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Pathology 2 > Dental Anomalies I > Flashcards

Dental Anomalies I Flashcards

1
Q

Ameloblasts:

A

extremely sensitive to external stimuli

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2
Q

Enamel defects
 Enamel defects may be caused by
 Enamel — does not occur after initial formation
 Abnormalities

A

local or systemic factors
remodeling
etched permanently on tooth surface

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3
Q

Stages of enamel development:
(3)

A

 (1) Matrix formation: enamel proteins laid down
 (2) Mineralization: minerals deposited, original proteins removed
 (3) Maturation: final mineralization, remaining original proteins removed
 Hard, translucent enamel

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4
Q

 Timing of injury:
 Final enamel:

A

affects location and appearance of defect
record of all significant insults received during tooth
development

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5
Q

Enamel defects
Clinical features:
(2)

A

 Enamel hypoplasia:
 Enamel opacities:

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6
Q

Clinical features:
 Enamel hypoplasia:
(2)

A

large areas of missing enamel
 Pits, fissures, grooves

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7
Q

 Enamel opacities:
(3)

A

areas of enamel hypomaturation
 diffuse or demarcated
 White, yellow, brown

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8
Q

Turner hypoplasia

A

Periapical inflammatory disease or trauma of overlying deciduous tooth

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9
Q

Turner hypoplasia
Clinical and Radiographic features:
 Observed in
 Traumatic cases –
 Focal areas of
 Extensive hypoplasia –
 RG: (2)

A

permanent teeth – MC premolar
max central incisors
white, yellow, brown discoloration
may involve entire crown
lack of enamel, irregular surface dentin

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10
Q

Antineoplastic therapy
 Developmental abnormalities secondary to use of
 Severity dependent on (4)
 — therapy – more severe alterations

A

radiation or chemotherapy
age of treatment, form of therapy, dose and field of radiation
Radiation

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11
Q

Antineoplastic therapy
 Clinical features:
 Radiation: (4)
 Chemotherapy: (3)

A

enamel hypoplasia, microdontia, radicular hypoplasia, Hypodontia
enamel hypoplasia, microdontia, occasionally radicular hypoplasia

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12
Q

Dental Fluorosis
(3)

A

 Ingestion of excessive FL → significant enamel defects
 Retention of amelogenin proteins in enamel → hypomineralized enamel
 Dose dependent

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13
Q

Dental fluorosis
 Clinical features:
(3)

A

 White, opaque enamel, with areas of brown/yellow discoloration
 Affected teeth are caries resistant
 Bilateral, symmetrical distribution

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14
Q

Treatment: enamel defects
(3)

A

 Most defects are cosmetic
 Focal loss of enamel – increased prevalence of caries
 Composite restorations, veneers, full crowns

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15
Q

Tooth wear
 Considered pathologic when the degree of destruction creates

A

functional,
aesthetic, or dental sensitivity problems

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16
Q

Attrition
(2)

A

 Loss of tooth structure due to tooth-to-tooth contact
 Poor-quality/absent enamel can accelerate process

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17
Q

Attrition
Clinical features:
(3)

A

 Incisal and occlusal surfaces
 Large, flat, smooth and shiny wear facets
 Slow loss of tooth structure, reparative secondary dentin forms

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18
Q

Abrasion
(2)

A

 Pathologic wearing of tooth structure secondary to an external agent
 Toothbrushing MC

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19
Q

Abrasion
Clinical features:
 Dependent on —
 Toothbrushing:
 Tobacco pipe, bobby pins:

A

cause
horizontal cervical notches on buccal surface
V-shaped notches on incisal edge

20
Q

Erosion
(2)

A

 Loss of tooth structure caused by a non-bacterial chemical process
 Exposure to acidic source, reduced salivary flow

21
Q

Erosion
Clinical features:
(2)

A

 Cupped lesion, central depression of dentin surrounded by elevated enamel
 May create concave sloping areas on palatal surfaces

22
Q

Tooth wear treatment
 — cause
 Detailed —, — measures
 Erosion:
 Restorative treatment:

A

Multifactorial
diagnosis, preventative
may consider limiting toothbrushing 1x daily
composite, veneers, full crown

23
Q

Extrinsic stains
 Arises from the surface accumulation of
 Usually can be removed with
 Ex (6)

