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Dental anomalies for FINALS > Eruption and exfoliation abnormalities; abnormalities of structure > Flashcards

Eruption and exfoliation abnormalities; abnormalities of structure Flashcards

1
Q

Types of dental abnormalities (5)

A 
Number
Size
Shape/ form
Eruption/ exfoliation
Structure
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2
Q

Eruption disturbances affect (7)

A

Premature (will be extracted as can cause problems)
-primary or secondary
-natal/ neonatal
-hbw (high birth weight)
-hormonal abnormalities
Delayed
-lbw/ pre-term
syndromes e.g. Down’s, Turner’s / endocrinopathies e.g. hypoparathyroidism, hypopituitarism
-impaction e.g. upper 8s on 7s, upper 6s on Es/ supernumerary
-early extraction of 1.
Differences: jaws, race and gender (2.)

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3
Q

Exfoliation disturbances affect (7)

A

Premature
-trauma
-extraction (these two not true exfoliation)
-immune e.g. cyclic neutropenia/ cementum deficiencies e.g. hypophosphatasia
Delayed
-infraocclusion (submerged): 1. > 2.; 4, 5, absent; genetic (may become ankylosed to bone)
-ectopic successors
-double 1.
-hypodontia

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4
Q

Abnormalities of structure (4)

A

All tissues
-arrested development
-odontodysplasia
Enamel defects
-hypomineralistion (defect 1) - altered translucency
-hypoplasia (defect 2) - variation in thickness
-discolouration (defect 3) - intrinsic discolouration
Dentine defects
Cementum defects

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5
Q

Regional ‘ghost teeth’ causes

A

Odontodysplasia
All of tooth germ is disrupted
Chemotherapy, radiotherapy **

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6
Q

Enamel defect types (3)

A
  1. Hypomineralisation: quality
    - opacity (porous)
  2. Hypoplasia: quantity
    - pits, grooves, areas, absence
  3. Discolouration (intrinsic)
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7
Q

Causes of enamel defects (2)

A

Circa 100 causes described

Different causes - same appearances

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8
Q

Aetiology of dental anomalies (3)

A 
Genetic (polygenic)
-primary involved enamel - Al
-associated with generalised disorders, syndromes
Environmental
-systemic/ chronological
-local
-timing (development, insult)
Multifactoral
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9
Q

Genetic factors in enamel defects (2)

A
  • non-chronological

* affect both dentitions to variable extent

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10
Q

Environmental factors in enamel defects (2)

A
  • chronological e.g. trauma, infection, systemic illness

* “non-chronological” e.g. prolonged fluoride e

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11
Q

Systemic effects leading to ?enamel defects? (2)

A

• Maternal/foetal conditions (rubella; 1° teeth)
• Pre-term/lbw/neonatal
• Fluoride
• Severe/chronic childhood illness
(fevers: measles, chicken pox; tetracyclines)

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12
Q

Localised defects leading to ?enamel defects? (2)

A
  • Infections/trauma

* Cleft lip/palate

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13
Q

Idiopathic/ environmental factors leading to ?enamel defects? (1)

A

• Molar-incisor hypomineralisation (MIH) (defect 1)

“Cheese molars” (Popcorn teeth)

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14
Q

Features of opacity (defect 1) (4)

A

Opaque patches (white/ cream; yellow/ brown)
Hypomineralisation (hypocalcified/ hypomature)
disruption to mineralisation at maturation stage; porosity (subsurface/ surface)
Appearance: altered translucency, altered texture (porosity)
Boundary: demarcated, diffuse
Distribution: localised (1 or 2 teeth), generalised (all teeth), symmetrical/ asymmetrical

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15
Q

Enamel opactities (defect 1) - poorly mineralised zones (4)

A 
• full enamel thickness
maturation permanently interrupted
• surface unaffected
ameloblasts returned to normal maturation
• Enamel “softer”
• May be lost (PEB)
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16
Q

Flouride-induced opacities (defect 1) (5)

A
  • Opacities (brown), enamel loss
  • Primary and permanent
  • Posterior and anterior (development)
  • Dose dependant (variety of appearances)
  • Symmetrical distribution
17
Q

Featuers of hypoplasia (defect 2) (5)

A 
Quantitative
Deficient matrix production 
Thin
Pits, grooves, areas
Chronological: 'matching' teeth affected
Systemic effect/ upset
18
Q

Localised hypoplasia (6)

A 
“Turner” tooth
• Affects 1-5 only
• Trauma or infection of 1°
• Damage to underlying developing permanent tooth germ
• May also exhibit hypomineralisation
• Commonly affects 4s and 5s
19
Q

Variation in tooth colour (defect 3) may be due to (4)

A

• changes in tooth thickness and/or structure -
i.e. hypoplasia or hypomineralisation
• incorporation of circulating substances/pigment
deposits - e.g. metabolic disorders - circulating bilirubin, tetracycline; during
development
• incorporation of pulp products e.g. loss of vitality and infection; not developmental
• exogenous agents
i.e. extrinsic, not developmental; e.g. bacterial, dietary

20
Q

Studies of developmental defects of enamel (7)

