
• Ambulatory with assistance
• Responsible adult present

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
1062

Administration
Intranasal
• Rapid onset
• Use atomizer: 1-cc syringe
• No first-pass metabolism
• Indicated for when patient refuses oral meds
1063

Administration
Intramuscular
• Faster absorption than oral route
• Ease of administration
• Potential for trauma to injection site
• Prolonged onset and recovery
• Painful
• Increased liability costs

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
1064

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
1065

Used
Meperidine (Demerol)
• Narcotic
• Analgesic
• Sedative
• Oral or parenteral
• Onset 30 minutes
• Dosage: 1-2mg/kg to maximum dose of 50mg
• Reversal agent
• Unpleasant taste
• Precautions
• CNS, CV, Respiratory depression

Used
Hydroxyzine (Vistaril, Atarax)
• Antihistamine, anti-emetic
• Analgesic
• CNS depression
• Used with other meds
• Dosage 1-2mg/kg orally
• Effect similar to nitrous oxide
• Pleasant taste
1066

Used
Benzodiazepines
• Anxiolytic, amnesic
• Muscle relaxant
• CNS depression
• Minimal CV, respiratory effects
• Reversal agent

Used
Diazepam (Valium)
• Dosage (general guide): 1mg/year of age
• Indications
• Minimal adverse reactions
• Contraindication – patients with narrow-
angle glaucoma
• Precautions
1067

Used
Midazolam (Versed)
• 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

Used
Complications of Midazolam
• Paradoxical negativism
• Hallucinations/nightmares
1068

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

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
1069

Using Drugs in Combination
• Benefits
• Potentiation effects

Emergencies
• Upper airway obstruction
• Respiratory depression
• Overdose of medications
• Seizure
• Allergic reaction
• Vomiting, aspiration
• Syncope
• Hypoglycemia
1070

Adverse Events
What are the common adverse
events in pediatric sedation?
• Respiratory arrest – 43%
• Respiratory depression – 30%
• Cardiac arrest – 8%
Cote, April 2000

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
1071

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

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
1072

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

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
1073

Emergency Preparedness
Personnel Training
Patient Factors
! Know medical history
! Know sedation specifics
! Pre-operative assessment

Follow Guidelines
• NPO status
• Monitoring
• Discharge criteria
1074

Emergency equipment
• Positive pressure oxygen
• Rescue drugs
• Nasal and oral airways – assorted sizes
• Masks – assorted sizes
• Training to use all of above

Quality assurance
1075

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Speech and Language Milestones

