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Pedo > Anomalies In Dentition > Flashcards

Anomalies In Dentition Flashcards

1
Q

What classifications of dental anomalies are there?

A
  1. Number
  2. Form
  3. Size
  4. Structure
  5. Colours
  6. Others
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2
Q

What anomalies in tooth number are there?

A
  1. Hypodontia
  2. Hyperdontia
  3. Variation in root number
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3
Q

How many teeth are there in primary dentition?

A

20

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4
Q

What is hyperdontia?
Where are they mostly found?
Are they mostly erupted?

A

Increase in tooth number. Presence of supernumeraries
Mostly found in premaxilla (90%) more common in males, permanent teeth.
Mostly unerupted (75%), usually incidental findings in radiograph

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5
Q

What are other names for supernumerary teeth?

A

Mesiodens (midline), paramolars (buccal/palatal of molar region), distomolars (distal of molars)

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6
Q

What is a supplemental supernumerary tooth?

A

Similar shape/size/form of tooth in the area that is found- may not be able to decide which is the supernumerary.

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7
Q

What are the forms of supernumerary teeth?

A

Conical, supplementary, tuberculate

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8
Q

What medical/dental conditions have higher association with supernumeraries

A 
Cleidocranial dysostosis (have no collar bone): have a lot of supernumeraries but many remain unerupted
Cleft palate (40% have supernumeraries in area of cleft due to disturbance of development of developing tooth buds)
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9
Q

What are the associated problems that supernumeraries cause?

A
  1. Impede/deflect path of eruption of permanent teeth
  2. Resorption of roots of adjacent teeth- buried supernumerary causing root resorption of nearby tooth
  3. Cyst @ buried supernumerary
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10
Q

What is the management for supernumeraries?

A
  1. Removal (extraction or surgery) Make sure the crown of associated tooth is fully formed- if not may cause hypoplastic permanent tooth, or dilaceration. Just have to extract before permanent tooth erupt, Scar tissue from extraction may cause difficulty in eruption
  2. Leave alone and review (if tooth is buried, not causing problem) X-ray every 5 years to see if any cystic changes
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11
Q

What is hypodontia?

A

Congenital absence of teeth
Oligodontia- 6 or more missing teeth
Anodontia- no teeth at all
Hypodontia associated with microdontia in severe cases

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12
Q

Is hypodontia more common in males or females?

A

Females

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13
Q

Which teeth are most often missing in hypodontia?

A

Caucasians- lower 5s followed by upper 2s

Mongoloids- lower incisors

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14
Q

What related syndromes/conditions are associated with hypodontia

A

Ectodermal dysplasia- scanty hair, eyebrows, pouty lips, bat ears
Ellis van Creveld Syndrome
Down’s syndrome
Cleft

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15
Q

What is the management for hypodontia?

A

Clinical and radiographic assessment
Regular preventive care (to prevent further loss of teeth)
Restore aesthetics/function

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16
Q

What extra/accessory root is common on lower 6s

A

Distolingual root

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17
Q

Which teeth commonly have extra/accessory roots?

A

Lower 6s, canines, premolars, teeth with large cusp of Carabelli (mesiopalatal of upper 6s/7s)

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18
Q

What dental treatment does extra roots affect and how?

A

Extractions- iatrogenic fracture/difficult to remove
Ortho- tooth might not move
Endo- missing root canal during endo will cause persistent infection

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19
Q

Which teeth are more affected by reduced root numbers

A

Single, pyramidal root form
<1% of 1st molars
15-40% of 2nd and 3rd molars

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20
Q

What are the two kinds of double teeth?

A

Fusion- 2 tooth buds join together, fewer total number of teeth
Gemination- 1 tooth germ splitting into 2, total tooth number correct

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21
Q

Which teeth are most commonly affected by double tooth

A

Incisors

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22
Q

What are implications of primary double tooth?

