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Oral Diseases > Theme 4 - Dental anomalies > Flashcards

Theme 4 - Dental anomalies Flashcards

1
Q

Why may teeth be impacted (aetiology)?

A

Local causes:
- Lack of space: overcrowding e.g. small arch or supernumary teeth
- Prematures/delayed loss of primary teeth
- Greater density of overlying bone e.g. osteopetrosis
- Fibrosis of overlying mucous membrane
- Pathology: cysts, odontomes, tumours

Postnatal systemic causes (interfere with growth of child):
- Anaemia
- Congenitas syphilis
- Endocrone dysfunction
- Malnutrition
- Irradiation
-TB

Prenatal systemic causes:
- Cleft lip and palate (often lateral incisors as lie in suture of maxilla)
- Cleidocranial dysplasia
- Garners syndrome

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2
Q

What syndromes are known for causing supernumary teeth?

A

Cleidocranial dysplasia (absent or hyperplastic clavicles too)

Gardners syndrome

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3
Q

What is the prevalence of impaction from most likely tooth to least?

A

8’s - upper 3 - upper 1 - lower 4 - lower 5 - supernumary

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4
Q

What are the complications associated with impaction?

A
  • Pericoronitis (mandibular 3rd molars)
  • Food trap
  • Resorption (when unerupted and in close proximity to other teeth)
  • Cystic change around follicle of crown
  • Mandibular fracture
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5
Q

What signs would make you suspect a tooth is impacted?

A
  • Retention of primary teeth
  • Tooth missing
  • Swelling
  • Mobility of adjacent tooth
  • Tilting of adjacent tooth
  • Loss of vitality of adjacent tooth
  • Periocoronitis
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6
Q

What is the most to least likely angle of impaction of mandibular 3rd molars?

A

Vertical - mesial angled - distal angled - horizontal

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7
Q

What features on a DPT would make you suspect there is communication of a mandibular 3rd molar with the IAN?

A
  • Darkening of the root
  • Diversion of the canal
  • Interruption of the cortical outline
  • Narrowing of the canal
  • Deflected roots
  • Narrowing of the rooth
  • Dark bifid root
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8
Q

When would a CBCT be appropriate when extracting mandibular 3rd molars?

A
  • If high risk IAN signs on plain film
  • Unusual root morpholoy
  • Superimpositions in unerupted teeth
  • Decision to perform surgical removal has been made
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9
Q

What is the
a) Coated vicryl suture
b) Coated vicry raptide suture
intended for closing?

A

a) General ST approximation and ligation, including opthalmic. NOT CVS or neuro tissue
b) superficial ST approximation and mucosa for short-term wound support (7-10 days)

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10
Q

For managing impacted/unerupted teeth, what is
a) Open exposure
b) Closed exposure

A

a) Through keratinized tissue, by tissue sacrifice (maintain gingival margins, small circular palatal mucosa removed and bone chiseled) or apically repositioned flap followed by a coverplate and co-pack (ZoE) for 2 weeks to prevent re-epithelialisation. If very superficial punch biopsy and pt keeps brushing tooth to prevent mucosa growth
b) Through non-keratinized tissue, mucoperiosteal flap raised, bone removed to expose crown only, etch prime bond (only using aspirator as 3in1 surgical emphysema) chain/wire ligature/brackets/magnets applied, ST closure. For when buccal tooth sits high in buccal sulcus.

Must be brought through keratinised tissue in order for PDL to form correctly

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11
Q

What is a transplant in the management of impacted teeth?
What are its complications?

A

Expose donor tooth (open apex tooth), carefully extract, reposition in surgically prepared socket, splinted for 2-4 weeks, antibiotic prophylaxis. Transplanted teeth can be moved orthodontically
Complications = root resorption and ankylosis, require RCT

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12
Q

When may a coronectomy be carried out? How is it done?