Hearing and Understanding Talking
Birth-3 Months Birth-3 Months
• Startles to loud sounds. • Makes pleasure sounds (cooing, gooing).
• Quiets or smiles when spoken to. • Cries differently for different needs.
• Seems to recognize your voice and quiets if crying. • Smiles when sees you.
• Increases or decreases sucking behavior in
response to sound.
4-6 Months 4-6 Months
• Moves eyes in direction of sounds. • Babbling sounds more speech-like with many different
• Responds to changes in tone of your voice. sounds, including p, b, and m.
• Notices toys that make sounds. • Vocalizes excitement and displeasure.
• Pays attention to music. • Makes gurgling sounds when left alone and when playing
with you.
7 Months-l Year 7 Months-l Year
• Enjoys games like peek-a-boo and pat-a-cake. • Babbling has both long and short groups of sounds such as
• Turns and looks in direction of sounds. “tata upup bibibibi.”
• Listens when spoken to. • Uses speech or non-crying sounds to get and keep
• Recognizes words for common items like “cup”, attention.
“shoe”, “juice”. • Imitates different speech sounds.
• Begins to respond to requests (“Come here”, • Has 1 or 2 words (bye-bye, dada, mama) although they may
“Want more?”). not be clear.
1-2 Years 1-2 Years
• Points to a few body parts when asked. • Says more words every month
• Follows simple commands and understands simple • Uses some 1-2 word questions (“Where kitty?”, “Go bye-
questions (“Roll the ball”, “Kiss the baby”, “Where’s bye?”, “What’s that?”).
your shoe?”). • Puts 2 words together (“more cookie”, “no juice”, “mommy
• Listens to simple stories, songs, and rhymes. book”).
• Points to pictures in a book when named. • Uses many different consonant sounds of the beginning of
words.
2-3 Years 2-3 Years
• Understands differences in meaning (“ go-stop”, • Has a word for almost everything.
“in-on”, “big-little”, “up-down”). • Uses 2-3-word “sentences” to talk about and ask for things.
• Follows two requests (“Get the book and put it on • Speech is understood by familiar listeners most of the time.
the table”). • Often asks for or directs attention to objects by naming
them.
3-4 Years 3-4 Years
• Hears you when call from another room. • Talks about activities at school or at friends’ homes.
• Hears television or radio at the same loudness • People outside family usually understand child’s speech.
level as other family members. • Uses a lot of sentences that have 4 or more words.
• Understands simple, “who?” “what?” “where?” • Usually talks easily without repeating syllables or words.
“why?” questions.
4-5 Years 4-5 years
• Pays attention to a short story and answers simple • Voice sounds clear like other children’s.
questions about it. • Uses sentences that give lots of details (e.g. “I like to read
• Hears and understands most of what is said at my books”).
home and in school. • 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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*VOEFSTUBOEUIBUTFEBUJPONBZQSPWFQBSUJBMMZPSDPNQMFUFMZJOFĊFDUJWFJONBOBHJOHNZDIJMEPSMFHBM
XBSE*OTVDIBOJOTUBODFUIFQMBOOFEUSFBUNFOUNBZOPUCFQPTTJCMFPSNBZSFRVJSFTFWFSBMBQQPJOUNFOUT
VTJOHUIFTFDPOTDJPVTTFEBUJPOUFDIOJRVFTUPDPNQMFUFUIFOFDFTTBSZEFOUBMXPSLBOEPSBOBMUFSOBUJWFUSFBUNFOU
NBZCFJOTUJUVUFE
*IBWFCFFOQSPWJEFEXJUIBOFYQMBOBUJPOPGBMUFSOBUJWFTUPUSFBUNFOUBOEVOEFSTUBOEUIFSJTLTPGOPUCFJOH
USFBUFEGPSUIFEFOUBMDPOEJUJPO
*IBWFDBSFGVMMZSFBEUIFBCPWFBOEJOBEEJUJPOIBWFIBEBMMPGNZRVFTUJPOTJOSFHBSEUPTFEBUJPOUPCF
BENJOJTUFSFE UIFPVUMJOFESJTLT BOETJEFFĊFDUTBOTXFSFE
*EPHJWFNZGSFFBOEWPMVOUBSZJOGPSNFEDPOTFOUUPUIFTBNF
%BUF@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@ 5JNF@@@@@@@@@@@@@@@@@@@@@
4JHOBUVSF @@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@ 3FMBUJPOTIJQ@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
8JUOFTT @@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
1081

  
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       


   
   
   
  
  
 

   


 






 

           
 
 
 
   
       

     
   
     
    
  
   







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
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

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


 



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
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 


                 
                
                 
 
               
                 
                 
                 
                 
                 
                 
                 
                 
                 
                 
                 



  


 
 
       
   
      
 
  
     





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
 
 
 
  
 
 


  




         
 


1083

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. You are unable to arouse your child.
2. Your child is unable to eat or drink.
3. Excessive vomiting or pain.
4. Your child develops a rash.
FOR THESE OR ANY OTHER CONCERNS about your child’s sedation, please
contact the doctor.
1084

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 A normally healthy patient.

Class II A patient with mild systemic disease (eg, controlled reactive airway disease).
Class III A patient with severe systemic disease (eg, a child who is actively wheezing).
Class IV A patient with severe systemic disease that is a constant threat to life (eg, a child with status
asthmaticus).
Class V 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
1085

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)
1086

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Reference Manual 2005-2006 Resource Section 239
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 Drug dosage Drug delivery

