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PEDO (Spring) > 5. Aquired Developmental Disturbances > Flashcards

5. Aquired Developmental Disturbances Flashcards

1
Q

Is amelogenesis imperfecta inherited

A

yes

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2
Q

inheritance patterns of amelogenesis imperfect

A
  • dominant
  • recessive
  • X-linked
  • sporadic
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3
Q

Amelogenesis imperfecta affects the three major stages of enamel formation which are

A
  • Elaboration of enamel matrix (hypoplastic)
  • Mineralization of the matrix (hypocalcified)
  • Maturation of the matrix (hypomaturation)
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4
Q

AI affects the (primary/permenant) teeth

A

both (uniformly throughout the dentition)

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5
Q

How many major types and subgroups of AI

A

4 major types and 14 subgroups

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6
Q

Dx of AI based on

A
  • Family history

- Clinical exam (teeth may be discolored, sensitive and prone to disintegration)

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7
Q

What malocclusion is AI commonly associated with

A

anterior open bite

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8
Q

what are the 4 major types of AI

A
  • Hypoplastic
  • Hypocalcified
  • Hypomaturation
  • Hypomaturation with taurodontism
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9
Q

Describe hypoplastic AI

A

-Insufficient quanity of enamel

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10
Q

Describe hypomaturation AI

A
  • Normal thickness

- Low mineral content

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11
Q

Describe Hypocalcified AI

A
  • Normal quantity
  • Poorly calcified
  • Soft and fragile
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12
Q

Describe hypomaturation with taurodontism for AI

A
  • Mottled and pitted
  • Enlarged pulp chambers
  • Associated with tricho-dento-osseous syndrome
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13
Q

Treatment for AI in primary dentition

A
  • SSC molars
  • Strip crow anteriors (resin or preformed)
  • Usually done under general anesthesia
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14
Q

Treatment of AI in mixed dentition

A
  • SSC molars

- Composite restorations on anterior teeth

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15
Q

When can you do a full coverage restoration on a child patient and why

A

when they are done growing… position of finishline will always change

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16
Q

Treatment for AI in permenant dentition

A

Full coverage crowns

Dentures/overdentures

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17
Q

Is dentinogenesis imperfecta inheritable

A

yes

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18
Q

inheritance pattern of DI

A

autosomal dominant

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19
Q

What is DI

A
  • Defect in predentin matrix
  • Histodifferentiation stage in tooth development
  • Amorphic disorganized atubular circumpulpal dentin
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20
Q

Describe the color of teeth with DI

A
  • Blue-brown (amber)
  • Translucence
  • Normal enamel (but tends to chip due to poor support)
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21
Q

DI radiographic findings

A
  • Bulbous crowns
  • Short roots
  • Early obliteration of pulp chamber/root canals
  • *Variation= shell teeth (large pulp chambers)
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22
Q

What are the three different types of DI

A

Sheilds types I, II, and III

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23
Q

Describe Sheilds Type I DI

A
  • Osteogenesis imperfecta
  • Brittle bones
  • Bowing limbs
  • Temporal bossing
  • **Blue sclera
  • Teet= periapical RLs and amber translucence
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24
Q

Which are more severely affected in Sheilds type I (primary/permanent) teeth

A

primary

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25
Q

Describe Sheilds Class II DI

A
  • Both dentitions affected

- Same clinical findings as Shield’s type I but without osteogenesis imperfecta

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26
Q

Shell teeth is most commonly seen in what type of DI

A

Sheild’s class III

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27
Q

Describe Sheild’s type III

A
  • Rare
  • Brandywine population
  • Bell shaped crowns
  • Shell teeth (short roots and large pulp chambers)
  • Multiple pulp exposures
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28
Q

Is dentin dysplasia an inherited disorder

A

yes

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29
Q

inheritance pattern of dentin dysplasia

A

autosomal dominant

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30
Q

What are the subtypes of dentin dysplasia

A

Sheilds Type I and II

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31
Q

Describe Sheild type I dentin dysplasia

A
  • Radicular
  • Normal color of crowns
  • Both dentitions affected
  • Short blunted roots
  • Obliterated pulp chambers
  • mobility
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32
Q

