Dental Anomalies II Flashcards
Abnormalities in tooth eruption?
Premature eruption:(primary and permanent teeth)
- Natal/neonatal - born with teeth or within first 30 days of life = can be wobbly and in a superficial position = may be inhaled by baby (usually removed)
- More likely when: Hormonal abnormalities and high birth weight
Delayed eruption:
- More common in low birth weight babies, pre-term syndromes, endrocrinopathies
- Can occur in impaction/ supernumerary/early extraction
Differences - jaws, race, gender
Abnormalities in exfoliation?
Premature abnormalities due to:
- Trauma
- Extraction
- Immune/cementum deficiencies
Delayed:
- Infraocclusion (submerged) = primary>permanent, 4 and 5 absent = genetic
- Ectopic successors
- Double primary
- Hypodontia
Abnormalities in structure?
All tissues:
- Arrested development
- Odontodysplasia - ghost teeth on radiographs (not radiopaque)
Enamel defects
- Hypomineralisation (defect 1)
- Hypoplasia (defect 2)
- Discolouration (defect 3)
Dentine defects
Cementum defects
Enamel defects?
- Hypomineralisation (1)
- Quality
- Opacity (porous)
- Altered translucency - Hypoplasia (quality) (2)
- Pits, grooves, areas, absence
- Variation in thickness - Discolouration (intrinsic) (3)
- Intrinsic discolouration
Aetiology of dental anomalies?
Genetic (polygenic)
- Primarily involving enamel = amelogenesis imperfecta
- Associated with generalised disorders, syndromes
- Non-chronological
- Affects both dentitions to variable extent
Environmental
- Systemic/chronological e.g. trauma, infection, systemic illness
- Non-chronological e.g. prolonged fluoride
- Local
- Timing (development, insult)
If combo of both = multifactorial determination
Examples of systemic effects that can impact tooth development?
Maternal/foetal conditions
Pre-term/low birth weight/neonatal
Fluoride
Severe/chronic childhood illness (fevers: measles, chicken pox, tetracyclines)
What can cause localised defects?
Infections/trauma
Cleft lip/palate
Example of an idiopathic/environmental defect?
Molar-incisor hypomineraisation (MIH) (defect 1)
Presentation of enamel opacity defects - type 1?
Opacity (defect 1)
- Opaque patches (white/cream, yellow/brown)
- Hypominerlisation (hypocalcified/hypomature)
- Disruption to mineralisation at maturation stage
- Porosity (subsurface/surface)
- Altered translucency and texture
- Boundary of opaque defects can be diffuse or demarcated
- Localised to 1 or 2 teeth, generalised (all teeth), symmetrical or asymmetrical
- Poorly mineralised zones through full enamel thickness (due to maturation permanently interrupted) OR surface unaffected (ameloblasts returned to normal maturation)
- Enamel may be softer and may be lost (post eruptive breakdown)
Fluoride induced opacities (defect 1) presentation?
Opacities (brown), enamel loss Primary and permanent Posterior and anteriors (development) Dose dependent Symmetrical distribution
Enamel hypoplasia (defect 2) presentation?
Deficient matrix production
Thin
Pits, grooves, areas
Chronological - matching teeth affected
Localised (turner teeth)
- Affects 1-5 only
- Due to Trauma or infection of primary tooth
- = Damage to underlying developing permanent tooth germ
- May also exhibit hypomineralisation
- Commonly affects 4s and 5s
Variation in tooth colour (defect 3) due to?
Changes in tooth thickness and/or structure - hypoplasia/hypomin
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
Exogenous agents
- E.g. intrinsic, not developmental - diet, bacterial
Prevalence of defects in opacity and hypoplasia in white school children?
Opacity - 68%
Hypoplasia - 14.6%
Amelogenesis imperfecta features?
Hereditary
1:700 to 1:14000
Enamel defects, not associated with systemic abnormalities
Cause - Single gene mutations, genes critical for enamel formation:
- Amelogenin (AMELX)
- Inheritance patterns - AD, AR, X-linked
Can present with hypomineralisation and hypoplastic (defects 1 and 2)
Diverse phenotypes
Bilateral symmetry but not always
Soft enamel wears away
Snowcapped - incisal portions of anterior and occlusal portions of posters can be affected
What is lyonisation?
Bands of normal and abnormal enamel
Seen in females
What disorders may cause enamel defects?
Epidermolysis bullosa
Tuberous sclerosis
Vitamin D dependent rickets
Genetic anomalies of dentine?
Limited to dentine:
- Dentinogenesis imperfecta (DI)
- Radicular dentine dysplasia (DD) = limited to root dentine
- Fibrous dysplasia
Associated with generalised disorders:
- Osteogenesis imperfecta (OI) with DI (type 1)
- Ehlers-danlos syndrome
- Vit D dependent and resistant rickets
- Hypophosphatasia
Dentinogenesis imperfecta features?
Hereditary opalescent dentine 1:8000, AD Defect in non-collagenous dentine matrix protein Defect in DSPP gene Variability in expression, severity
Teeth opalescent on transillumination, blue or brown in colour
All teeth, both dentitions
Primary > permanents
Bulbous crowns, short, thin roots Pulp chamber obliteration Flattened ADJ Enamel chips away, soft dentine quickly wears Dentine abnormal: - Tubules decreased and irregular - Cellular inclusions from pulp - Gradual pulp obliteration
Can have large pulps that are flamed shaped and shell shaped teeth with thin dentine and enamel
Dentine defects caused by genetic abnormalities (type 1 DI)?
Osteogenesis imperfecta
- Group of CT disorders
- Mutation in type 1 collagen genes
- Bone fragility, deformity
- Lax joints
- Opalescent dentine (90% collagenous protein)
- Blue sclera
Primary teeth resemble DI
Permanent teeth variable, better prognosis
Dentine dysplasia features?
Rootless teeth Normal, bluish or brown colour Both dentitions RG normal crown morphology and crown dentine Roots short, blunt, teeth mobile Rare
Fibrous dysplasia of dentine features?
Lacunae
Cellular inclusions
More common in permanent dentition, rare
Environmental dentine defects due to?
Local trauma
Nutritional deficiencies
Drugs
Interglobular dentine, predentine and osteoid