Allergic reaction Hives, itching, edema, erythema 1. Discontinue all sources of Diphenhydramine 1 mg/kg Oral
(mild or delayed) of skin, mucosa, conjunctiva allergy-causing substances Child: 10-25 mg qid
2. Administer diphenhydramine Adult: 25-50 mg qid
Allergic reaction Urticaria – itching, flushing, This is a true, life- Epinephrine 1:1000 IM or SubQ
(sudden onset): hives; rhinitis; wheezing/difficulty threatening emergency 0.01 mg/kg every 5 min
anaphylaxis breathing; bronchospasm; 1. Call for medical help until recovery or until
laryngeal edema; weak pulse; 2. Administer epinephrine help arrives
marked fall in blood pressure; 3. Administer oxygen
loss of consciousness 4. Monitor vital signs
Acute asthmatic Shortness of breath, wheezing, 1. Sit patient upright or in a 1. Try patient’s inhaler or Inhale
attack coughing, tightness in chest, comfortable position one from emergency kit
cyanosis, tachycardia 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 1. Assess and support airway, Supplemental oxygen Mask
vision and/or speech, changes in breathing, and circulation
mental status, confusion, agitation, 2. Administer oxygen
tinnitis, tremor, seizure, tachypnea, 3. Monitor vital signs
bradycardia, unconsciousness, 4. Transport to emergency
cardiac arrest center as indicated
Anesthetic reaction: Anxiety, tachycardia/palpitations, 1. Reassure patient Supplemental oxygen Mask
vasoconstrictor restlessness, headache, tachypnea, 2. Assess and support airway,
chest pain, cardiac arrest breathing, and circulation
3. Administer oxygen
5. Transport to emergency
center as indicated
Overdose: Somnolence, confusion, diminished 1. Assess and support airway, Flumazenil 0.01 mg/kg IV
benzodiazepine reflexes, respiratory depression, breathing, and circulation (not to exceed a total of 1 mg)
apnea, respiratory arrest, 2. Administer oxygen at a rate not to exceed
cardiac arrest 3. Monitor vital signs 0.2 mg/min
4. Establish IV access and
reverse with flumazenil
5. Monitor recovery
Overdose: narcotic Decreased responsiveness, 1. Assess and support airway, Naloxone 0.01 mg/kg IV, IM,
respiratory depression, respiratory breathing, and circulation (may repeat after 2-3 min) or SubQ
arrest, cardiac arrest 2. Administer oxygen
4. Reverse with naloxone
5. Monitor recovery
Seizure Warning aura; disorientation, 1. Recline and position to Diazepam IV
blinking, or blank stare; prevent injury Child up to 5 y: 0.2-0.5 mg
uncontrolled muscle movements; 2. Ensure open airway and slowly every 2-5 min with
muscle rigidity; unconsciousness; adequate ventilation maximum=5 mg
postictal phase: sleepiness; 3. Monitor vital signs Child 5 y and up: 1 mg
confusion; amnesia; slow recovery 4. If status is epilepticus, every 2-5 min with
give diazepam maximum=10 mg
Syncope (fainting) Feeling of warmth, skin pale and 1. Recline, feet up Ammonia in vials Inhale
moist, pulse rapid initially then 2. Loosen clothing that
gets slow and weak, dizziness, may be binding
hypotension, cold extremities, 3. Ammonia inhaler
unconsciouness 4. Administer oxygen
5. Cold towel on back of neck
6. Monitor recovery
1088
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1089

Guidelines for Infection Control

in Dental Health-Care Settings — 2003
INSIDE: Continuing Education Examination

1090

MMWR
CONTENTS
(52
@2?62@<3=B/960.A6<;@6@=B/96@521/FA52 Introduction ......................................................................... 1