Describe Sheild Type II dentin dysplasia

A
  • Coronal
  • Amber colored primary teeth
  • Normal root length
  • Permanent tooth look normal but on X-ray –> Thistle tube shaped pulp and multiple pulp stones
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33
Q

Contraindications for patients with Osteogenesis imperfecta and why

A

physical restraint (can break their bones)

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34
Q

DI and DD treatment in permanent dentition

A
  • Full coverage restorations
  • Denture/overdenture (short roots –> early failure)
  • Bonded restorations prone to failure
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35
Q

Another name for vitamin D resistant rickets

A

familial hypophosphatemic rickets

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36
Q

Inheitance pattern of VItDRR and what is the gene involves

A

X-linked PHEX gene

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37
Q

Describe VitDRR

A
  • Decreased tubular reabsorption of phosphate in the kidney leads to hypophosphatemia
  • Low levels of phosphate –> defective calcification of teeth and bones (bowing legs and frontal bossing)
38
Q

Treatment for VitDRR

A

-Phosphate and calcitriol

39
Q

Oral manifestations of VitDRR

A
  • Abnormal dentin and enamel
  • Large pulp chambers (can extend into DEJ)
  • Spontaneous abscesses (25% have multiple abscesses in normal primary teeth)
  • Variable penetration (depends on when treatment was intiated)
40
Q

Treatment for VitDRR

A

Selants

  • Prophylatic full coverage restorations (large pulps)
  • Endo therapy for pulpally involved permanent teeth
41
Q

Sources of intrinsic stains of teeth

A
  • Congenital porphyrie- Purple brown *heme build up)
  • Hyperbilirubinemia Absent bile duct –> bile accumulation
  • Anemia - gray
  • Cystic Fibrosis - (disease/therapy)= (yellow/brown)
  • Tetracycline
42
Q

Colors of hyperbilirubinemia

A
  • Biliary atresia= green

- Rh incompatibility (erythroblastosis fetalis)= blue-green/brown

43
Q

What is the name of the disease where there is enamel hypoplasia on one or more permanent molars and incisors

A

molar incisor hypomineralization (MIH)

44
Q

Causes of Molar incisor hypomineralization

A

Systemic insult during child’s first 3 years of life

  • Medical condition
  • Antibiotic usage
  • Preterm birth
  • Environmental pollutants (PCDD in breast milk)
45
Q

Prevalence of MIH

A

4-25%

46
Q

Difficulties with treating MIH teeth are

A

Teeth are sensitive

  • OH difficult
  • Anesthesia difficult (pulps are chronically inflammed)

Poor bonding

47
Q

Treatment for MIH teeth

A
  • Remineralization therapy (MI paste and fluoride varnish)
  • Fuji sealants (retention is poor- frequent replacing)
  • Incisors= microabrasion, composite bonding and veneer
  • *depends on the severity**
48
Q

Treatment for molars affected with MIH

  • Mild
  • Moderate
  • Severe
A
  • Mild= composite restorations
  • Moderate= SSC
  • Severe= Exo
49
Q

Fluorosis stains are (intrinsic/extrinsic)

A

intrinsic (white brown)

50
Q

What causes fluorosis

A

excess fluoride disrupts enamel formation

51
Q

Disruption of enamel formation by excess fluoride is commonly caused when

A

during the first few years of life

52
Q

The enamel in fluorosis is (hypoplastic/hypomineralized/Hypomaturated)

A

hypomineralized

53
Q

Current recommendation for water fluoridation is

A

0.7 ppm

54
Q

Incidence of mild and moderate fluorosis in 12-15 year olds

A

8% mild and 5% moderate

55
Q

Potential sources of fluoride causing fluorosis are

A
  • Halo effect
  • Infant formula
  • Toothpaste consumption
  • Inappropriate fluoride supplements
56
Q

