Eruption and exfoliation abnormalities; abnormalities of structure Flashcards
Types of dental abnormalities (5)
Number Size Shape/ form Eruption/ exfoliation Structure
Eruption disturbances affect (7)
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.)
Exfoliation disturbances affect (7)
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
Abnormalities of structure (4)
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
Regional ‘ghost teeth’ causes
Odontodysplasia
All of tooth germ is disrupted
Chemotherapy, radiotherapy **
Enamel defect types (3)
- Hypomineralisation: quality
- opacity (porous) - Hypoplasia: quantity
- pits, grooves, areas, absence - Discolouration (intrinsic)
Causes of enamel defects (2)
Circa 100 causes described
Different causes - same appearances
Aetiology of dental anomalies (3)
Genetic (polygenic) -primary involved enamel - Al -associated with generalised disorders, syndromes Environmental -systemic/ chronological -local -timing (development, insult) Multifactoral
Genetic factors in enamel defects (2)
- non-chronological
* affect both dentitions to variable extent
Environmental factors in enamel defects (2)
- chronological e.g. trauma, infection, systemic illness
* “non-chronological” e.g. prolonged fluoride e
Systemic effects leading to ?enamel defects? (2)
• Maternal/foetal conditions (rubella; 1° teeth)
• Pre-term/lbw/neonatal
• Fluoride
• Severe/chronic childhood illness
(fevers: measles, chicken pox; tetracyclines)
Localised defects leading to ?enamel defects? (2)
- Infections/trauma
* Cleft lip/palate
Idiopathic/ environmental factors leading to ?enamel defects? (1)
• Molar-incisor hypomineralisation (MIH) (defect 1)
“Cheese molars” (Popcorn teeth)
Features of opacity (defect 1) (4)
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
Enamel opactities (defect 1) - poorly mineralised zones (4)
• full enamel thickness maturation permanently interrupted • surface unaffected ameloblasts returned to normal maturation • Enamel “softer” • May be lost (PEB)
Flouride-induced opacities (defect 1) (5)
- Opacities (brown), enamel loss
- Primary and permanent
- Posterior and anterior (development)
- Dose dependant (variety of appearances)
- Symmetrical distribution
Featuers of hypoplasia (defect 2) (5)
Quantitative Deficient matrix production Thin Pits, grooves, areas Chronological: 'matching' teeth affected Systemic effect/ upset
Localised hypoplasia (6)
“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
Variation in tooth colour (defect 3) may be due to (4)
• 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
Studies of developmental defects of enamel (7)
Prevalence Aetiology Indices FDI DDE 1982, 1992 Enamel Defects Index EDI 2001 • Hong Kong • British school children • Romano-Britons • Low birthweight
Enamel defect prevalence in white Caucasian school children (4)
Population prevalence -68% opacity -14.6% hypoplasia Tooth prevalence -opacity 13.5% -hypoplasia 1.7%
Amelogenesis imperfecta epidemiology (5)
• 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
Amelogenesis imperfecta classification (5)
• 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)
Amelogenesis imperfecta - what does it look like? (5)
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
