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dental anomalies Flashcards

1
Q

types

A

number
size and shape
structure - hard tissue defects
eruption and exfoliation

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2
Q

prevalence of hypodontia in the primary dentition

A

1%

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3
Q

prevalence of hypodontia in permanent dentition

A

3-6%

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4
Q

prevalence of missing L premolars

A

usually 5s

2%

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5
Q

prevalence of missing U2s

A

1-2%

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6
Q

teeth least likely to be missing in hypodontia

A

FPMs

U1s

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7
Q

pattern of hypodontia

A

if a tooth is missing it tends to be the last in a series

except L incisors - central more likely to be absent because of genetic programming - L2 coded before L1

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8
Q

conditions associated with hypodontia

A
  • ectodermal dysplasia
    • sparse hair
    • lack of sweating
  • Down syndrome
  • Cleft palate
  • Hurler’s syndrome
  • incontinentia pigmentii
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9
Q

hypodontia problems

A
  • abnormal shape/form
  • spacing
  • submergence/ infraocclusion
  • deep overbite - reduced LFH
  • over-eruption of L canines can be a Rx problem when U2s are missing
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10
Q

hypodontia solutions

A 
overenture
RPD
composite build ups
porcelain veneers
fixed prostheses - crowns and bridges
ortho
implants
preventative tx - enhanced prevention
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11
Q

what might hypodontia pts need before implants?

A

may need bone augmentation, sinus lift, distraction osteogenesis

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12
Q

which txs for hypodontia should not be done until early 20s and why?

A

porcelain veneers
fixed prostheses - crowns and bridges
implants
need gingival margin to have stabilised

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13
Q

prevalence of supernumeraries

A

2%

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14
Q

gender distribution of supernumeraries

A

M:F 2:1

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15
Q

what groups are supernumeraries more common in?

A

Japanese

cleidocranial dysplasia - stranger things boy

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16
Q

which jaw are supernumeraries more common in?

A

maxilla

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17
Q

types of supernumerary

A
  • conical - cone shaped
  • tuberculate - barrel shaped, has tubercles
  • supplemental - looks like tooth of normal series
  • odontome - irregular mass of dental hard tissue, compound/complex
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18
Q

what is the most common cause of delayed eruption of the permanent incisors?

A

supernumerary

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19
Q

what is the most common supplemental and what should you do with it?

A

lateral incisor
the extra one may be a bit smaller
keep whichever tooth is best for ortho

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20
Q

when should you remove a conical supernumerary?

A

usually wait until 7-8yrs to remove to avoid damaging developing central incisors

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21
Q

abnormalities of size and shape

8

A

microdont
macrodontia
double teeth
odontomes
taurodontism
dilaceration
accessory cusps
dens in dente

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22
Q

microdont statistics

A

2.5%

F>M

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23
Q

example of microdont

A

peg shaped lateral incisors

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24
Q

macrodontia stats

A

rare
<1% for single teeth
0.1% in generalised form in Caucasians

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25
Q

double teeth 2 types

A

gemination - 1 tooth splits into 2

fusion - 2 teeth join to form one

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26
Q

taurodontism

A

6.3% in UK
flame shaped pulp
teeth look normal - issue with exposing pulp if placing restoration

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27
Q

dilaceration types

A

crown or root

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28
Q

accessory cusps

A

talon cusps

often do selective grinding - encourage pulp to go back

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29
Q

dens in dente

A
  • enamel organ invaginates into the dental papilla during tooth development.
  • deep, V-shaped invagination or pocket within the crown

tx

  • immediately seal areas to prevent bacterial ingress - you won’t be able to do endo for this tooth
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30
Q

short root anomaly - which teeth are normally affected?