Fluorosis treatment

A

Esthetics only

  • Microabrasion
  • Bonding
  • veneer
57
Q

Eruption cyst is the soft tissue analog of

A

dentigerous cyst

58
Q

What causes an eruption cyst

A

when the dental follicle forms around the crown of an erupting tooth

59
Q

what is the name of an eruption cyst filled with blood

A

eruption hematoma

60
Q

Treatment for eruption cyst

A

None-usually spontaneously erupts on its own

-Can excise the roof of the cyst to aid in eruption

61
Q

Radiographic evidence of ankylosis

A

Loss of PDL (sometimes not evident)

62
Q

Clinical sign of ankylosis

A

solid sound on percussion

-Marginal ridge discrepancy

63
Q

Ankylosis in anterior teeth is common following

A

trauma

64
Q

T?F the alveolar bone around the impacted tooth doesn’t continue to growth

A

f it does

65
Q

Incidence of ankylosis in primary molars

A

2-4%

66
Q

Ankylosis is more common in the (maxilla/mandible)

A

mandible

67
Q

T/F Exfoliation of ankylosed teeth usually occurs normally

A

t

68
Q

Under what circumstances should you extract an ankylosed tooth

A

-Marginal ridge discrepancy is severe (tipping of adjacent teeth into the space (prevent trapping erupting teeth)

69
Q

What is ectopic eruption

A

when a permanent tooth causes either resorption of a primary tooth other than the one it is supposed to replace or resorption of an adjacent primary tooth

70
Q

Ectopic eruption is most commonly seen in what teeth

A
  • Lateral incisor
  • First maxillary molar
  • Maxillary canines
71
Q

In what arch is the lateral incisor often involved in ectopic eruption

A

both arches

72
Q

Describe what happens when a lateral incisor ectopically erupts

A

premature exfoliation of the primary canine

73
Q

Ectopic eruption of the lateral incisors typically indicates

A

crowding

74
Q

Treatment for ectopic eruption of the lateral incisor

A
  • If unilateral, consider extraction of the other primary canine to prevent midline shift
  • LLHA with a spur
  • Refer to orthodontitis
75
Q

Ectopic eruption of the maxillary first molar leads to early exfoliation of what tooth

A

primary 2nd molar

76
Q

Prevalence of ectopically erupted maxillary first molar

A

3-4%

77
Q

How many ectopically erupted maxillary first molars self-correct

A

66%

78
Q

Treatment options for ectopically erupted maxillary first molars

A
  • Ortho separator
  • Brass wire
  • Ortho appliances
  • Severe case will result in loss of 2nd primary molar
79
Q

Consequence of ectopic eruption of maxillary first molar

A
  • Space loss

- 2nd primary molar may develop access (requiring exo)

80
Q

Ectopically erupting maxillary canines (impacted) are positioned how

A

mesioangular (possible overlap with the root of the lateral incisor)

81
Q

How many impacted maxillary canines are palatally and labially positioned

A 
Palatal= 2/3
Labial= 1/3
82
Q

Incidence of impacted maxillary canines

A

1.5-2%

83
Q

Palatal impaction of the canine can be suspected when

A

the canine buldge can’t be palpated

84
Q

Impacted maxillary canine is more commonly seen when

A

the lateral incisor is missing or small

85
Q

Improvement of the eruption path of the impacted canine can be improved how

A

extraction of the primary canine

  • Overlapping less than half the lateral incisor –> 91% success
  • When overlap is more than 1/2 extraction is 64% successful
86
Q

What will happen if eruption of the impacted canine is unsuccessful

A

remains impacted

87
Q

The maxillary incisor is ectopic or impacted in _% of the population

A

2

88
Q

Causes of impacted/ectopic maxillary incisor

A
  • Supernumerary tooth
  • Trauma
  • Pulpal treatment of primary incisor
89
Q

Treatment of impacted maxillary incisor

A

Impaction
-Exo supernumerary tooth or overretained primary tooth

Ectopic

  • Depends on severity and etiology
  • Exo overretained primary tooth
  • Supernumerary tooth- consider root development of permanent incisors
90
Q

Permanent mandibular incisors often erupt (buccally/lingually) relative to the primary

A

lingually

91
Q

O and P can be extracted when

A

24 and 25 (lingually erupted are mostly erupted and O and P aren’t mobile

PEDO (Spring) (9 decks)

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