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PATH II > dental anomolies 1 > Flashcards

dental anomolies 1 Flashcards

1
Q

Enamel defects
 Ameloblasts sensitivity?
 Enamel defects may be caused by what factors?
 Enamel remodeling?
 Abnormalities etched?

A

Enamel defects
 Ameloblasts: extremely sensitive to external stimuli
 Enamel defects may be caused by local or systemic factors
 Enamel remodeling does not occur after initial formation
 Abnormalities etched permanently on tooth surface

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2
Q

Stages of enamel development

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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3
Q

Enamel defects
 Timing of injury: affects?
 Final enamel: record of?

A

 Timing of injury: affects location and appearance of defect
 Final enamel: record of all significant insults received during toothdevelopment

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4
Q

 Enamel hypoplasia

A

large areas of missing enamel
 Pits, fissures, grooves

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5
Q

enamel opacities

A

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

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6
Q
A

enamel hypoplasia of a systemic cause due to more generalized app

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7
Q
A

enamel opacities

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8
Q

turner hypoplasia
 Clinical and Radiographic features:
 Observed in which tooth? MC?
 Traumatic cases?
 app?
 Extensive hypoplasia may involve?
 RG?

A

 Periapical inflammatory disease or trauma of overlying deciduous tooth

 Clinical and Radiographic features:
 Observed in permanent teeth – MC premolar
 Traumatic cases – max central incisors
 Focal areas of white, yellow, brown discoloration
 Extensive hypoplasia – may involve entire crown
 RG: lack of enamel, irregular surface dentin

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9
Q

severity of turner hypoplasia depends on?

A

timing on development, earlier= more severe

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10
Q

Antineoplastic therapy and development
 Severity dependent on?
 which is more severe?

A

 Developmental abnormalities secondary to use of radiation orchemotherapy
 Severity dependent on age of treatment, form of therapy, dose and field ofradiation
 Radiation therapy – more severe alterations

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11
Q

Antineoplastic therapy
 Clinical features:
 Radiation:
 Chemotherapy:

A

 Radiation: Hypodontia, microdontia, radicular hypoplasia, enamel hypoplasia

 Chemotherapy: enamel hypoplasia, microdontia, occasionally radicular hypoplasia

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12
Q

what previous medical tx likley occurred in this pt

A

antineoplastic tx

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13
Q

Dental Fluorosis
 Ingestion of?
 mechanism?
 Dose?

A

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

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14
Q

fluorosis clinical features
 color?
 caries?
 distribution?

A

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

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15
Q
A

fluorosis

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16
Q

Treatment: enamel defects
most defects are?
focal lose of enamel may lead to?
options?

A

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

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17
Q

Tooth wear
 Considered pathologic when?

A

 Considered pathologic when the degree of destruction creates functional, aesthetic, or dental sensitivity problems

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18
Q

Attrition
 Loss of tooth structure due to?
 what can accelerate process?

A

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

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19
Q

attrition clinical features

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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20
Q

Abrasion
 defined?
 MC agent

A

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

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21
Q

abrasion clinical features
 Clinical features:
 Dependent on?
 Toothbrushing?
 additional causes?

A

 Dependent on cause
 Toothbrushing: horizontal cervical notches on buccal surface
 Tobacco pipe, bobby pins: V-shaped notches on incisal edge

22
Q

Erosion
 Loss of tooth structure caused by?
 Exposure to?

A

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

23
Q

 erosion Clinical features:

A

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

24
Q

Tooth wear treatment
 cause?
 Detailed?
 Erosion: may consider?
 Restorative treatments?

A

Tooth wear treatment
 Multifactorial cause
 Detailed diagnosis, preventative measures
 Erosion: may consider limiting toothbrushing 1x daily
 Restorative treatment: composite, veneers, full crown

25
Q

Extrinsic stains
 Arises from?
 Usually can be removed with?
 examples?