A

double permanent tooth, hypodontia or hyperdontia possible
Caries at joint
Resorption affect exfoliation and eruption

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23
Q

What are the management options for double tooth

A

Place fissure sealant if deep grooves present.
Monitor root resorption of primary double tooth to prevent delayed eruption of permanent successor
May need to divide tooth for aesthetic/ortho reasons (if they have separate pulp chambers)

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24
Q

When to intervene for double tooth

A

When permanent tooth supposed to be erupting

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25
Q

Where is talons cusp most prominent

A

Upper central incisors

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26
Q

How can you classify anomalies affecting enamel and dentine?

A

Genetic- enamel/dentine only OR systemic?

Environmental- localised or generalised?

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27
Q

Where is cusp of carabelli located

A

Mesiopalatal of upper 6, may also be seen on upper second primary molar

Usually bilateral

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28
Q

Implication of cusp of carabelli

A

May have associated root if large, be careful during exo

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29
Q

What is paramolar cusp

A

Extra cusp on buccal of molars

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30
Q

What are characteristics of hypomineralised AI

A
  • Initial normal thickness of enamel
  • Dark yellow/brown/chalky white depending on degree of hypomin
  • Enamel may wear away to expose rough sensitive dentine
  • Xray: difficult to distinguish enamel and dentine–> moth eaten appearance
  • Hypomaturation- snowcapped teeth, some parts chalky white
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31
Q

What is dens in Dante

A

Severe form of dens invaginates, look like tooth within a tooth

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32
Q

Complications of dens invaginatus

A

Caries may develop in invaginatus

Enamel lining may be incomplete or very thin, dentin deficient hence when there are caries there is rapid involvement of th pulp —> direct communication with pulp leading to acute dental alveolar infection

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33
Q

Characteristics of X-linked AI

A
  • males more severely and uniformly affected (no normal x chrom to balance out)
  • females vertical bands of normal/abnormal enamel (1 normal x chrom)
  • no male-to-male transmission
  • heterozygous females may pass trait to children of any sex
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34
Q

Dens invaginatus more common in males or females

A

Males

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35
Q

What is dens evaginatus

A

Enamel covered tubercle projecting from tooth surface, usually occlusal

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36
Q

Which teeth are more likely to have dens evaginatus

A

Premolars
Canines, molars
Lower more likely than upper

Usually bilateral

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37
Q

Management of Leong’s premolar

A

PRR soon after eruption, reinforce tubercle with CR. This is to prevent fracture, allow slow natural attrition, allowing pulp to recede and lay down reactionary dentine

If evaginatus in occlusion, PRR with pulpal protection (always assume pulp exposed). Compare with baseline 6 months later on xray to check for continued root development ie vitality

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38
Q

Management of dilacerated tooth

A

If mild, tooth may erupt, then you can reshape for aesthetics

If fail to erupt, track down orthodontically or remove surgically.

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39
Q

What are the dental changes in a patient with congenital syphilis

A

Moon/mulberry molar

Hutchinson’s incisor

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40
Q

What is management for Molar-incisor hypomin

A
  • SSC for molars if not suitable for CR/GIC
  • CR veneers for incisors if aesthetics compromised
  • If molars severly compromised, analyse occlusion, KIV extraction (timing to allow 7s to erupt in place of 6, extract when 7s’ furcation beginning to form)
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41
Q

What is moon’s and mulberry molar

A

Moon’s molar: reduction/narrowing of crown form towards occlusal surface of 6s

Mulberry: hypoplasia of early mineralising parts of 6s, cusps and fissures cannot be seen clearly

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42
Q

What syndrome is globodontia associated with

A

Otodental syndrome

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43
Q

How can you classify anomalies affecting enamel?

A

Genetic- enamel only OR systemic?

Environmental- localised or generalised?

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44
Q

How is amelogenesis imperfecta inherited?

A

AD, AR and X-linked

45
Q

What are the different classifications of AI?