=612:6<9<4F $?<4?.: #33602 2;A2?@ 3<? 6@2.@2 Background ......................................................................... 2
<;A?<9 .;1 $?2C2;A6<; )' 2=.?A:2;A <3 Previous Recommendations .............................................. 3
2.9A5.;1B:.;'2?C602@A9.;A. Selected Definitions .......................................................... 4
Review of Science Related to Dental Infection Control ......... 6
SUGGESTED CITATION Personnel Health Elements of an Infection-Control
2;A2?@3<?6@2.@2<;A?<9.;1$?2C2;A6<;B61296;2@ Program .......................................................................... 6
3<?;320A6<;<;A?<96;2;A.92.9A5.?2'2AA6;4@ Preventing Transmission
I !!*& "<&&
,6;09B@6C2=.42 of Bloodborne Pathogens ................................................ 10
;B:/2?@- Hand Hygiene ................................................................ 14
Personal Protective Equipment ........................................ 16
Contact Dermatitis and Latex Hypersensitivity ................. 19
Centers for Disease Control and Prevention
Sterilization and Disinfection of Patient-Care Items ......... 20
B962 2?/2?16;4!!$ Environmental Infection Control ..................................... 25
" Dental Unit Waterlines, Biofilm, and Water Quality ......... 28
Special Considerations ...................................................... 30
6E62';612??!!$
Dental Handpieces and Other Devices Attached
"#"$ " #"
to Air and Waterlines .................................................... 30
'B@.;+5B$5!'$ Saliva Ejectors ................................................................ 31
"!!" " Dental Radiology ............................................................ 31
Aseptic Technique for Parenteral Medications ................. 31
Epidemiology Program Office Single-Use or Disposable Devices ................................... 32
'A2=52;(5.082?!!'0 Preprocedural Mouth Rinses ........................................... 32
" Oral Surgical Procedures ................................................ 32
Handling of Biopsy Specimens ........................................ 33
Office of Scientific and Health Communications Handling of Extracted Teeth ............................................ 33
<5;**.?1! Dental Laboratory ........................................................... 33
" Laser/Electrosurgery Plumes or Surgical Smoke .............. 34
" !!*& ! M. tuberculosis ................................................................. 35
Creutzfeldt-Jakob Disease and Other Prion Diseases ...... 36
'BG.;;2!2D6AA!$ Program Evaluation ........................................................ 37

" !!*& ! Infection-Control Research Considerations ..................... 38
.F':6A586;!1 Recommendations ............................................................. 39
" " Infection-Control Internet Resources ................................. 48
Acknowledgement ............................................................. 48
.F':6A586;!1 References ......................................................................... 48
<B49.@**2.A52?D.E Appendix A ....................................................................... 62
"" ! Appendix B ........................................................................ 65
Appendix C ....................................................................... 66
2C2?9F<99.;1 Continuing Education Activity* ....................................... CE-1
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Pediatric Anaphylaxis/Allergic Response
Assess ABCs Transport ASAP and

contact med control
Patient alert, responsive Establish patent airway

with localized alergic 100% oxygen by non-rebreather mask or
reaction 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 No
Reassess: is patient hemodynamically stable?
Trendelburg position
Continue oxygen and Consider fluid bolus at
support; monitor 20 cc/kg NS
Repeat prn
For Wheezing, Albuterol 2.5-5.0 mg in

2-3 cc NS by nebulizer prn
Continue tx and support

Diphenhydramine 1-2 mg/kg IV/IM
prn during transport
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1100

(AAPD) Comprehensive Review of Pediatric Dentistry (B-Ok - Xyz)

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(AAPD) Comprehensive Review of Pediatric Dentistry (B-Ok - Xyz)

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Comprehensive

American Academy of Pediatric Dentistry

WARNING: The copyright proprietor

is not responsible in any way for the

This educational activity is a DVD format.

The American Academy of Pediatric

the requirements of other governing

1. The major clinical and knowledge

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! Light, continuous forces

" Tooth movement begins

" This process is called “FRONTAL RESORPTION”

Frontal resorption occurs on the osseous

Tooth movement (mm)

Undermining resorption results loss of vitality of

Direction of Force Application

! Center of Rotation --- The point around which rotation

! Center of Resistance --- A point on the tooth around

+3",4%3#) ()*'+,U",, #A''

+3",4%3#) ()*'+,U",, #A''

Orthodontic Forces and Tooth

! Optimal force levels

Degree of Force Summary

! In the range of 10 to 200 grams.

Force Continuous and

• Key to producing tooth movement:

als1 photos of dental open bite and skeletal oopen bite

als2 missing laterals

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Constance M. Killian, D.M.D.

Trauma is a part of Anticipatory

1. “Primum non nocere”

2. Never treat a stranger

• Identify adult bringing the child

• Dental trauma is a subset of head

• Bruising behind ear -

• Abnormal vital signs

• Glasgow Coma Scale – see

Glasgow Coma Scale

What else should make you think ICI?

What overrides the dental injury?

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