dental anomalies Flashcards
1
Q
types
A
number
size and shape
structure - hard tissue defects
eruption and exfoliation
2
Q
prevalence of hypodontia in the primary dentition
A
0.1-0.9%
3
Q
prevalence of hypodontia in permanent dentition
A
3.5-6.5%
4
Q
prevalence of missing L premolars
A
usually 5s
1.2-2.5%
5
Q
prevalence of missing U2s
A
1-2%
6
Q
teeth least likely to be missing in hypodontia
A
FPMs
U1s
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
8
Q
conditions associated with hypodontia
A
ectodermal dysplasia - sparse hair - lack of sweating Down syndrome Cleft palate Hurler syndrome incontinentia pigmenti
9
Q
hypodontia problems
A
abnormal shape/form spacing submergence deep overbite reduced LFH over-eruption of L canines can be a Rx problem when U2s are missing
10
Q
hypodontia solutions
A
overenture RPD composite build ups porcelain veneers fixed prostheses - crowns and bridges ortho implants preventative tx - enhanced prevention
11
Q
what might hypodontia pts need before implants?
A
may need bone augmentation, sinus lift, distraction osteogenesis
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
13
Q
prevalence of supernumeraries
A
1.5-3.5%
14
Q
gender distribution of supernumeraries
A
M:F 2:1
15
Q
what groups are supernumeraries more common in?
A
Japanese
cleidocranial dysplasia
16
Q
which jaw are supernumeraries more common in?
A
maxilla
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
18
Q
what is the most common cause of delayed eruption of the permanent incisors?
A
supernumerary
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
20
Q
when should you remove a conical supernumerary?
A
usually wait until 7-8yrs to remove to avoid damaging developing central incisors
21
Q
abnormalities of size and shape
A
microdont macrodontia double teeth odontomes taurodontism dilaceration accessory cusps dens in dente
22
Q
microdont statistics
A
2.5%
F>M
23
Q
example of microdont
A
peg shaped lateral incisors
24
Q
macrodontia
A
rare
<1% for single teeth
0.1% in generalised form in Caucasians
25
double teeth
gemination - 1 tooth splits into 2
| fusion - 2 teeth join to form one
26
taurodontism
6.3% in UK
flame shaped pulp
teeth look normal - issue with exposing pulp if placing restoration
27
dilaceration
crown or root
28
accessory cusps
talon cusps
| often do selective grinding - encourage pulp to go back
29
dens in dente
tooth within a tooth
| immediately seal areas to prevent bacterial ingress - you won't be able to do endo for this tooth
30
short root anomaly - which teeth are normally affected?
permanent maxillary incisors
31
short root anomaly prevalence
2.5% incidence
| 15% of these children also have short roots on the canines and premolars
32
short root anomaly aetiologies
radiotherapy
dentine dysplasias
accessory roots
33
short root anomaly impact on tx
means danger for ortho tx
34
types of amelogenesis imperfecta
hypoplastic
hypomineralised
hypomaturational
mixed forms (with taurodontism)
35
env enamel hypoplasia
systemic
nutritional
metabolic e.g. rhesus incompatibility, liver disease
infection e.g. measles
36
localised enamel hypoplasia
trauma or infection to primary tooth
| infection to primary molars can lead to spots on premolars
37
hypomineralisation
secretory phase fine, correct thickness of enamel
mineralisation phase affected
white/brown/yellow patches
38
hypoplastic
happens at earlier phase of amelogenesis
secretory phase affected
quality of enamel usually fine as mineralisation phase unaffected
39
aetiology of hard tissue defects
localised - trauma, caries then abscess of primary
| generalised - env, hereditary
40
fluorosis aetiology
generalised and env
41
fluorosis presentation
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
tx of fluorosis
microabrasion
veneers
vital bleaching
43
MIH aetiology
generalised and env
associated with childhood illness or chronological hypo mineralisation e.g kidney or liver failure
see different levels of abnormality on different teeth - they develop at different times
44
generalised env enamel defects - prenatal
```
rubella
congenital syphillis
thalidomide
F
maternal A and D deficiency
cardiac and kidney disease
```
45
generalised env enamel defects - neonatal
up to 8 weeks
| prematurity, meningitis
46
generalised env enamel defects - post-natal
```
otitis media
measles
chickenpox
TB
pneumonia
diphtheria
deficiency of vits A,C,D
heart disease
long term health problem e.g. organ failure
```
47
aetiology of AI
generalised and hereditary
48
prevalence of AI
1 in 14000
49
types of AI
hypoplastic
hypomineralised
hypomaturation
mixed with taurodontism
50
AI inheritance
familial inheritance
| autosomal dominant, recessive and X-linked
51
does AI have an associated systemic disorder?
