DP01 developmental anomalies of teeth Flashcards

(46 cards)

1
Q

Teeth form from the ectoderm and ectomesenchyme (from neural crest). What does the ectoderm give rise to?

A

Enamel

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2
Q

Teeth form from the ectoderm and ectomesenchyme (from neural crest). What does the ectomsenchyme give rise to?

A

Dentine, pulp, cementum, PDL, bone

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3
Q

What is the inductive theory?

A

IEE (preameloblasts) induce the dental papillae to differentiate preodontoblasts. Odontoblasts produce dentine. Dentine stimulates preameloblast maturation into ameloblasts which form enamel.

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4
Q

What might anomalies affect in teeth?

A

Size, number, form, structure, sequence of eruption, position

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5
Q

What are the anomalies of size?

A

Macrodontia
Microdontia

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6
Q

What is macrodontia of the roots caused by?

A

Rare disease - oculo-facio-cardio-dental syndrome
X-linked - lethal in males
Involves BCOR gene

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7
Q

What effects does oculo-facio-cardio-dental syndrome have?

A

→ Ocular: congenital cataracts, microphthalmia, secondary glaucoma
→ Facial: long narrow face, high nasal bridge, pointed nose with cartilages separated at the tip, cleft palate, submucous cleft palate
→ Cardiac: atrial/ventricular septal defects, floppy mitral valve
→ Dental: canine radiculomegaly, delayed dentition, oligodontia, persistent primary teeth, variable root length
If the canines have v long roots (due to no apoptosis of HERS), there may be issues if the tooth must be extracted as it may fracture

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8
Q

What is STHAG?

A

Selective tooth agenesis - having fewer teeth than normal

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9
Q

What are the types of STHAG?

A

Anodontia
Hypodontia = <6 teeth are absent
Oligodontia = > 6 teeth are absent

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10
Q

Is syndromic or non-syndromic hypodontia more common?

A

Non-syndromic

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11
Q

What is Bolk’s terminal line reduction theory?

A

Hereditary trait - ‘last in each series of teeth tends to be more commonly missing’

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12
Q

What molecular signalling pathways may regulate tooth number?

A

WNT family
Ectodysplasin A (EDA)

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13
Q

What might mutations of WNT antagonists cause?

A

AXIN2 - tooth agenesis
APC - Gardner’s syndrome, supernumerary teeth

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14
Q

Syndromic hypodontia - what diseases may hypodontia be associated with?

A

Ectodermal dysplasia
Cleft palate
Down syndrome
Axenfeld-Rieger syndrome

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15
Q

What is ectodermal dysplasia and what does it cause?

A

X-linked, autosomal recessive; ectodermal components affected: smooth dry skin, absent sweat glands -> hyperthermia, anodontia (total/partial), conical cuspids and molars, hypotrichosis (lack of hair)

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16
Q

Where do most supernumary teeth occur?

A

Maxilla

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17
Q

What are the most common supernumaries?

A

Mesiodens > 4th molars > upper laterals > lower 2nd premolars

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18
Q

What syndromes can cause hyperdontia?

A

Cleidocranial dysplasia
Gardner’s syndrome
Cleft lip/palate

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19
Q

What disturbances in eruption might there be?

A

Premature teeth which erupt early:
→ Natal teeth: present at birth; neonatal teeth: erupt during the first 30 days after birth
→ Commonly deciduous mandibular central incisors are affected
→ May predispose to premature eruption of permanent teeth
→ May also induce irritation of the mucosa/ulceration of ventral surface of tongue
→ Premature loss of teeth may occur
→ May be associated w hyperthydroidism

20
Q

What disturbances in the shape of teeth are there?

A

Dilaceration
Taurodontism
Dens invaginatus (dens in dente, invaginated odontome)
Supernumerary cusps
Cervical enamel projection/enameloma/enamel pearl
Supernumerary roots
Gemination
Fusion

21
Q

How does dents invaginatus occur?

