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BDS4 Paeds > Developmental Anomalies > Flashcards

Developmental Anomalies Flashcards

1
Q

What is hypodontia?

A

Reduced number of teeth

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2
Q

What are the types of developmental dental anomaly?

A

Number
Size and shape
Structure- hard tissue defects
Eruption and exfoliation

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3
Q

Which teeth are most commonly involved in hypodontia?

A

Very uncommon in primary

Most common in permanent- 8, lower 5s, upper 2s (tends to be the last one in the series)

Most common lower incisor missing is central- lateral is coded before central genetically (more detail and shape, larger)

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4
Q

Which conditions are associated with hypodontia?

A

Ectodermal Dysplasia

Down Syndrome

Cleft Palate

Hurler’s syndrome

Incontinentia pigmentii

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5
Q

What are the features of ectodermal dysplasia?

A

Blonde, saddle shaped noses, intolerance to sweating, sparse hair

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6
Q

What can cause a restorative issue when upper laterals are missing?

A

Over-eruption of lower canines

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7
Q

What are the treatment options for hypodontia? (chronological order)

A

Enhanced prevention

Removable prostheses- overdenture

Orthodontics

Composite build-ups

Veneers

Crowns and bridges (resin retained)

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8
Q

What are the problems with hypodontia in children and their solutions?

A

Abnormal tooth shape and form-> composite build up

Spacing (in mixed dentition)- partial denture

Submergence-> overdenture

Deep overbite

Reduced LFH

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9
Q

Why is enhanced prevention so important in hypodntia patients?

A

As it is important that teeth they do have are healthy and are not at risk of loss (treated as high caries risk)

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10
Q

What is hyperdontia?

A

When there are extra (supernumerary) teeth

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11
Q

In what demographics is hyperdontia more common?

A

Japanese people

Males (2:1)

Maxilla

In patient with cleidocranial dysplasia

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12
Q

What are the types of supernumerary teeth?

A

Conical (cone shaped)

Tuberculate (barrel shaped, has tubercles- premolar like)

Supplemental (looks like tooth of normal series)

Odontome (irregular mass of dental hard tissue, compound or complex)

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13
Q

What is the most common type of supernumerary?

A

Conical, in maxilla and unerupted
-> Most likely to cause issues in eruption

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14
Q

How can you which tooth is supplementary?

A

Supplemental tooth is usually smaller and doesn’t look quite the same as other side

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15
Q

How do you decide which tooth to extract when you have a supplemental tooth?

A

Decide which tooth would be easier to fix with Ortho

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16
Q

What age should you wait until to remove supernumerary teeth and why?

A

Wait until child is 7/8 to remove supernumerary tooth as there is a high chance of damaging developing teeth

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17
Q

What are the developmental dental anomalies of size and shape?

A

Microdontia (peg-shaped lateral incisors)

Macrodontia

Double teeth
-> Gemination (one tooth splits into 2)
-> Fusion (two teeth join to form 1)

Odontomes

Taurodontism (flame shaped pulp)

Dilaceration (crown or root)- caused by trauma

Accessory cusps e.g. talon cusp

Dens in dente- tooth within a tooth (invaginations in tooth with their own pulp system)

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18
Q

What is the treatment for accessory cusps?

A

Selective grinding with FV over time (helps shrink pulp)

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19
Q

What is the issue with dens in dente?

A

RCT is impossible- so seal all areas to prevent ingress of bacteria

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20
Q

Which root structure anomalies can occur?

A

short roots- permanent maxillary incisors
-> can happen due to Ortho

Radiotherapy

Dentine dysplasias

Accessory roots

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21
Q

What are the types of enamel structure anomaly?

A

Amelogenesis imperfecta

Environmental enamel hypoplasia

Localised enamel hypoplasia

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22
Q

What are the causes of environmental enamel hypoplasia?

A

Systemic- liver/kidney failure

Nutritional- poor during development of dentition

Metabolic- rhesus incompatibility, liver disease

Infection e.g. measles

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23
Q

What are the cause of localised enamel hypoplasia?

A

Trauma

Infection of primary tooth

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24
Q

What is hypo-mineralisation and its features?

A

All tooth is there, normal shape (correct thickness of enamel matrix in secretory phase)

-> Something has gone wrong with mineralisation
-> Appears as white, brown, yellow patches

