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Module 6 > Dental Anomalies > Flashcards

Dental Anomalies Flashcards

1
Q

In tooth formation, what are the interacting tissues at initiation?

A

The interaction between the epithelium and the ectomesenchyme

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2
Q

The tooth germ is organised into 3 parts - what are these 3 parts and what do they each produce?

A

Enamel organ - ameloblasts, root sheath
Dental papilla - odontoblasts, pulp
Follicle - cementoblasts, osteoblasts, fibroblasts

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3
Q

When does the process of tooth formation start?

A

Week 5 of embryonic life

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4
Q

When does the dental lamina form?

A

Week 6 of embryonic life

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5
Q

When does the primary tooth germ form?

A

Week 8 of embryonic life

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6
Q

When does the permanent tooth germ form?

A

Week 14 of embryonic life

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7
Q

What are the 3 phases of enamel formation?

A
  1. Pre-secretory - shape of the crown determined, ameloblasts develop and prepare to secrete organic matrix
  2. Secretory - ameloblasts lay down organic matrix
  3. Maturation - ameloblasts transport specific ions to mineralise the matrix
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8
Q

When does dentine/enamel formation of primary teeth start to occur?

A

Week 18 of embryonic life

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9
Q

When does dentine/enamel formation of permanent 1st molars start to begin?

A

32 weeks of embryonic life

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10
Q

When does the mineralisation of primary teeth begin?

A

14-18 weeks of embryonic life

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11
Q

When do crowns of first permanent molars begin mineralisation?

A

7-8 months gestation

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12
Q

When do permanent incisors begin mineralisation?

A

Within the 1st year of life

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13
Q

At what point should all permanent teeth (excluding 8s) have begun mineralisation?

A

Before 6 years old

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14
Q

What are 2 quantitative developmental anomalies?

A

Hypodontia
Supernumeraries - cleidocranial dysplasia

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15
Q

What is the term used to describe a total lack of teeth in one or both dentitions?

A

Anodontia

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16
Q

What is the name of a rare condition that involves >6 primary or permanent missing teeth ?

A

Oligodontia

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17
Q

In order state the 4 most commonly missing teeth?

A
  1. 8s
  2. Lower 5s
  3. Upper 2s
  4. Upper 5s
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18
Q

Which syndromes might Hypodontia be associated with?

A

Trisomy 21 (Down syndrome)
Ectodermal dysplasia
Autosomal dominant inheritance pattern in some families
Mutations in the MSX1 gene on chromosome 4

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19
Q

List some common features of ectodermal dysplasia

A

Males (X-linked)
Thin, sparse hair
Absence of sweat glands - Heat intolerance
Multiple missing teeth
Microdontia (peg laterals especially)

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20
Q

How might you treat multiple missing teeth?

A

Detection
Refer as necessary - multidisciplinary input
Maintain excellent dental health
Undertake restorative treatment as necessary

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21
Q

How might you treat missing upper laterals?

A

Treatment planning based around the eruption of canine and patient’s wishes

2 treatment options:
- Space closure – bring canine into lateral position
- Space opening – placement of prosthesis.

Often a staged treatment plan, with temporary space maintenance (aesthetic considerations!) until full maturity

Will usually require a joint orthodontic/restorative opinion

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22
Q

What are a type of supernumerary teeth that are found in the midline and usually peg-shaped known as?

A

Mesiodens

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23
Q

What are supplemental teeth?

A

A type of supernumerary tooth that looks like a normal tooth

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24
Q

What might happen if conical supernumaries are inverted?

A

They may migrate superiorly towards the nose

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25
Q

What can happen with tuberculate supernumaries?

A

They can impede eruption of adjacent teeth

26
Q

What is cleidocranial dysplasia/dysostosis?

A

A rare autosomal dominant condition

27
Q

What are the skeletal features of cleidocranial dysplasia?

A

Hypoplasia/aplasia of clavicles
Delayed closure of the frontanelles
Underdevelopment of bones and joints

28
Q

What are the dental features of cleidocranial dysplasia?

A

Delayed loss of primary teeth
Delayed/failed eruption
Supernumerary teeth

29
Q

How do you manage supernumerary teeth?

A

Usually based around extraction/monitoring, spontaneous alignment, and use of orthodontics where necessary

Determining which teeth to take out can sometimes be difficult if supplemental (look identical)

Liaison with orthodontics

30
Q

List 5 different abnormalities that affect the size/form of the teeth?

A

Microdontia
Macrodontia
Double teeth
Dens in dente
Talon cusps

31
Q

What are 2 old terms that have been used to classify double teeth?

A

Fusion - an abnormal shaped tooth resulting from the fusion of 2 separate tooth germs, normal number of crowns

Germination - 2 teeth develop from one tooth germ, look abnormally wide, extra crown (count the number of crowns

32
Q

What is dens in dente/dens invaginatus?

A

A tooth within a tooth
Localised area of the crown folded inwards

33
Q

What are the complications associated with dens in dente?

A

Can result in an area of caries, leading to pulpitis and PA infection - often difficult/impossible to treat endodontically

34
Q

Why should you NOT shave down a talon cusp?

A

As it may contain its own bit of pulp

35
Q

List 2 different hereditary disturbances of tooth structure

A
  1. Amelogenesis Imperfecta
  2. Dentinogenesis imperfecta
36
Q

What is Amelogenesis Imperfecta?

A

A spectrum of hereditary defects in the function of ameloblasts and mineralisation of enamel matrix

Affects both primary and permanent dentition

37
Q

What is the prevalence of Amelogenesis Imperfecta?

A

1:700-4,000

38
Q

How might you classify Amelogenesis imperfecta?

A

By inheritance or phenotype

39
Q

What are the 2 different phenotypic classifications of Amelogenesis Imperfecta?