A

Invagination of a portion of EO into DP before mineralisation
Upper laterals most commonly affected

22
Q

What supernumerary cusps are there?

A

Carabelli cusp
Dens evaginatus
Talon cusp

23
Q

What is concrescence?

A

2+ roots united by cementum after root formation (unlike fusion which occurs during development)

24
Q

How does concrescence occur and which teeth are most affected?

A

Due to trauma/crowding
Upper molars more common

25
What can cause hypercementosis?
Increased/decreased forces on tooth Pagets disease of bone - may be caused by virus Hyperpituitarism Chronic infection in adjacent area
26
How does Pagets disease of bone present on radiograph vs histologically?
Cotton wool on rad Mosaic pattern histologically - reversal lines seen where osteoclasts stop breaking down bone and osteoblasts start laying it down
27
What might patients with Pagets disease and hypercementosis develop later?
Ankylosis - obliteration of PDL
28
What are the environmental causes of enamel structure disturbance?
Bacterial and viral infections (syphilis, scarlet fever), inflammation, nutritional deficiencies, chemical injury, trauma Focal or generalised
29
What is focal enamel hypoplasia?
1-2 teeth only; chalky E, white opacity Turner tooth - brown staining Result of inflammation/trauma during tooth development e.g. if former tooth has periapical inflammatory focus following pulp necrosis If deciduous caries -> abscesses that damage developing successors May be idiopathic
30
What is generalised enamel hypoplasia?
E defect due to short term systemic/environmental factors - Horizontal lines, small pits of grooves on crown
31
Congenital syphilis can also appear as generalised enamel hypoplasia. What can this cause in the dentition?
Notched Hutchinson incisors, Mulberry molars, moon molars (round!)
32
What are some causes of intrinsic staining?
Tetracycline staining - yellow brown Congenital porphyria - red brown Bilirubin - green/blue Haemoglobin and products - pink
33
How does fluoride mottling occur?
Increased F Disturbed AM function --> defective enamel matrix formation and calcification Malformed HAp crystallisation
34
What can cause extrinsic staining of teeth?
Chromogenic bacteria Foods/drinks Habits: tobacco, betel nut chewing Chemicals - CHx
35
What hereditary disturbances in enamel structure are there?
Amelogenesis imperfecta - X-linked AD disease
36
What are the types of AI?
Hypomineralised Hypoplastic
37
What is hypomineralised AI?
Hypocalcified - defective mineralisation of E matrix, normal thickness, less dense, chalky -> cannot resist masticatory forces -> abrasion/atrition/exposed D Hypomaturation - normal thickness, mottled, soft, snow-capped teeth
38
What is hypoplastic AI?
Decreased enamel matrix formation, thin E, pitting, grooving, X-linked Absent prismatic structure of E, normal underlying D
39
What hereditary disturbances in D structure are there?
Osteogenesis imperfecta Dentinogenesis imperfecta Dentinal dysplasia I
40
What happens in osteogenesis imperfecta?
(type I) - Defective type I collagen, blue sclera (whites of eyes), fragile bones, bleeding problems
41
What happens in dentinogenesis imperfecta?
Opalescent teeth, undermineralised D, obliteration of pulp chamber Autosomal dominant Tooth fractures and chips away easily due to defective ADJ (E on top of defective D) -> exposed D and functional attrition, leading to crown and pulp loss
42
What is dentinal dysplasia I?
Radicular D affected, pulp stones Tiny roots affecting entire dentition
43
What metabolic disturbances can affect dentinogenesis?
Rickets - deficiency/resistance to vit D Hypophosphatasia - reduced ALP in serum
44
What effect does rickets have on dentine?
Incompletely calcified Prominent interglobular D
45
What effect does hypophosphatasia have on dentine?
Abnormal dentine, premature loss of teeth, lack of calcification of calvarium
46
What is regional odontodysplasia (ghost teeth)?
Developmental disturbance of several adjacent teeth Deciduous and permanent affected E and D - thin and irregular Not adequately mineralised (lots of preD) -> less radiopaque Delayed eruption