25
What is hypoplasia and its features?
Chunks of enamel missing- occurs at earlier phase of amelogenesis (issues with secretory phase) -> Mineralisation occurs normally but tooth lacking in quantity
26
How are localised hard tissue defects treated?
Check history for trauma or abscesses to primary teeth -> cover with composite
27
What are the types of generalised environmental enamel defects?
Fluorosis MIH- assoc. with childhood illness, kidney/liver disease
28
How does fluorosis appear?
White flecks in enamel (bleached appearance)- dark parts of the tooth can remain after treatment (make sure patient knows) Can appear as brown spots (severe)
29
How if Fluorosis treated?
MA Veneers Vital bleaching
30
How does MIH appear?
Appears as lines where enamel has not formed properly (during the time of illness) -> Marks appear in different places in different teeth depending on stage of development at time of illness
31
What are the prenatal causes of generalised environmental enamel defects?
Rubella Congenital syphilis Thalidomide Fluoride Maternal A&D deficiency, cardiac & kidney disease
32
What are the causes of enamel defects during neonatal period (ups to 8 weeks)?
Prematurity Meningitis
33
What are the post-natal (up to 2 years) causes of enamel defects?
Otitis media Measles Chickenpox TB Pneumonia Diphtheria Deficiency of Vits A,C&D Heart disease Long term health problem e.g. organ failure
34
What is an example of hereditary enamel defect?
Amelogenesis imperfecta
35
What pattern does amelogenesis imperfecta inheritance follow?
Tends to be an autosomal dominant trait in USA and Europe (but can be recessive or x-linked) Can be new mutation or not noticed before in family
36
Which gene mutations are associated with AI?
Mutations involving: Enamel extracellular matrix molecules Amelogenin/ Enamelin Kallikrein 4
37
What are the main types of Amelogenesis imperfecta? (hundreds)
Hypoplastic- enamel crystals do not grow to the correct length Hypocalcified- crystallites fail to grow in thickness and width Hypomaturational- enamel crystals grow incompletely in thickness or width but to normal length with incomplete mineralisation Mixed forms- assoc. with taurodontism
38
What factors are important when diagnosing AI?
Family history Generally affects both dentitions Affects all teeth Abnormal tooth size, structure, colour Radiographs- no obvious change in radiolucency between enamel and dentine
39
What are the issues caused by AI?
Sensitivity Caries/ acid susceptibility Poor aesthetics- brown colour Poor oral hygiene Delayed eruption Anterior open bite Bonding issues
40
What treatment are available for AI?
Preventive therapy Composite veneers/ composite wash Fissure sealants Metal onlays Stainless steel crowns Orthodontics
41
Which systemic conditions are associated with enamel defect? (not AI)
Epidermolysis bullosa Incontinenta pigmenti Down’s Prader-Willi Porphyria Tuberous sclerosis Pseudohypoparathyroidism Hurler’s
42
Which anomalies of dentine structure can occur?
Dentinogenesis Imperfecta (rarer than AI) Dentine dysplasia Odontodysplasia Systemic disturbances- nutrition, metabolic, drugs
43
What are the features of dentine dysplasia?
Normal crown morphology Amber radiolucency Pulpal obliteration Short constricted roots
44
What are the features Odontodysplasia?
Localised arrest in tooth development Thin layers of enamel and dentine Large pulp chambers Appear as Ghost Teeth on radiographs
45
What are the types of dentinogenesis imperfecta?
Type I- osteogenesis imperfecta Type II- autosomal dominant Brandywine
46
What are the features of patients with OI/DI (type I)?
Wheel chair bound Multiple bone fractures Bulbous crowns (amber translucent- grey) Blue sclera Pulp obliteration (difficult to RCT)
47
What are the features of DI radiographically?
Appear like primary teeth with normal root formation Large pulps- become obliterated Occult abscess formation (no demonstrable clinical disease)
48
What are the issues with DI?
Aesthetics Caries / acid susceptibility Spontaneous abscess formation -> poor prognosis
49
What are the treatment options for DI?
Prevention Composite veneers Overdentures Removable prostheses Stainless steel crowns- lack of tissue to bond to
50
Why is enamel lost in DI?
No connection at ADJ- just falls off due to no support
51
How is generalised wear in children with DI treated?
SSC on posterior and composite on anteriors
52
What hereditary types of dentine defect are limited to dentine only?
Dentinogenesis imperfecta type II Dentine dysplasia Types I & II Fibrous dysplasia of dentine
53
Which hereditary disorders are associated with dentine defects?
Osteogenesis imperfecta Ehlers-Danlos syndrome Brachio-skeletal genital syndrome Rickets Hypophosphatasia
54
What are the causes of anomalies in cementum structure?
Cleidocranial dysplasia- hypoplasia of cellular component of cementum Hypophosphatasia- hypoplasia or aplasia of cementum (leads to early loss of primary teeth)
55
What are the causes associated with premature eruption of teeth?
High birth weight Precocious puberty
56
When are neonatal teeth removed?
If issue with feeding or inhalation risk
57
What are the causes of delayed eruption?
Pre-term & low birth-weight children Malnutrition Associated general conditions: Downs, hypothyroidism, hypopituitarism, cleidocranial dysplasia Gingival hyperplasia/ overgrowth
58
What are the causes of premature exfoliation?
Trauma Following pulpotomy Hypophosphatasia Immunological deficiency e.g. cyclic neutropaenia Chediak-Higashi syndrome Histiocytosis X
59
What re the causes of delayed exfoliation?
Infra-occlusion (ankylosis/trauma) -> majority exfoliate normally by age 11-12 yrs Double primary teeth Hypodontia Ectopic permanent successors Trauma

BDS4 Paeds (2 decks)

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