A

exogenous pigment
surface treatment
Tobacco, bacterial stains, food + beverages, iron, restorative materials, medications

24
Q

Intrinsic stains
 Arises from
 Cannot be removed by —
 Ex (6)

A

endogenous materials that are incorporated into enamel and dentin
prophylaxis
Amelogenesis imperfecta, dentinogenesis imperfecta, dental fluorosis, hyperbilirubinemia, trauma, medications

25
Q

Internal Resorption
 Loss of tooth structure on the
 Commonly arises secondary to
 Continues if

A

dentinal walls of the pulp
inflammatory reaction
vital pulp tissue remains

26
Q

Internal Resorption
 Clinical and Radiographic features:
 Inflammatory resorption:
 Replacement resorption:
 Coronal pulp affected →

A

resorbed dentin replaced by inflamed granulation tissue
pulpal dentinal wall is resorbed with bone and cementum-like bone
pink tooth of Mummery

27
Q

 Inflammatory resorption:
 RG:

A

resorbed dentin replaced by inflamed granulation
tissue
well-circumscribed radiolucent enlargement of pulp chamber

28
Q

External resorption
 Loss of tooth structure along
 Exposure of
 Common causes: (4)
 Common!

A

external surface of root
adjacent mineralized cementum to cemetoclasts
localized pressure (ie: orthodontic therapy), excessive
occlusal forces, cysts, tumors

29
Q

External resorption
 Clinical and Radiographic findings:
(2)

A

 “moth-eaten” loss of tooth structure
 Over pulp chamber, radiolucency superimposed

30
Q

Ankylosis
(2)

A

 Anatomic fusion of tooth cementum with the alveolar bone
 May be caused by trauma, chemical/thermal irritation, genetically
decreased PDL

31
Q

Ankylosis
 Clinical features:
(5)

A

 MC 1st-2nd decade
 MC mandibular primary first molar
 Mandible 10:1
 Ankylosis of permanent teeth uncommon
 Sharp, solid sound upon percussion

32
Q

Ankylosis
 Radiographic features:
(3)

A

 Absence of PDL space (difficult to detect)
 Adjacent teeth inclined towards affected tooth
 Supraeruption of opposing tooth

33
Q

Ankylosis
 Treatment:

A

 For primary teeth (lack of exfoliation) → extraction

34
Q

 Anodontia:

A

total lack of development of teeth

35
Q

 Hypodontia:

A

lack of development of one or more teeth

36
Q

 Oligodontia:

A

lack of development of 6 or more teeth

37
Q

 Hyperdontia:

A

development of an increased # of teeth – supernumerary

38
Q

Tooth number anomalies
(3)

A

 More than 200 genes associated with odontogenesis
 Syndromic and non syndromic
 MC genes implicated: PAX9, MSX1, AXIN2 genes (hypodontia)

39
Q

Hypodontia
 Prevalence of
 Absence of
 Syndrome associated:

A

3-10% in permanent teeth
primary teeth correlates strongly with missing successor
Ectodermal dysplasia

40
Q

Hypodontia
 Clinical features:
(2)

A

 After 3rd molars, MC in 2nd premolar and lateral incisor
 MC in females

41
Q

Hyperdontia
 Most cases represent
 Syndromes: (2)
 Positively correlated with —

A

single-tooth supernumerary
Cleidocranial dysplasia, Gardner
macrodontia

42
Q

Hyperdontia
 Clinical features:
(3)

A

 Single tooth hyperdontia: MC in anterior maxilla – mesiodens
 Accessory 4th molar: distomolar/distodens
 2: 1 male

43
Q

Microdontia
(4)

A

 Presence of unusually small teeth
 Genetic and environmental factors play a role
 Conditions: Down syndrome, pituitary dwarfism
 Isolated cases more common than diffuse cases

44
Q

Microdontia
 Clinical features:
(2)

A

 Isolated microdontia: MC in max lateral – peg lateral
 MC in females

45
Q

Macrodontia
(4)

A

 Teeth larger than average
 Genetic and environmental factors play a role
 Conditions: pituitary gigantism, XYY males, pineal hyperplasia,
hyperinsulinism
 Isolated cases more common than diffuse cases

46
Q

Macrodontia
 Clinical features:
(2)

A

 Isolated macrodontia: MC in incisors or canines
 MC in males

Pathology 2 (12 decks)

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