A

permanent maxillary incisors

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31
Q

short root anomaly prevalence

A

2.5% incidence

15% of these children also have short roots on the canines and premolars

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32
Q

short root anomaly aetiologies

A

radiotherapy
dentine dysplasias
accessory roots

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33
Q

short root anomaly impact on tx

A

means danger for ortho tx

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34
Q

types of amelogenesis imperfecta

A

hypoplastic
hypomineralised
hypomaturational
mixed forms (with taurodontism)

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35
Q

env enamel hypoplasia aetiology

A

systemic
nutritional
metabolic e.g. rhesus incompatibility, liver disease
infection e.g. measles

36
Q

localised enamel hypoplasia

A

trauma or infection to primary tooth

infection to primary molars can lead to spots on premolars

37
Q

hypomineralisation

A

secretory phase fine, correct thickness of enamel
mineralisation phase affected
white/brown/yellow patches

38
Q

hypoplastic

A

happens at earlier phase of amelogenesis
secretory phase affected
quality of enamel usually fine as mineralisation phase unaffected

39
Q

aetiology of hard tissue defects

A

localised - trauma, caries then abscess of primary

generalised - env, hereditary

40
Q

fluorosis aetiology

A

generalised and env

41
Q

fluorosis presentation

A

mild - white flecks
- explain to pt that tx will remove the white flecks not the normal darker tissue
severe - brown patches
tends to be on the surface layer of enamel

42
Q

tx of fluorosis

A

microabrasion
veneers
vital bleaching
fluorosis (mild case)

43
Q

MIH aetiology

A
  • generalised and env
  • associated with childhood illnessor chronological hypo mineralisation e.g kidney or liver failure
  • see different levels of abnormality on different teeth - they develop at different times
44
Q

generalised env enamel defects - prenatal

A

rubella
congenital syphillis
thalidomide
Fluoride
maternal A and D deficiency
cardiac and kidney disease

45
Q

generalised env enamel defects - neonatal

A

up to 8 weeks

  • prematurity,
  • meningitis
46
Q

generalised env enamel defects - post-natal

A

otitis media
measles
chickenpox
TB
pneumonia
diphtheria
deficiency of vits A,C,D
heart disease
long term health problem e.g. organ failure

47
Q

aetiology of AI

A

generalised and hereditary

48
Q

prevalence of AI

A

1 in 14000

49
Q

types of AI

A

hypoplastic
hypomineralised
hypomaturation
mixed with taurodontism

50
Q

AI inheritance

A

familial inheritance

autosomal dominant, recessive and X-linked

51
Q

does AI have an associated systemic disorder?

A

not thought to

52
Q

different inheritance patterns of AI more common in certain areas

A
  • Autosomal dominant most common in USA and Europe,
  • A-recessive in Middle East
  • Generally AI is more common in Scandanavia
53
Q

AI genetics

A
  • E formation needs multiple genes to transcribe the process of crystal growth and mineralisation
  • gene mutations affecting enamel ECM molecules
    • amelogenin
    • enamelin
    • kallikrein 4- KLK4
54
Q

diagnosis of AI

A
  • FH (but can be a new mutation)
  • generally affects both dentitions
    • tends to be worse in permanent dentition
    • often not diagnosed until then
  • affects all teeth
  • tooth size, structure, colour
  • radiographs
    • can’t see obvious change in radiolucency between E and D - can’t see ADJ
55
Q

hypoplastic AI

A

enamel crystals do not grow to correct length

56
Q

hypo mineralised AI

A

crystallites fail to grow in thickness and width

57
Q

hypomaturational AI

A

enamel crystals grow incompletely in thickness/width but to normal length with incomplete mineralisation

58
Q

AI problems

A 
sensitivity
caries/acid susceptibility
poor aesthetics
poor OH - hard to brush teeth properly as sore
delayed eruption
AOB
59
Q

systemic disorders associated with enamel defects (not AI)

A

epidermolysis bullosa
incontinenta pigmentii
Down Syndrome
Hurler’s
Prader-Willi
porphyria
tuberous sclerosis
pseudohypoparathyroidism

60
Q

AI solutions

A 
preventive therapy - enhanced prevention
composite veneers/composite wash
FS
metal onlays
SSCs
 - often when young and 6s just through, replace when older
ortho
 - brackets may debond - may need metal bands around teeth
61
Q

anomalies of structure - dentine

A

dentinogenesis imperfecta (most common)
dentine dysplasia
odontodysplasia
systemic disturbance

