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Pedo > Dental Anomalies II: Structure, Colour, Eruption/Exfoliation > Flashcards

Dental Anomalies II: Structure, Colour, Eruption/Exfoliation Flashcards

1
Q

What is odontodysplasia?

A
  • Localised, non-hereditary developmental abnormality affecting enamel, dentin and pulp
  • Affects either dentition
  • “Ghost teeth”
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2
Q

What is the presentation of teeth with odontodysplasia?

A
  • Small brown teeth with rough soft surface (often mistaken for caries)
  • May have pain, swelling & delayed eruption
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3
Q

What is the histology for teeth affected by odontodysplasia?

A
  • Markedly irregular enamel
  • Amorphous coronal dentine
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4
Q

What is the radiographic appearance of teeth with odontodysplasia?

A
  • Mild: root formation almost normal or develop a few years after normal teeth
  • Severe: little differentiation of dental tissues => ghost-like
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5
Q

What dental anomalies affect all structures of a tooth?

A
  1. Odontodysplasia
  2. Arrest of tooth germ development
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6
Q

What are causes of arrest of tooth germ development?

A
  • Osteomyelitis
  • Irradiation of jaw in childhood
  • Fracture of jaw
  • Severe trauma or untreated chronic
    pulpal infection (rare) of primary teeth
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7
Q

What is amelogenesis imperfecta?

A

Inherited enamel defects affecting both dentitions

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8
Q

What are the different classifications of amelogenesis imperfecta?

A
  1. Hypoplasia: Quantitative, reduced thickness of enamel
  2. Hypocalcification: Qualitative, hypomineralisation
    - Failure at transition phase (earlier)
    - Less dense than dentine => softest
  3. Hypomaturation: Qualitative, hypomineralisation
    - Failure at maturation phase (later)
    - Same density as dentine
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9
Q

What are the modes of inheritance of AI?

A
  1. Autosomal dominant
  2. Autosomal recessive
  3. X-linked
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10
Q

What are features of hypoplastic AI?

A

Thin enamel: smooth/rough/pitted/grooved
May have:
- Delay in eruption
- Replacement resorption of unerupted teeth
- AOB (60% of cases)

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11
Q

What are features of hypomaturation AI?

A

Normal thickness of enamel
Enamel slightly softer than normal, chips from crown
Radiographically: enamel approximately same radiodensity as dentine

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12
Q

What are features of hypocalcified AI?

A
  • Initially, normal thickness of enamel
  • At eruption, appears dark yellow to brown to chalky white (depending on degree of hypomineralisation)
  • Enamel may wear away to expose rough sensitive dentine
    Radiographically: enamel less RO than dentine
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13
Q

What is the management for AI?

A
  • Genetic counselling
  • Good preventive program – teeth v sensitive
  • SSC for molars or overdentures to maintain VD
  • CR veneers for anterior teeth
  • Ortho for AOB
  • Definitive crowns/veneers deferred until late teens
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14
Q

What are challenges that patients with AI will face?

A
  1. Functional problems
    - Pain + eating difficulties
    - Tooth hypersensitivity
    - Rapid wear => loss of OVD
    - Malocclusion
  2. Poor aesthetics => negative social outcomes
  3. Protracted course of treatment
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15
Q

What are genetic systemic disorders that result in enamel defects?

A
  1. Junctional epidermolysis bullosa
  2. Tricho-dento-osseous syndrome
  3. Molar-Incisor hypomineralisation
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16
Q

What is the presentation of patients with junctional epidermolysis bullosa?

A
  • Multiple bullae of mucous membrane and skin
  • Dystrophic nails
  • Fine-pitting hypoplasia => resemble honeycomb
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17
Q

What is the presentation of patients with tricho-dento-osseous syndrome?

A
  • Type IV AI (hypoplasia + hypomaturation + taurodontism): enamel appears thin + hypoplastic
  • Tight curly hair
  • Thick & cornified nails
  • Increased thickness of cranial bones
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18
Q

What is Molar-Incisor hypomineralisation?

A
  • Qualitative defect (hypomineralisation of systemic origin)
  • Affects 1-4 permanent first molars and incisors
  • Characterised by very rapid breakdown of enamel and is very sensitive
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19
Q

What are the difficulties in management of patients with MIH?

A
  1. Poor adhesion of restorative materials to hypomineralised enamel
  2. Hypersensitivity
    - Difficulty achieving anaesthesia
    - Sensitivity => avoid brushing => prone to caries
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20
Q

What is the management of patients with MIH?