A

 Arises from the surface accumulation of exogenous pigment
 Usually can be removed with surface treatment
 Tobacco, bacterial stains, food + beverages, iron, restorative materials,medications

26
Q

Intrinsic stains
 Arises from?
 Cannot be?
 examples?

A

 Arises from endogenous materials that are incorporated into enamel and dentin
 Cannot be removed by prophylaxis
 Amelogenesis imperfecta, dentinogenesis imperfecta, dental fluorosis, hyperbilirubinemia, trauma, medications

27
Q

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

A

 Loss of tooth structure on the dentinal walls of the pulp
 Commonly arises secondary to inflammatory reaction
 Continues if vital pulp tissue remains

28
Q

forms of internal resorb

A

inflammatory and replacement

29
Q

inflammatory internal resorb clinical and radio features

A

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

30
Q

replacement internal resorb clinical and radio findings

A

pulpal dentinal wall is resorbed with bone and
cementum-like bone
 RG: partial obliteration of canal by bone (radiopacity)

31
Q

pink tooth of mummery

A

occurs when coronal pulp is affected by internal resorb

32
Q
A

internal resorbtion (inflammatory)

33
Q

External resorption
 Loss of?
 Exposure of?
 Common causes:
 Commonality vs internal?

A

 Loss of tooth structure along external surface of root
 Exposure of adjacent mineralized cementum to cemetoclasts
 Common causes: localized pressure (ie: orthodontic therapy), excessive occlusal forces, cysts, tumors
 More Common!

34
Q

External resorption
 Clinical and Radiographic findings:

A

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

35
Q
A

external resorbtion

36
Q

Ankylosis
 Anatomic fusion of?
 May be caused by?

A

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

37
Q

Ankylosis
 Clinical features:
 MC age?
 MC tooth?
 Mandible vs maxilla ratio
 Ankylosis of permanent teeth?
 percussion?

A

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

38
Q

Ankylosis
 Radiographic features:

A

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

39
Q

ankylosis tx

A

 For primary teeth (lack of exfoliation) → extraction

40
Q

what can be noticed?

A

ankylosis of the primary molar

41
Q

Tooth number anomalies
 Anodontia:
 Hypodontia:
 Oligodontia:
 Hyperdontia:

A

 Anodontia: total lack of development of teeth
 Hypodontia: lack of development of one or more teeth
 Oligodontia: lack of development of 6 or more teeth
 Hyperdontia: development of an increased # of teeth – supernumerary

42
Q

Tooth number anomalies
 More than ___ genes associated with odontogenesis
 Syndromic or non syndromic?
 MC genes implicated:

A

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

43
Q

Hypodontia
 Prevalence of ?% in permanent teeth
 what correlates strongly with missing successor?
 Syndrome associated:

A

 Prevalence of 3-10% in permanent teeth
 Absence of primary teeth correlates strongly with missing successor
 Syndrome associated: Ectodermal dysplasia

44
Q

Hypodontia
 Clinical features:
 MC teeth?
 MC sex

A

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

45
Q
A

AMLI

46
Q

Hyperdontia
 Most cases represent?
 Syndromes:
 Positively correlated with?

A

 Most cases represent single-tooth supernumerary
 Syndromes: Cleidocranial dysplasia, Gardner
 Positively correlated with macrodontia

47
Q

Hyperdontia
 Clinical features:
 Single tooth hyperdontia: MC in?
 Accessory 4th molar?
 sex ratio

A

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

48
Q

Microdontia
 Presence of?
 factors playing a role?
 Conditions:
 Isolated cases vs diffuse cases?

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

49
Q

Microdontia
 Clinical features:
 Isolated microdontia: MC in?
 MC sex

A

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

50
Q

Macrodontia
 Teeth size?
 factors playing a role?
 Conditions:
 Isolated cases vs diffuse

A

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

51
Q

Macrodontia
 Clinical features:
 Isolated macrodontia: MC in
 MC sex

A

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

PATH II (25 decks)

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