62
Q

dentine dysplasia

A

normal crown morphology
amber radiolucency
pulpal obliteration
short constricted roots

63
Q

odontodysplasia

A

localised arrest in tooth development, thin layers of E and D, large pulp chambers, “ghost teeth”

64
Q

systemic disturbances in dentine structure

A

nutritional
metabolic
drugs

65
Q

DI prevalence

A

uncommon

much less common than AI

66
Q

types of DI

A

3

67
Q

type 1 DI

A

osteogenesis imperfecta (blue sclera)

68
Q

type 2 DI

A

Autosomal dominant

tends not to be associated with other systemic conditions

69
Q

type 3 DI

A

Brandywine, Maryland USA - Native American Indian, Irish, Afro-American - not really any new genes - inbreeding

70
Q

DI problems

A
  • aesthetics
  • caries/acid susceptibility
  • spontaneous abscess
  • v poor prognosis
71
Q

DI diagnosis

A
  • appearance
  • FH
  • associated Osteogenesis imperfecta
  • both dentitions affected
  • radiography
    • bulbous crowns
    • obliterated pulps (1 and 2) - initially large
      pulp but vvv quickly become obliterated
  • enamel loss - because no proper connection at ADJ
  • cult abscess formation - no obvious disease related to crown of tooth
72
Q

DI solutions

A
  • prevention
  • composite veneers (but not much to bond onto)
  • overdentures
  • removable prostheses
  • SSCs
73
Q

other hereditary dentine defects - limited to dentine only

A

dentinogenesis imperfecta type 2
dentine dysplasia types 1 and 2
fibrous dysplasia of dentine

74
Q

other hereditary dentine defects - associated with a systemic disorder

A

OI
EDS
brachio-skeletal genital syndrome
rickets
hypophosphatasia

75
Q

tooth structure defects - tx overview

A
  • prevention and pain control
  • restoration of lost tissue
  • harness growth
  • continuous dental care
  • management of growth and development
  • interceptive ortho
  • removable prostheses
  • crowns and bridges
76
Q

anomalies of structure - cementum (related syndromes)

A
  • cleidocranial dysplasia
  • hypophosphatasia
77
Q

cleidocranial dysplasia

A
  • no clavicle
  • hypoplasia of cellular component of cementum
  • supernumeraries
  • delayed eruption
78
Q

hypophosphatasia

A

hypoplasia or aplasia of cementum
early loss of primary teeth
- nothing holding teeth into bone

79
Q

anomalies of eruption - premature

A

high birth weight
precocious puberty
natal/neonatal tooth

80
Q

natal tooth

A

1:2000-3000 live births
extract if inhalation risk or issues feeding
but tend to be teeth of normal series so if you can try to keep them they will form normal tooth

81
Q

anomalies of eruption - delayed

A
  • pre-term and low birth weight children
  • malnutrition
  • associated general conditions
    • Down syndrome
    • hypothyroidism
    • hypopituitarism
    • cleidocranial dysplasia
  • gingival hyperplasia/overgrowth
    • pseudo delayed eruption
82
Q

premature exfoliation

A

trauma
following pulpotomy
hypophosphatasia
immunological deficiency e.g. cyclic neutropenia
Chediak-Higashi syndrome
Histiocytosis X

83
Q

delayed exfoliation

A

infra-occlusion
following trauma

‘double’ primary teeth
hypodontia
ectopic permanent successors
=these have no permanent tooth to push out primary tooth

84
Q

infraocclusion prevalence

A

1-9%

M=F

85
Q

infra occlusion - which is the most common?

A

L D - congenital absence of premolar

86
Q

infra-occlusion time course

A

majority exfoliate normally by 11-12 years
tooth isn’t sinking into gum, it just isn’t moving
some ankylosed - will need extracted - difficult

paeds (7 decks)

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