A

High risk lower 3rd molars. Expose amelo-cemental junction, fissure bur to section crown, avoid disturbing exposed pulp, primary closure of STs

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13
Q

For hypodontia:
a) M or F
b) Permanent or primary
c) Genes affected?
d) Pattern?
e) Other clinical findings

A

a) Females more
b) Permanent more
c) homeobox genes MSX1 and PAX9
d) 8s then upper 2s then lower 5s
e) often present teeth are microdont, opposing teeth overerupt, primary teeth important for retaining bone

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14
Q

For hyperdontia with supernumary teeth:
a) M or F
b) Permanent or primary
c) Types

A

a) Female more
b) Permanent more
c) Abnormal form (conical), Mesiodens (midline), Paramolar (another tooth to the side), Distomolar (extra tooth behind a molar)

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15
Q

For hyperdontia with supplemental teeth:
a) Shape
b) Pattern

A

a) Normal form
b) Upper 2s then lower 5s then upper 5s

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16
Q

What syndromes is hypodontia linked to?

A
  • Hypohidrotic ectodermal dysplasia
  • Cleft lip and palate
  • Crouzon syndrome
  • Ellis-van Creveld syndrome
  • Orofacial digital syndrome
  • Down syndrome
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17
Q

What syndromes is hyperdontia linked to?

A
  • Garner syndrome
  • Orofacial digital syndrome
  • Cleft lip and palate
  • Cleidocranial dysplasia
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18
Q

For hypohidrotic ectodermal dysplasia, what are the:
a) General features
b) Dental anomalies
c) Genetics

A

a) Smooth dry skin, sparse hair, protruded earts, absence of sweat glands, nail abnormalities, reduced lower face height
b) Ano/hypodontia, delayed eruption, deformed teeth, conical crowns
c) X-linked recessive (rare in F)

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19
Q

For cleidocranial dysplasia, what are the:
a) General features
b) Dental anomalies
c) Genetics

A

a) Absent or hypoplastic clavicles, fontanelled and sutures persist, helmet like skull, hypertolerism
b) High narrow palate, maxilla hypoplastic, retained primary teeth, supernumary teeth, delayed eruption
c) Autosomal dominant

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20
Q

What syndromes are known to affect the size of teeth?

A
  • Ehlers Danlos syndrome
  • Downs syndrome
  • Congenital heart disease
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21
Q

For Ehler’s Danlos syndrome, what are the:
a) General features
b) Dental anomalies

A

a) Defect of collagen, hypermobile joints, hyperextensibility of skin
b) Microdontia, short roots, pulp stones, fragile mucosa, juvenile periodontitis (aggressive as collagen not produced)

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22
Q

What is a) fusion and b) gemination that create double teeth?

A

a) Union between dentine and/or enamel of 2 or more separate teeth (will find 2 roots)
b) The partial development of 2 teeth from a single tooth bud following incomplete division

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23
Q

What are the different abnormalities of form in the shape of teeth?

A
  • Double teeth
  • Concresence
  • Taurodontism
  • Dilaceration
  • Peg-shaped laterals
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23
Q

What are the different abnormalities of form in the shape of teeth?

A
  • Double teeth
  • Concresence
  • Taurodontism
  • Dilaceration
  • Peg-shaped laterals
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24
Q

What is concrescence? (affects shape of teeth)

A

The roots of 2 or more teeth are united by cementum alone after formation of the crown

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25
Q

What is taurodontism (affects the shape of teeth)?

A

Pulp chamber has a greater apico-occlusal height and no cervical constriction (looks like a bull running at you on the xray). Permanent molars.

26
Q

What can taurodontism be a feature of?

A

Amelogenesis imperfects
Klinefelter syndrome (XXY)
Localised failure of tooth development

27
Q

What is dilaceration (affects shape of teeth)?

A

The crown of the tooth is displaced from its normal alignment with the root. Permanent upper incisors. Aquired - mechanical trauma

28
Q

What are the a) local causes and b) general causes of abnormalities of enamel?

A

a) Trauma/infection to the primary dentition. Idiopathic enamel opacity.
b) Genetic - amelogenesis imperfecta
Systemic - chronological hypoplasias/mineralisation:
- Excess fluoride (more than 2ppm)
- Infections e.g. rubella, syphilis
- Chronic disease e.g. CHD, endocrone
- Nutritional deficiency e.g. vit D
- Chemotherapy

29
Q

What is a turner tooth?

