Dental Anomalies in Children Flashcards
1
Q
What enamel defects can affect the deciduous dentition?
A
- May be discoloured by abnormal pigments circulating in the blood
- Severe neonatal jaundice: yellow teeth maybe with bands of greenish discolouration
- Congenital porphyria: red or purple teeth
- Tertacycline given during dental development
2
Q
What can be the cause of enamel defects in single permanent teeth
A
- Local causes such as PA infection of a predecessor (Turner teeth)
- Trauma from intubation while a preterm neonate
3
Q
What is the aetiology and incidence of amelogenesis imperfecta?
A
- Group of hereditary conditions that affect the structure and appearance of dental enamel, often in conjunction with changes in other EO, IO tissues
Aetiology
- Mutations in genes that encode enamel matrix proteins or other proteins/enzymes required to process or mineralise the matrix
- Most cases familial
- Initial stages of enamel formation: secretion of matrix proteins enamelin, amelogenin and ameloblastin
- Later stages: mineralisation and maturation
Incidence
- 1:14,000 usually
4
Q
What are the clinical features of Amelogeneis imperfecta? What is the differential diagnosis
A
- Characteristically all teeth are affected (deciduous and permanent)
- Defects involve the whole enamel or randomly distributed patches of it
- Eruption often delayed
- Sensitivity, caries/acid susceptibility (rapid wear), poor aesthetics, poor OH and AOB
- Pulpal calcification, pathological crown/root resorption, taurodontia
Differential diagnosis
- Dental fluorosis
- MIH
- Enamel chronological hypoplasia
- Trauma
5
Q
What is the classification of amelogeneis imperfecta?
A
- Based on pattern of inheritance, type of defect and appearance
Hypoplastic
- Cause: ameloblasts fail to produce appropriate thickness of enamel
- Features: matrix formation reduced, but normal in structure. Enamel randomly pitted, grooved or uniformly thin, hard and translucent. Defects tend to become stained
- Inheritance: autosomal dominant, recessive and X-linked forms
Hypomature
- Cause: Defect in final protein processing and crystallite growth causing defective matrix thus defective mineralisation
- Features: Normal enamel thickness but soft and vulnerable to attrition. Opaque white to brown-yellow patches - Mottled appearance
- Inheritance: autosomal recessive or X-linked
Hypocalcified
- Cause: Defect in initial crystallite mineralisation causing defective matrix thus defective mineralisation
- Features: Commonest type causing normal enamel thickness and form but enamel is poorly calcified, chalky, very soft and teeth tend to stain
- Inheritance:
6
Q
How is amelogeneis imperfecta managed?
A
Principles
- Pain management
- Prevention (OHI, diet, TSL, early dx, FS)
- Stabilisation - maintain OVD
- Restore any defects - aesthetics
- Maintenance
Primary dentition
- GIC/composite (anterior)
- SS crown/GIC (posterior)
Mixed dentition
- FPM: PMC or gold only/crown
- Delayed eruption: operculectomy for OH or GIC
- Permanent incisors: composite veneer
Premolars
- If sensitivity not issue and not in occlusion then no intervention (no aesthetic issue)
- If is an issue then full coverage restoration
Canines
- More likely to be aesthetic concern/wear/sensitivity
- Composite veneer
Quality/quantity of enamel
- Enamel intact but discoloured - bleaching and/or microabrasion to improve aesthetics
- If enamel or dentine cannot be bonded - full coverage restoration will be required
7
Q
What are the features of chronological hypoplasia and what may they result from
A
- Any severe disturbance of metabolism can halt enamel formation (dentine is less sensitive to insult so usually have normal shaped tooth with band of enamel missing)
Typical Effect:
- One or more rows of horizontally disposed pits, grooves or completely missing band of enamel horizontally across the crowns
- Pattern can aid in determining the timing of the systemic disease
May result from:
- Systemic infection: rubella, measles, childhood fevers, severe infantile gastroenteritis
- Nutritional defects, protein deficiency, lack of vitamins (A,C,D (rickets))
- Metabolic disturbance in utero (e.g. maternal disorder) or around birth affects primary teeth
8
Q
What is the features, aetiology and management of MIH?