A 
Prevalence
Aetiology
Indices FDI DDE 1982, 1992
Enamel Defects Index EDI 2001
• Hong Kong
• British school children
• Romano-Britons
• Low birthweight
21
Q

Enamel defect prevalence in white Caucasian school children (4)

A 
Population prevalence
-68% opacity
-14.6% hypoplasia
Tooth prevalence 
-opacity 13.5%
-hypoplasia 1.7%
22
Q

Amelogenesis imperfecta epidemiology (5)

A

• Hereditary
• 1:700 to 1:14000 prevalence
• Enamel defects, not associated with systemic
abnormality (antr open bite, cone-rod dystrophy, hearing
impairment, renal calcifications; Heimler syndrome)
• Single gene mutations, genes critical for enamel
formation:
e.g. amelogenin (AMELX), enamelin (ENAM)
PEX1 and 6
• Inheritance patterns – AD, AR, X-linked

23
Q

Amelogenesis imperfecta classification (5)

A

• Hypomineralised (defect 1) - hypomature
- hypocalcified
• Hypoplastic (defect 2)
• Mixed (14-15 types), diverse phenotypes
• Classification:
Clinical and radiographic appearance, mode of inheritance,
molecular defect, biochemical result (2003);
Hypoplastic, hypomature, hypocalcified and
hypomature hypoplastic with taurodontism (2006)
• 1° and 2° affected by most types (2° worse)

24
Q

Amelogenesis imperfecta - what does it look like? (5)

A 
Decreased matrix, mineralisation normal
• Bilateral symmetry, but not always
• RG contrast lost
• Soft enamel wears away
• Snowcapped- incisal portions of anterior
occlusal portions of posterior
25
Q

Amelogenesis imperfecta - variation in expression - why? (3)

A 
• Different clinical pictures with same gene
• Non-penetrant
No expression of gene
Due to modifying effects of other genes
• Environmental factors
26
Q

Amelogenesis imperfecta - variation in expression (5)

A 
• Within families
• Within individuals
-between dentitions
-within dentition
-within tooth
27
Q

Lyonisation (3)

A

• In females, random inactivation of one X chromosome
(Mary Lyon, 1961)
• Bands of normal and abnormal enamel
• Not seen in males (XY)
Thin enamel – more severely and uniformly affected

28
Q

Other genetic enamel defects associated with generalised disorders (4)

A
  • epidermolysis bullosa
  • tuberous sclerosis
  • vitamin D-dependent rickets
  • microdento-osseous syndrome
29
Q

Anomalies of dentine categories (2)

A

Genetic

Environmental

30
Q

Genetic anomalies of dentine (7)

A 
Limited to dentine:
1. Dentinogenesis Imperfecta (DI)
2. (Radicular) Dentine Dysplasia (DD)
3. Fibrous Dysplasia
Associated with generalised disorder:
1. Osteogenesis Imperfecta (OI) w DI (type I)
2. Ehlers-Danlos Syndrome
3. Vit D-dependent and -resistant rickets
4. Hypophosphatasia
31
Q

Dentinogenesis imperfecta (DI) (6)

A

• Hereditary opalescent dentine
• Commonest form
• Prevalence 1 : 8000, AD, DSPP gene
• Defect in non-collagenous dentine matrix proteins
(DSP, DPP and DGP; 10%)
• Variability in expression, severity
(so reclassified from DI type II, III and DD type II)

32
Q

DI epidemiology and diagnosis (4)

A 
• Teeth opalescent on transillumination,
blue or brown in colour
• All teeth, both dentitions
• 1o > 2o severity
• Severity varies between
and within families
33
Q

DI clinical features (5)

A 
• Bulbous crowns; short, thin roots
• Pulp chamber obliteration
• Flattened ADJ
• Enamel chips away, soft dentine (hypomineralised)
• Dentine abnormal:
tubules↓ and irregular
cellular inclusions from pulp
gradual pulp obliteration
34
Q

DI other variants - continuum of expressions (2)

A

• Thistle or flame-shaped pulps
• “Shell Teeth”
rare, 1o dentition, severely affected cases
large pulp chamber, thin dentine and enamel
“Brandywine isolate hereditary opalescent dentine”
- USA, isolated population

35
Q

Type 1 DI (3)

A

Associated with Osteogenesis Imperfecta (OI)
• group of CT disorders (type I collagen)
• mutation in collagen type 1 genes
• bone fragility, deformity
• lax joints
• blue sclera
• opalescent dentine (90% collagenous protein)
1o teeth resemble DI
2o variable, better prognosis

36
Q

Dentine dysplasia: Rootless teeth radicular dentine dysplasia (5)

A
  • Normal, bluish or brown colour
  • Both dentitions
  • RG normal crown morphology and crown dentine
  • Roots short and blunt, teeth mobile
  • Rare
37
Q

Fibrous dysplasia of dentine (3)

A
  • Lacunae
  • Cellular inclusions
  • 2o, rare
38
Q

Environmental dentine defects (4)

A
  • Local trauma
  • Nutritional deficiencies
  • Drugs
  • Interglobular dentine, predentine and osteoid
39
Q

READ UP ON CEMENTUM DEFECTS

A

READ UP ON CEMENTUM DEFECTS

Dental anomalies for FINALS (4 decks)

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