A

Enamel hypoplasia in tooth that was underneath an infected primary tooth

30
Q

If a ridge had grooves, pits and altered shape when did disturbance occur in development? If a tooth has a white/brown mark but good shape when did distrubance occur?

A

a) early (matrix affected)
b) later (mineralisation affected)

31
Q

What is chronological hypoplasia?

A

Lines across teeth that correspond to injury in utero e.g. mother very poorly

32
Q

How does congenital syphilis affect the structure of teeth?

A

Infection of tooth by Treponema pallidum
Hutchinson’s incisors - screw driver shape with notch
Mulberry molars - nodular cusps, breaks off with whisps of pulp
Children can be born blind and is an extremely rare condition

33
Q

How does excess fluoride consumtion/fluorosis present in teeth? What is a problem in 3rd world countries?

A

Hypoplastic/hypomineralised enamel as toxic to tooth germ. White flecks/patches or yellow/brown/black discolouration.

Bony fluorosis

34
Q

What is amelogenesis imperfecta?
What are the 2 groups it is classified into?

A

Rare heriditary defect of enamel - autosomal or X-linked
Hypoplastic type and hypomineralised/hypomaturation type

35
Q

What are the features of the hypoplastic type of amelogenesis imperfecta?

A

Defective matrix production, enamel hard, variable thickness.
Clinical appearance:
- Generalised thinning
- Vertical grooving
- Pitting
- Teeth appear small
- Abnormal cusp morphology

36
Q

What are the features of the hypomineralised type of amelogenesis imperfecta?

A

Defective mineralization, enamel soft, normal thickness
Normal morphology when first erupting with soft chalky enamel. Chips off exposing dentine.

37
Q

What are the a) local causes b) dentinal dysplasia c) Dentinogenesis imperfecta and d) environmental abnormalities of dentine?

A

a) Trauma/infection (turner tooth)
b) Type 1 = radicular, Type 2 = coronal
c) Type 1 = in osteogenesis imperfecta, Type 2 = teeth only/shell teeth, Type 3 = Brandywine isolate
d) Rickets, hypophosphatasia, juvenile hypoparathyroidism

38
Q

What is Type 1 Dentinogenesis imperfecta in osteogenesis imperfecta?
What are the clinical features?

A

Defect in type 1 collagen, rare autosomal dominant disease. Managed with bisphosphonates
CF:
- Slender bones (weak)
- Deformity, fractures and deafness due to bones in ear
- Hypermobile ligaments
- Thin transluscent skin, blue sclera
- Dentinogenesis imperfecta: dark, worn dentition, flat ADJ not scalloped so enamel not bonded to dentine.

39
Q

What is Type II Dentinogenesis imperfecta?
What are the clinical features?

A

Rare autosomal dominant M=F. Hypomineralised dentine.
CF:
- Discoloured teeth (grey/brown tint)
- Bulbous crown
- Rapid attrition
- Thin short blunt roots
- Pulp chamber obliterated

40
Q

What is the histopathology of type II dentinogenesis imperfecta?

A

Thin layer of normal mantle dentine
Circumpulpal denine = reduced no of tubules and irregular wide tubules
Cellular and vascular inclusion
ADJ straight not scalloped

41
Q

What is type I dentinal dysplasia?

A

Normal crowns, short roots
Pulp obliterated
Roots composed of dysplastic dentine
Dentinal tubules disorganised
Calcified globules of abnormal dentine

42
Q

What is type II dentinal dysplasia?

A

Primary teeth look like dentinogenesis imperfecta
Permanent teeth look normal
Pulp obliterated
Pulp stones
Thistle shaped pulp

43
Q

What is rickets? How does it occur? What are the clinical features?

A

Failure of calcification due to vit D deficiency

Diet, absorption (GIT disease), lack of UV, renal disease, drugs

CF = short stature, bow legs, bone deformity and fracture
Teeth = delayed eruption, enamel hypoplasia and dentine abnormalities

44
Q

What is regional odontodysplasia?

A

Ghost teeth: hypoplastic, abnormal form, delayed eruption, very delicate so hard to remove
Rare - affects primary and permanent, usually unilateral and anterior maxilla

45
Q

What is the histopathology of the enamel and dentine in regional odontodysplasia (ghost teeth)?