A
  1. Preventive
    - Regular fluoride varnish application
    - FS
  2. Restorative
    Molars:
    - If not suitable for CR/GIC => SSC
    - If severely compromised, exo at 10-11 y/o => 5 can drift to fill space
    Incisors: CR veneers if aesthetics compromised
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21
Q

What are environmental reasons for enamel defects?

A

Localised: Infection/trauma of primary teeth
Generalised: Enamel fluorosis (excessive ingestion of F), prematurity, malnutrition, exanthematous fevers

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22
Q

What is the presentation of patients with enamel fluorosis and what is the difference compared to patients with AI?

A

Generally: mottled enamel
Mildest form: Hypomineralisation of enamel => opacities
Severe form: Manifest as hypoplasia

Differentiate from AI: AI teeth more sensitive

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23
Q

What is the presentation of patients with MIH?

A
  • Enamel friable => “cheese molars”
  • White caps on incisors
  • Defective enamel is normal thickness with smooth surface and can be white, yellow or brown
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24
Q

What are some differences between AI and MIH?

A
  1. MIH only affects permanent teeth, AI affects both dentitions
  2. AI has more generalised defect to dentition compared to MIH
  3. AI can be qualitative or quantitative problem, MIH is qualitative problem
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25
Q

How do you differentiate between MIH and caries?

A

Caries occur at caries prone sites eg proximal surfaces and P&F while teeth as part of MIH do not have post eruptive breakdown at these areas – will usually occur at smooth surfaces

26
Q

What is type IV AI?

A

Hypomaturation-hypoplastic with taurodontism

27
Q

What is the etiology of enamel fluorosis?

A

Developing ameloblasts are affected by the ingestion of high fluoride content water resulting in mottled enamel

28
Q

What are 2 genetic disorders that only affect dentine, with no systemic effect?

A
  1. Dentinogenesis Imperfecta
  2. Dentine Dysplasia (Coronal/Radicular)
29
Q

What is the mode of inheritance of DI and which teeth does it affect?

A

Autosomal dominant. All teeth affected, primary teeth usually worse

30
Q

What is the clinical presentation of teeth with DI?

A
  • Opalescent bluish/brownish colour
  • Soft dentine base supporting enamel => enamel chip away at DEJ => exposed dentine wears away rapidly
31
Q

What is the radiographic appearance of teeth with DI?

A

Radiographic Appearance
- Bulbous crowns
- Short roots
- Obliteration of pulp chamber & root canals by abnormal dentine

32
Q

What is the tx for teeth with DI?

A
  • Difficult due to unstable dentine base for resto work
  • SSC for posterior, strip crown for anterior
33
Q

What is a systemic genetic condition that affects dentine?

A

Osteogenesis Imperfecta
50% have DI (opalescent dentine)

34
Q

What is the clinical presentation of dentine dysplasia?

A
  • Affects both dentitions & all teeth
  • “Rootless teeth”
  • Crowns of teeth are normal in shape & form, colour may be normal or light brown/blue
35
Q

What is the radiographic appearance of teeth with radicular DD?

A
  • Crowns normal shape
  • Roots short & blunt
  • Pulp chamber small/obliterated
36
Q

What is the clinical presentation of teeth with coronal DD?

A
  • Primary: amber & translucent
  • Permanent: normal colour
37
Q

What are the differences between hypocalcified AI and coronal DI?

A

Hypocalcified AI teeth have sensitivity while DI teeth do not.

Hypocalcified AI teeth enamel less RO, DI teeth enamel normal

Hypocalcified AI teeth have normal pulp, DI teeth have thistle-shaped pulp

37
Q

What is the radiographic appearance of teeth with coronal DD?

A
  • Thistle/flamed shaped pulp chambers
  • Multiple pulp stones
  • Thin root canals
38
Q

What is Turner’s tooth?

A

Severe trauma/infection in primary teeth => formation of interglobular dentine below area
of hypoplastic enamel on succedaneous teeth

39
Q

What are some environmental causes for generalised dentine defects?

A
  1. Tetracycline taken during tooth formation => discolour dentine + delay dentinogenesis
  2. Irradiation & hypothyroidism retards dentinogenesis in children
40
Q

What are 2 defects of pulp?

A
  1. Pulp stones
    - Usually in coronal pulp of older px (90% of >50 y/o)
    - Asymptomatic, incidental findings on x-rays
  2. Diffuse pulpal calcification
    - Obliteration of pulp chamber & root canals by abnormal dentine in DI
    - May follow trauma => gradual obstruction of root canal
41
Q

What are 2 genetic conditions affecting teeth and bones that result in cementum defects?