A
  1. Hypoplastic type
    - affects the quantity of enamel
    - thin, hard enamel, normal bond strength
    - teeth affected before eruption
  2. Hypomineralised type
    - affects the quality of enamel
    - teeth affected after eruption
    - full-thickness enamel but very soft, impaired bond strength
    - can be sub-categorised into hypocalcified and hypomature
40
Q

What is the most common inheritance pattern seen in Amelogenesis Imperfecta?

A

Autosomal dominant, X-linked

41
Q

What are the other associated dental defects of Amelogenesis imperfecta?

A

Pulp calcification
Taurodontism
Delayed eruption
Gingival overgrowth
Skeletal anterior open bite (~50% of patients)

42
Q

How would you manage amelogenesis imperfecta?

A

Composite restorations on anteriors
- can be added to as teeth further erupt
- bonding can be an issue

If hypoplastic consider if there enough enamel to bond onto.

If hypomature – pre-treatment with sodium hypochlorite is required to remove proteins and aid bond

If hypocalcified – dentine bonding where enamel has broken down

In the posterior dentition full coverage restorations are often required - particularly hypocalcified where further breakdown likely

43
Q

What is dentinogenesis imperfecta?

A

Autosomal dominant inherited condition

44
Q

What is the prevalence of dentinogenesis imperfecta?

A

1:80,000

45
Q

What are the 3 different types of dentinogenesis imperfecta?

A

Type I - associated with osteogenesis imperfecta (OI)
Type II - dentinogenesis imperfecta on its own
Type III - “Brandywine isolate”

46
Q

What are common findings associated with Dentinogenesis type 1?

A

Osteogenesis imperfecta
Likelihood of skeletal abnormalities, bone fractures, cardiac defects
>70% class III skeletal pattern
Bisphosphonates routinely used in management

47
Q

What are the characteristics associated with dentinogenesis imperfecta in primary dentition?

A

Colour - amber
Attrition
Pulp obliteration
Spontaneous abscesses

48
Q

What are the characteristics associated with dentinogenesis imperfecta in permanent dentition?

A

Colour - grey/translucent
Short roots
Pulp obliteration
Spontaneous abscesses

49
Q

What are the 4 main clinical problems associated with dentinogenesis imperfecta?

A

Poor aesthetics
Chipping and attrition of enamel
Exposure of dentine
Poor OH, gingivitis, caries

50
Q

What are the general treatment objectives for dentinogenesis imperfecta?

A

Maintain occlusal face height
Maintain OH
Address sensitivity/infection/abscesses
Preserve function, aesthetics and normal growth
Protect incisors/first permanent molars from wear

51
Q

What are the treatment options for dentinogenesis imperfecta (primary and permanent teeth) ?

A

Primary dentition:
- Monitor wear
- Overdenture
- SSCs for posteriors, composite crowns for anteriors
- Fluoride applications for sensitivity
- Extractions if abscessed

Permanent dentition:
- Monitor wear
- Cast restorations on occlusal surfaces of 1st permanent molars (and premolars if required)
- Composite veneers
- Orthodontics - with care

52
Q

List 3 non-hereditary disturbances in fomration?

A

MIH
Turners tooth
Fluorosis

53
Q

What is MIH?

A

Qualitative developmental defect in enamel structure - altered enamel structure with less mineral content
- caused by disruption to the maturation/late transitional stage of amelogenesis

54
Q

Which teeth are most frequently affected by MIH?

A

Typically 1st permanent molars and central incisors

55
Q

What are the clinical findings that you may observe in MIH?

A

Demarcated enamel opacities, ranging in colour - creamy white to yellow/brown

Can appear hypoplastic (patchy enamel), normally as a result of post-eruptive breakdown

Patients can present c/o breakdown off teeth, sensitivity, aesthetic concerns, failed restorations

56
Q

How do you treat MIH?

A

Prevention of caries and post-eruptive breakdown

May need temporisation with restorative material or SS crown

Child anxiety and pain during tx. has to balance against restoration type

Desensitisation and remineralisation:
- Repeated application of 5% sodium fluoride varnish
- Use of commercially available ‘sensitive toothpastes’
- Use of 0.4% stannous fluoride gels
- CPP-ACP

Long-term treatment plan:
- Decide (and discuss with the child/parent) whether to restore the teeth definitively or extract them
- Long-term prognosis of the affected molar teeth
- Occlusion/ malocclusion
- Aesthetic impact of any anterior lesions

Maintenance

57
Q

What are the complications of MIH?

A

More susceptible to caries, tend to be hypersensitive – may increase dental anxiety

Defects vary in size and shape

Dramatic transition between hard normal enamel and defective enamel (opacities)

Defective enamel fractures under normal occlusal forces - result in excessive chipping/wear of these areas leading to sensitivity/pain

No typical etching pattern achieved

Crown form often compromised in terms of both the quantity and the quality of the remaining tooth tissue, which makes defining an appropriate cavity form very difficult

Anxiety - due to need for lot of treatment/repeat treatment, increased sensitivity, young age, ineffective LA

Poor mechanical and physical properties - therefore difficult teeth to restore long term

58
Q

In a class 1, uncrowded occlusion, when would you extract a 1st permanent molar of poor prognosis, with MIH, in the absence of pain/infection?

A

Should be extracted when the calcification of the bifurcation of the second permanent molars can be seen radiographically

59
Q

What is fluorosis and how is it caused?

A

Irregular enamel opacities, stained if severe
It results from ingestion of high F concentrations during amelogenesis

Only affects teeth that are developing during time of excessive fluoride (chronological)

60
Q

What is turners tooth and which teeth are affected by it?

A

Hypoplastic enamel following infection around the inter radicular area of a primary tooth

Affects the permanent successors (often secondary premolar)

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