A

Enamel:
- Irregular mineralisation
Dentine:
- Thin
- Wide pulp chamber with open apices
- Wide predentine zone
- Interglobular dentine
- Pulp stones
- Calcification of follicle

46
Q

What are the abnormalities of cementum?

A

Hypo or hypercementosis/ankylosis

47
Q

What is hypercementosis? Why does it occur?

A

Overproduction of cementum, PDL removed and direct link with bone
Infection, overloaded teeth, functionless/unerupted teeth, paget’s disease

48
Q

What is hypocementosis? Why does it occur?

A

Rare defect of mineralisation, autosomal recessive. Causes premature tooth loss as nothing for collagen fibres to attach to.
Cleidocranial dysplasia, hypophosphatasia

49
Q

What are the possible causes of delayed eruption if it is localised?

A
  • Retained primary teeth
  • Hyperdontia
  • Abnormal crypt position
  • Reduced space (crowded arch/impacted)
  • Dentigerous/eruption cyst
50
Q

What are the possible causes of delayed eruption if it is generalised?

A
  • Hypothyroidism
  • Rickets
  • Cleidocranial dysplasia (plus multiple supernumaries)
  • Downs syndrome
51
Q

What are the problems with premature eruption e.g. natal/neonatal tooth?

A
  • Hypoplastic enamel/rootless
  • Mobile - exfoliate risk to airway
  • Interfere with feeding
  • Ulcerated tongue
  • If removed these teeth are part of the normal dentition so will stay missing until permanent erupt
52
Q

In orthognathic surgery, what is distraction osteogenesis?

A

Bones are gradually separated using distraction screws allowing bony deposition as jaw is moved

53
Q

What are the 5 management options of impacted teeth?

A

1) Leave
2) Open exposure
3) Closed exposure
4) Transplant
5) Extract

54
Q

If you see a cystic change around an unerupted/impacted tooth, what are your differential diagnoses?

A

Dentigerous cyst
Keratocyst
Ameloblastoma

55
Q

For localisation of an unerupted tooth, what radiographs could you get?

A

Parrallax views (SLOB):
- 2 PAs (Clarks method)
- Occlusal and DPT
3D view - CBCT
If tooth palatal, on DPT it is magnified

56
Q

What are submerging/infraoccluding teeth?

A

Deciduous tooth ankyloses to alveolus and adjacent structures continue to grow - gives appearance of submerging. Remove when they sink below the contact points. Hard to clean, caries, and failure of eruption of successor tooth

57
Q

When there is primary failure of eruption and nothing is impeding eruption, why does it occur and why is it a problem?

A

Unfavourable rooth formation - often engaging with inferior cortex of lower border of mandible
Don’t respond favourably to orthodontic traction and hard to remove as often associated with IAN

58
Q

What is an odontome?

A

Amorphous collections of tooth tissue, complex and compound forms. Can prevent movement of teeth orthodontically and deflect eruption path of developing teeth

59
Q

When exposing an unerupted tooth, why must there be
a) minimal follicle removal
b) Not beyond the CEJ

A

a) avoids ankylosis
b) so cementum not damaged with can cause external resorption

60
Q

What are orthodontic implants?

A

Used for anchorage - midline of palate for arch expansion.
Shorter tan dental implants so can be reversed out of bone after Tx
Bone microscrews/TAD less invasive as tapped in, but must be positioned away from adjacent roots

61
Q

What are the indications for a labial frenectomy?

A

Facilitate closure of a diastema
Reduce chance of diastema relapse
Aid tooth burhsing
Eliminate tension on gingivae
Lip lengthening

62
Q

If a patient has a diastema
a) What size makes it less likely to resolve
b) what can you see radiographically
c) What should you check for
d) How is it excised
e) If a frenectomy is dont prior to ortho what is the benefit and drawbacks?

A

a) more than 2 mm
b) notching of alveolar crest
c) Mesiodens
d) Vertically, or z-plasty. Closed in horizontal or vertical direction
e) Benefit = assist closure. Drawback - can lead to fibrous scarring which can inhibit closure

Oral Diseases (12 decks)

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