A

Hypoplasia (deficiency in tissue matrix) quantitative defect

Hypomineralisation- hypocalcification (more severe, very soft enamel) and hypomaturation qualititative defect

46
Q

What are characteristics of hypoplastic AI

A

Thin enamel: smooth/rough/pitted/grooved
Generalised spacing if enamel uniformly thin
May have delay in eruption, unerupted teeth undergo replacement resorption
AOB in 60% of cases

47
Q

Which teeth do globodontia affect

A

Canines and posterior teeth of both dentition

48
Q

Otodental syndrome associated with

A

High frequency deafness

Globodontia

49
Q

What other disorders is taurodontism associated with

A

Klinefelter’s syndrome
Ectodermal dysplasia
Amelogenesis imperfecta (20%)

50
Q

Etiology of taurodontism

A

Delayed invagination fo HERS

51
Q

Presentation of taurodontism

A

Apical extension fo trunk of teeth resulting in enlarged pulp chamber and short roots

Cervical constriction may not be obvious

52
Q

Implications of taurodontism

A

Harder to rct

Roots more likely to fracture during exo

53
Q

Megadontia associated with

A

Pituitary hypergigantism (generalised megadontia)

Hypertrichosis

Hereditary gingival hyperplasia

On the side with hemifacial hypertrophy

54
Q

How to differentiate megadontia and gemination

A

Lack of incisal notching and pulpal bifurcation

55
Q

Microdontia most common affects which teeth

A

Permanent upper lateral incisors and 8s

56
Q

Microdontia associated with

A

Pituitary dwarfism
Ectodermal dysplasia
Down’s syndrome

Severe microdontia associated with hypodontia

57
Q

Increase in root size which tooth most commonly

A

Upper canines

58
Q

Increase in root size associated with

A

Megadontia

59
Q

Characteristics of autosomal dominant A.I.

A
  • 50% chance of passing condition
  • Both genders equally affected
  • Both dentitions affected (perm more severe)
  • Many phenotypes (hypomin/hypoplastic)
  • unerupted teeth with coronal resorption, taurodontism, AOB
60
Q

Characteristics of autosomal recessive AI

A
  • Parental consanguinity, limited gene pool
  • both parents unaffected careers, 1/4 chance pass on
  • associated with ocular effects
61
Q

Characteristics of X-linked AI

A
  • males more severely and uniformly affected (no normal x chrom to balance out)
  • females vertical bands of normal/abnormal enamel (1 normal x chrom)
  • no male-to-male transmission
  • heterozygous females may pass trait to children of any sex
62
Q

Decrease in root size associated with

A

Dentin and pulp dysplasia
Hypoparathyroidism
Excessive irradiation of jaw during root formation

63
Q

What can cause arrest of tooth germ development

A

Osteomyelitis

Irradiation of jaw during childhood (tumour, lack of shielding)

Severe trauma

Untreated chronic pulpal infection of primary tooth predecessor

Fracture of jaw (if tooth germ in the line of fracture)

64
Q

Cause of odontodysplasia

A

Disturbance of blood supply during perinatal period

65
Q

Odontodysplasia affects primary and/or secondary dentition, which part of dentition

A

Either dentition (primary usually more severe)

Segment in the arch ie REGIONAL, not entire dentition affected

66
Q

Presentation of odontodysplasia

A

Small brown teeth with rough soft surface

Pain, swelling, delayed eruption

X ray:
Mild cases root formation almost normal or roots develop a few years after normal teeth. Tooth may be restorable depending on amount of coronal structure

In severe cases, there is little differentiation of dental tissues

67
Q

Which AI would be easier to treat? hypoplastic or hypomin

A

Hypoplastic- still have enamel of good quality, can bond CR to it, in fact the pits and grooves could increase retention

68
Q

What is the management of AI?