not thought to
52
different inheritance patterns of AI more common in certain areas
AD most common in USA and Europe, AR in Middle East
| Generally AI is more common in Scandanavia
53
AI genetics
E formation needs multiple genes to transcribe the process of crystal growth and mineralisation
gene mutations found so far involve enamel ECM molecules amelogenin and enamelin and kallikrein 4
54
diagnosis of AI
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
hypoplastic AI
enamel crystals do not grow to correct length
56
hypo mineralised AI
crystallites fail to grow in thickness and width
57
hypomaturational AI
enamel crystals grow incompletely in thickness/width but to normal length with incomplete mineralisation
58
AI problems
```
sensitivity
caries/acid susceptibility
poor aesthetics
poor OH - hard to brush teeth properly as sore
delayed eruption
AOB
```
59
systemic disorders associated with enamel defects (not AI)
```
epidermolysis bullosa
incontinenta pigmenti
Down Syndrome
Prader-Willi
porphyria
tuberous sclerosis
pseudohypoparathyroidism
Hurler's
```
60
AI solutions
```
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
anomalies of structure - dentine
dentinogenesis imperfecta (most common)
dentine dysplasia
odontodysplasia
systemic disturbance
62
dentine dysplasia
normal crown morphology
amber radiolucency
pulpal obliteration
short constricted roots
63
odontodysplasia
localised arrest in tooth development, thin layers of E and D, large pulp chambers, "ghost teeth"
64
systemic disturbances in dentine structure
nutritional
metabolic
drugs
65
DI prevalence
uncommon
| much less common than AI
66
types of DI
3
67
type 1 DI
osteogenesis imperfecta (blue sclera)
68
type 2 DI
AD
| tends not to be associated with other systemic conditions
69
type 3 DI
Brandywine, Maryland USA - Native American Indian, Irish, Afro-American - not really any new genes - inbreeding
70
DI problems
aesthetics
caries/acid susceptibility
spontaneous abscess
v poor prognosis
71
DI diagnosis
appearance
FH
associated OI
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
DI solutions
```
prevention
composite veneers (but not much to bond onto)
overdentures
removable prostheses
SSCs
```
73
other hereditary dentine defects - limited to dentine only
dentinogenesis imperfecta type 2
dentine dysplasia types 1 and 2
fibrous dysplasia of dentine
74
other hereditary dentine defects - associated with a systemic disorder
```
OI
EDS
brachio-skeletal genital syndrome
rickets
hypophosphatasia
```
75
tooth structure defects - tx overview
```
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
anomalies of structure - cementum
cleidocranial dysplasia
| hypophosphatasia
77
cleidocranial dysplasia
no clavicle
| hypoplasia of cellular component of cementum
78
hypophosphatasia
hypoplasia or aplasia of cementum
early loss of primary teeth
- nothing holding teeth into bone
79
anomalies of eruption - premature
high birth weight
precocious puberty
natal/neonatal tooth
80
natal tooth
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
anomalies of eruption - delayed
```
pre-term and low birth weight children
malnutrition
associated general conditions
- Down syndrome
- hypothyroidism
- hypopituitarism
- cleidocranial dysplasia
gingival hyperplasia/overgrowth
- pseudo delayed eruption
```
82
premature exfoliation
```
trauma
following pulpotomy
hypophosphatasia
immunological deficiency e.g. cyclic neutropenia
Chediak-Higashi syndrome
Histiocytosis X
```
83
delayed exfoliation
infra-occlusion
following trauma
'double' primary teeth
hypodontia
ectopic permanent successors
=these have no permanent tooth to push out primary tooth
84
infraocclusion prevalence
1-9%
| M=F
85
infra occlusion - which is the most common?
L D - congenital absence of premolar
86
infra-occlusion time course
majority exfoliate normally by 11-12 years
tooth isn't sinking into gum, it just isn't moving
some ankylosed - will need extracted - difficult