A
Features
- Hypomineralisation of all first permanent molars and incisors
- Molars usually worse affected than incisors
- Teeth erupt normally and have patchy opaque and yellow patches on enamel of occlusal third of crown
- Enamel surface is hard, but the underlying enamel is soft and breaks down, leaving stained rough and soft surface that is prone to caries
- Teeth affected are hypersensitive
Aetiology
- Wide range of illnesses => failure of enamel maturation
Management mildly affected molars
- Fluoride varnish with partially erupted
- FS when fully erupted
- CR restorations if breakdown or caries
Management mildly affected incisors
- Etch-bleach-seal approach in younger children for brown-yellow defects
- Resin infiltrate
- White defects: micro abrasion followed by CR if needed
- CR restorations following enamel reduction
Management moderate/severe affected molars
- xla
- Fluoride varnish or GIC in partially erupted
- CR restorations for up to 3 surfaces
- PMCs or full porcelain crown in adulthood
Management moderate/severe affected incisors
- Wait until defect gets better as mineralisation may occur in salivary environment
- CR restorations or veneers following micro abrasion
- Porcelain veneer if needed in adulthood
9
Q
What is the aetiology and features of osteogenesis imperfecta with opalescent teeth (defective dentine)
A
Aetiology
- Uncommon collagen type I gene defect - collagen formation affected - bone and dentine formation disturbed
- Relative severity of the teeth/bone defect depends on the mutation
- Types III and IV are those more frequently associated with dentine defects
Features
- Dentine is soft and has abnormally high water content
- Primary teeth usually opalescent, discoloured and show attrition
- Class III malocclusion is associated in >70% of pts
10
Q
Aetiology of dentinogeneis imperfecta
A
- Hereditary developmental disturbance of the dentine. May be seen alone or in conjunction with the systemic hereditary disorder of the bone, osteogenesis imperfecta
Aetiology
- This condition produces identical changes in appearance and structure of teeth to those in osteogenesis imperfecta but is caused by mutations in dentine sialoprotein, a dentine matrix protein rather than collagen genes
11
Q
What are the features of dentinogenesis imperfecta
A
- Enamel uniformly grey-brown-purple and translucent (giving opal appearance)
- Affects primary and permanent dentitions
- Dentine is dysplastic with large tubules, uncalcified matrix, odontoblasts and BVs trapped in advancing front of dentine formation
- Dentine formation progresses to obliterate the pulp chamber at an early age
- Crown shape and size normal, but slender and stunted roots
- Weak zone in the dentine just below the ameldodentinal junction, and the lack of resilient dentine to support the enamel allows enamel to chip away, exposing the dentine which is soft and wears rapidly
- No predisposition to caries
- Radiographically the teeth have bulbous crowns, cervical constructions, thin roots and early obliteration of the root canal and pulp chambers due to excessive dentine production
12
Q
What is the management of dentinogenesis imperfecta
A
- Tx aims: preserve VD, avoid xla to prevent space loss and allow normal alveolar bone growth for implants later
- Routine restorative techniques can be used to treat mild-moderate DI
- Full coverage restorations for more severe cases with significant enamel wear
- Ideally restorative stabilisation of dentition completed before excessive wear and loss of VD
- Bleaching has been reported to lighted colour with success
13
Q
What are the features of dental dysplasia and what is the aetiology?
A
Features
- Crown shape and size normal but roots absent or very short and conical
- Pulp chambers are obliterated by multiple nodules of poorly organised dentine
- There are pulpal extensions through dentine to the enamel, and vitality lost quickly
- Lack of root predisposes to periodontitis
- Normal coronal E and D, but abnormal tubule patterns in the foot
- Both dentitions affected
Features of less severe
- Deciduous: dentition opalescent (same as DI)
- Permanent: appears normal/nearly normal in colour but with larger pulps
Aetiology
- Defect in dentine sialoprotein gene (classified as severely affected form of DI)
14
Q
What is the aetiology, features and treatment of regional odontodysplasia (defect of D and E)?
A
Aetiology
- Sporadic (not inherited) => possibly a somatic mutation, or vascular or traumatic
Features
- Arrested dental development in localised area, usually unilateral (upper incisors ± canines >80%)
- Affects deciduous and permanent in that one region
- ‘Ghost teeth’: hypoplastic thin hypocalcified enamel, dysplastic thin poorly mineralised dentine, greatly enlarged pulp chambers
- Teeth often fail to erupt and are susceptible to caries and fracture
Treatment
- If they can be preserved and restored, crown and root dentine continue to form and teeth survive long enough to allow normal development of alveolar ridge and occlusion
- However, xla often needed eventually
15
Q
What are the features of segmental odontomaxillary dysplasia (defect of E and D)?
A
- Can be mistaken for regional odontodysplasia (which does not affect bone) or fibrous dysplasia (which does not affect tooth germs)
- Unilateral expansion of alveolar process of maxilla
- Enlargement due to both fibrous enlargement of gingiva and swelling of alveolar bone
- In affected area: delayed eruption of teeth, hypoplastic teeth with enlarged pulps, thin pitted enamel, an irregular pulp/dentine interface, permanent successors may be absent
- Antrum is small, and maxilla is distorted, although rarely to the extent of causing facial asymmetry