A
  • Genetic counselling
  • Good preventive program
  • SSC for molars, overdenture to maintain VD, prevent overclosure
  • CR veneers
  • Orthodontic, orthognathic for AOB
  • Definitive crowns/veneers deferred till late teens
69
Q

What is tricho-dento-osseous syndrome

A

SYSTEMIC disorder leading to enamel defects, amongst other ectodermal defects

  • tight curly HAIR
  • Cortical OSTEOSCLEROSIS
  • Thick and cornified NAILS
  • TEETH as in mixed AI
70
Q

What is epidermolysis bullosa dystrophica

A
  • Multiple bullae of mucus membrane (for e.g. GIT) and skin
  • Dystrophic nails
  • Fine pitting hypoplasia of enamel (honeycomb octogonal shape), similar to hypoplastic AI
71
Q

Is Molar-incisor hypomineralisation systemic or enamel only?

A

Systemic origin, aetiology uncertain, probably multifactorial with genetic disposition+environmental insult

72
Q

What does molar-incisor hypomineralisation present as?

A

Hypomin of 1-4 of 1st permanent molars, with affected permanent incisors

  • Cheese molars, enamel friable
  • Defects well demarcated, asymmetric distribution (indicating genetic and not environmental)
  • Incisors less severely affected (irregularly distributed mottling) similar to fluorosis but fluorosis will be timebased
73
Q

What is management for Molar-incisor hypomin

A

SSC for molars if not suitable for CR/GIC

74
Q

What can cause localised enamel defect due to environmental changes?

A

Infection, trauma of primary teeth

75
Q

What can cause generalised enamel defect due to environmental changes?

A

Environmental changes during tooth development
- Prematurity
- Malnutrition
- Exanthematous fevers (viral fevers like measles, mumps, chicken pox)
- Excessive ingestion of F
Can be seen as a horizontal band of hypomin across the teeth

76
Q

What are the genetically determined dentine defects involving dentition only? (3)

A
  1. Dentinogenesis Imperfecta
  2. Coronal dentine dysplasia
  3. Radicular dentine dysplasia
77
Q

What is the mode of inheritance for D.I.

A

Autosomal dominant, rare

78
Q

Which teeth are affected by D.I.?

A

All teeth, primary teeth usually worse

79
Q

What is another name for D.I.?

A

Hereditary opalescent dentine

80
Q

Appearance of teeth affected by DI

A

Opalescent bluish/brownish
Enamel chips way at ADJ exposing soft dentine which wears away rapidly (enamel supported by soft dentine, reduced scalloping at ADJ, so chip away)
Severe attrition and wear

81
Q

Appearance of teeth on X-ray in DI

A

Bulbous crown, short roots (mostly dentine), obliteration of pulp chamber and root canals by abnormal dentine

82
Q

Is enamel affected in DI?

A

Yes- in 1/3 of cases, enamel hypomineralised

83
Q

What are histological findings in DI?

A
  • 1/3 of cases enamel hypomin
  • Flattening of ADJ
  • Dentine matrix amorphous
  • Tubulues abnormal size and shape, haphazard
84
Q

What is the main challenge in treating DI?

A

Difficult because unstable base for restorative work

85
Q

Features of coronal dentine dysplasia

A
  • Primary teeth amber and translucent
  • Permanent teeth normal colour
  • X-ray thistle/flame shaped pulp chambers, multiple pulp stones, thin root canals
86
Q

Features of radicular dentine dysplasia

A

All teeth affected

  • Normal colour or light brown to bluish, clinically difficult to detect
  • Rootless teeth/ non opalescent dentine
  • Xray: Crowns normal shape, roots short and blunt, pulp chambers small/obliterated
87
Q

What are possible problems that may appear in radicular dentine dysplasia?

A

Sudden dentoalveolar infection- pulpal necrosis, unable to do RCT because pulp chamber small/obliterated

88
Q

What are features of Osteogenesis imperfecta?

A

Systemic condition

  • Impaired hearing
  • Brittle bones, bowed legs, easily fractured
  • Blue sclera
  • 1/2 have DI, not all permanent teeth equally affected
89
Q

Can trauma cause only dentine defect without enamel defect?

A

No. Severe trauma/infection to primary teeth may cause formation of interglobular dentine below area of hypoplastic enamel on succedaneous teeth.