A
  1. Cleidocranial Dysplasia (AD inheritance)
  2. Hypophosphatasia (AR/AD inheritance)
42
Q

What is cleidocranial dysplasia?

A
  • AD inheritance, affects development of teeth & bones
  • Hypoplasia of cementum
  • May be related to eruption delay/failure
43
Q

What is hypophosphatasia?

A
  • AR inheritance, affects development of teeth & bones
  • Aplasia/hypoplasia of cementum
  • Lack of periodontal attachment
  • Premature loss of primary teeth

*aplasia: slight development, less than hypoplasia
*hypoplasia: underdeveloped

44
Q

What is hypercementosis and what are 2 causes of it?

A

Hypercementosis: excessive deposition of cementum
May result from:
- Chronic infection
- Traumatic occlusion

45
Q

What are some reasons for extrinsic discolouration of teeth, and what is the mx?

A
  • Food, drinks
  • Medication
  • Chromogenic bacteria (stains will form again unless microflora change)

Mx: clean w pumice, NaOCl if stubborn stain

46
Q

What are reasons for localised intrinsic discolouration of teeth?

A
  1. Caries
  2. Internal resorption
  3. Trauma/infection of primary tooth
47
Q

What are some reasons for generalised intrinsic discolouration?

A
  • AI, DI
  • Tetracycline/excessive F- during tooth formation
  • Blood borne pigments such as bilirubin, hemosiderin, porphyria
48
Q

What is the normal sequence of eruption for permanent teeth?

A

Max: 61245378
Mand: 61234578

49
Q

When is eruption of primary teeth considered premature?

A

Erupt prior to 3 months of age
- Natal teeth (at birth)
- Neonatal teeth (within 1st month of birth)

50
Q

Which kind of teeth are the most commonly seen in premature eruption?

A
  • 90% true primary teeth, 10% supernumerary
  • Most common: lower incisors
51
Q

What is the clinical appearance of prematurely erupted primary teeth, what are concerns with them?

A

Lack root dev => mobile

Concerns:
- Trauma during feeding (tooth rub against
non-keratinised ventral tongue => ulcer)
- Danger of aspiration if dislodge

52
Q

What is the mx for prematurely erupted teeth?

A
  1. Leave to firm up
  2. Extract if:
    - Major lack of structure
    - Partially detached from tissue
    - Causing major ulcer

Only exo when >10 days old

53
Q

What are causes of ectopic eruption?

A
  1. Ectopic crypt position
  2. Presence of supernumerary teeth/odontomes
    => deflect eruption path
54
Q

When should maxillary canine impaction be suspected?

A

When
1. Canine bulge not palpable at 9-10yo
2. Asymmetric canine eruption
3. Peg shaped laterals (small laterals) => less guidance for canines to erupt

55
Q

What are some reasons for localised delayed eruption of permanent teeth?

A
  1. Ankylosis
  2. Impaction
  3. Supernumerary teeth/odontomes
  4. Trauma
  5. Crowding – could be due to early loss of pri teeth (eg early loss of primary molars => delay eruption of PMs due to lack of space)
  6. Retained primary
56
Q

What are some reasons for generalised delayed eruption?

A
  • Premature/low birth weight babies
  • Down’s syndrome
  • Turner’s syndrome
  • Cleidocranial dysplasia
  • Gross malnutrition
  • Growth hormone deficiency
57
Q

What are 2 reasons for localised premature exfoliation?

A
  1. Pulpal infection spread to periradicular tissue
  2. Ectopic eruption of 6 (mesially) => resorb distal root of E => early exfoliation
58
Q

What are 2 reasons for generalised premature exfoliation?

A
  1. Hypophosphatasia
  2. Histiocytosis X
59
Q

What are 3 reasons for localised delayed exfoliation?

A
  1. Primary double teeth
  2. Congenital absence of permanent successor
  3. Infraocclusion due to ankylosis (mand E most often affected)
    - Majority will exfoliate spontaneously if successor tooth present
    - Monitor need/timing for extraction (may require surgery)
60
Q

What are some 2 syndromes associated with generalised delayed exfoliation?

A
  1. Down’s syndrome
  2. Turner’s syndrome
61
Q

What are some reasons for pathological resorption of teeth?

A
  • Trauma
  • Infection
  • Excessive ortho forces
  • Impacted/supernumerary teeth

Pedo (15 decks)

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