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
double teeth 2 types
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 types
crown or root
28
accessory cusps
talon cusps | often do selective grinding - encourage pulp to go back
29
dens in dente
* 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
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 aetiology
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 fluorosis (mild case)
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 **Fluoride** **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
* Autosomal dominant most common in USA and Europe, * A-recessive 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 affecting enamel ECM molecules * **amelogenin** * **enamelin** * kallikrein 4- **KLK4**
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 pigmentii** **Down Syndrome** **Hurler's** Prader-Willi porphyria tuberous sclerosis pseudohypoparathyroidism
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
Autosomal dominant | 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 **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
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 (related syndromes)
* cleidocranial dysplasia * hypophosphatasia
77
cleidocranial dysplasia
* no clavicle * hypoplasia of cellular component of **cementum** * supernumeraries * delayed eruption
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