90
Q

What could lead to generalised environmental dentinal defect

A
  • Tetracycline taken during tooth formation, discolouring dentine, delaying dentinogenesis
  • Irradiaation and hypothyroidism retards dentinogenesis
91
Q

What are the defects of pulp?

A
  • Pulp stones–> Coronal pulp of older patients (90% of >50 y/o), asymptomatic, incidental xray finding, problem with RCT
  • Diffuse pulpal calcification–> May follow trauma, gradual obstruction of root canal, or associated with D.I.
92
Q

What are the genetic defects of cementum?

A

Genetic

  • Cleidocranial dysostosis (AD)–> hypoplasia of cementum, may be related to delay/failure of eruption
  • Hypophosphatasia (AR)–> Aplasia/hypoplasia of cementum, lack of perio attachment, early loss of primary teeth (teeth are whole without root resorption when exfoliating)
93
Q

What are the environmental defects of cementum?

A

Excessive deposition of cementum (hypercementosis)

  • Chronic infection
  • Traumatic occlusion
94
Q

What are causes of extrinsic tooth staining/discolouration?

A
  • Chromogenic bacterial flora–> very tenacious stains, cannot be removed just with prophy cup, use spoon excavator to scrape and agitate a bit before prophy. When moving into mixed dentition, flora may change, stains will stop
  • Food/drinks/poor oral hygiene- tea, coffee
  • Supplements high in iron
95
Q

What are causes of intrinsic tooth stains

A
  • Localised: caries, internal resorption (pink tooth), trauma, infection of primary teeth
  • Generalised: tetracycline, fluorosis, AI, DI, biliary atresia (blockage of bile duct, teeth look yellow-green)
96
Q

What are the anomalies of tooth eruption?

A
  • Premature
  • Ectopic
  • Delayed
97
Q

What is the difference between natal and neonatal teeth?

A

Natal (at birth), neonatal (within 1st month of birth) 1:2000/3000 births

98
Q

Are natal/neonatal teeth supernumeraries or primary teeth

A

May be supernumeraries but usually primary teeth

99
Q

What are the problems with premature eruption?

A
  • Mobile (lack of root development)
  • Surrounding gingiva may be inflamed
  • May cause trauma during feeding or danger of aspiration
100
Q

What is the management of prematurely erupted teeth?

A

Leave to firm up or extract if not supported sufficiently

101
Q

What is the cause of ectopic eruption?

A
  1. Ectopic crypt position

2. Presence of supernumerary teeth/odontomes causing deflection of path of eruption

102
Q

What are causes for generalised delayed eruption

A
  1. Down’s and Turner’s syndrome
  2. Premature/low birth weight
  3. Cleidocranial dysostosis
  4. Gross malnutrition
  5. Reduced growth hormones
103
Q

What are causes for localised delayed eruption?

A
  1. Early loss of primary molars (<7 years) may delay eruption of premolars
  2. Supernumerary teeth/ odontomes
  3. Fibrous tissue overlying erupting tooth
104
Q

What causes premature localised exfoliation?

A
  1. Pulpal infection spreading to periradicular tissue

2. Ectopic eruption of 6–> resorption of distal root and early loss of E

105
Q

What causes premature generalised exfoliation?

A
  1. Hypophosphatasia- cementum defect, periodontal attachment missing
  2. Histocytosis X
106
Q

What causes localised delayed exfoliation?

A
  1. Primary double teeth
  2. Congenital absence of permanent successor
  3. Infraocclusion of primary tooth
107
Q

What causes generalised delayed exfoliation?

A

Down’s and Turner’s syndrome

108
Q

When does physiological root resorption begin in primary teeth?

A

Soon after root formation complete at 3-4 years

Intermittent process with process of repair

109
Q

What causes pathological root resorption?

A

Complication following trauma, infection, excessive ortho forces, impacted/supernumerary teeth

Pedo (12 decks)

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