Dental anomolies/abnormalities Flashcards
4 Stages of tooth development
- Initiation - correct number of teeth in the right jaw
- Morphodifferentiation - teeth shape
- Cytodifferentiation - different tissues formed
- Tooth formation
Aetiology of developmental abnormalities
Genetic - Part of a disorder e.g. Down's, Ectodermal dysplasia - Specific gene mutation e.g. DSPP in DI Environmental - Local - Systemic/generalised
Types of tooth development abnormalities (general) [6]
Tooth number Tooth shape Tooth size Tooth eruption Tooth tissues Root abnormalities
Tooth number abnormalities [7]
Hypodontia - Oligodontia (6+ missing teeth) - Adontia Hyperdontia/supernumeraries - Accessory = atypical - Supplemental = normal - Mesiodens in midline
Aetiology of hypodontia and associated factors
Environmental e.g. low birth weight, multiple births, old mother
Associated with Dwarfism, ectodermal dysplasia and Down’s syndromes (+microdontia)
Single gene mutations e.g. PAX9 - U2s
More common in females
Hyperdontia associated factors [6]
More common in males
Associated with cleft palate, invaginated teeth and syndromes e.g. Gardner’s syndrome, Cleidocranial dysplasia, orofacial digital syndrome
Can affect the eruption of teeth
Primary hyperdontia is associated with secondary teeth hyperdontia
Abnormalities of tooth size
Microdontia
- More common in females
- Generalised e.g. Down’s, ectodermal dysplasia
Megadontia
- More common in males
- Generalised e.g. pituitary gigantism, facial hyperplasia
Can be specific to one tooth, generalised, affecting crown, root or whole tooth.
Developmental abnormalities in tooth shape [4]
Double teeth
Invaginated tooth (dens-in-dente)
Evaginated tooth
Accessory cusps
Invaginated teeth [4]
Enamel epithelium grows into dental papilla
Invagination can be into enamel, dentine or pulp
Caries spreads v quickly into the pulp and can be difficult to treat
Most commonly affecting maxillary incisors, and bilateral
AKA dens-in-dente
Diagnose early and prevention (FS, OHE) bc RCT can be difficult w abnormal pulps.
Accessory cusps and problems associated [4] [5]
Evaginations - an outgrowth of dental tissues or focal hyperplasia of ectomesenchyme
Accessory cusps e.g. cusp of carabelli, talon cusps on incisors
Can cause wear on opposing teeth, altered occlusion, plaque retention, fractures, irritated tongue.
Double teeth [4]
Can be 1 tooth germ splitting, or 2 fusing
Can share pulp chambers/canals - more difficult to manage
More common in primary dentition
Can cause eruption problems bc takes longer to resorb the root
Conscrescence
Excess cementum causes teeth to fuse after they’ve formed
Developmental abnormalities of roots
[4]
[3]
Taurodontism Short or large roots Fused/pyramidal roots Extra roots/growths e.g. enamel pearls. Dentine dysplasia and irradiation therapy can affect root formation and cause short roots
Taurodontism [5]
Crown elongated at the expense of roots
No CEJ/neck of the tooth is lost
Large pulp space
Caused by problems to Hertwig’s root sheath and associated w syndromes e.g. AI
Dental eruption developmental abnormalities
[3]
[4]
Premature eruption
- If tooth germ developed too close to epithelium/in the wrong place
- Need to XLA bc these can be mobile, risk of inhalation, get caries, cause trauma, problems feeding
- Found in large birth weight babies or hormonal problems like excessive growth hormone or thyroid hormone
Delayed eruption
- Impacted or ectopic
- Slow development, low birth weight babies, pre-term
- Hormonal abnormalities e.g. hypopituitary or hypothyroid
Dental exfoliation developmental abnormalities
[2]
[2]
Premature exfoliation
- Cementum hypoplasia/aplasia stops PDL from inserting into teeth so they become mobile and fall out
- Nutritional or immune deficiencies destroy PDL
Delayed exfoliation
- No successor tooth
- Submerged/ankylosed
- XLA and maintain space
Abnormalities in tooth tissue structure - environmental aetiology [4] and examples [8]
Environmental
- All or some tissues can be affected
- Depends on timing/severity of insult and what part of the tooth was developing at the time
- Can show as chronological
- Can be localised or generalised
- E.g. chemo, trauma, fluoride, tetracycline, bilirubin, measles, neonatal complications, nutritional deficiencies
Developmental enamel abnormalities
[4]
AI
Hypomineralisation
Hypoplastic enamel
Discoloured
Amelogenesis imperfecta
Autosomal dominant/recessive and X-linked inherited
Gene mutations = AMELX, ENAM, MMP20
4 types:
- Hypomature enamel (hypomineralised)
- Hypocalcified enamel (hypomineralised)
- Hypoplastic enamel
- All + taurodontism
Affects primary and secondary teeth but 2 worse
Associated w AOB, eye and hearing problems
Lots of post-eruptive breakdown bc enamel is weak, poor quality or pitting/grooves/areas of absences
Opacities or brown staining
X-linked - in females, if they have 1 normal copy and 1 mutated, then ameloblasts will be 1 normal, 1 mutated and have a banding pattern on the enamel where some abnormal and then some normal etc. = lyonisation
Enamel Hypomineralisation
Less mineralised = weaker porous enamel, opacities, white/brown/staining.
Can be generalised, localised, have a clear boundary or be diffuse.
Can be fluoride-induced
Teeth get post-eruptive breakdown
Enamel hypoplasia
Less enamel = pitting, grooves, areas of absence
Can be localised, generalised, chronological
Can be due to trauma to the primary tooth which affects the underlying tooth germ (Turner tooth)
Enamel discolouration causes
Intrinsic - fluoride, enamel hypomineralisation or hypoplastic, tetracycline staining (grey/brown), bilirubin into teeth if pt has a hepatic disorder during tooth development (green staining)
Developmental
dentine abnormalities
DI
Fibrous dysplasia affecting dentine (hollows and spaces in the dentine)
Radicular dentine dysplasia
- OI, Ehler’s Danlos affect collagen formation so affect the dentine too (90% collagenous proteins)
Cementum aplasia/hypoplasia
Stops PDL attaching to tooth so teeth get mobile and fall out
