pedo abnormalities

Question 1

Hyperdontia: presence of supernumerary teeth
prevalence : male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 1

prevalence: male>female, <1% in primary teeth, permanent teeth 1.5-3.5%, 90% in premaxilla, 75% unerupted
etiology: cleidocranial dysostosis, cleft palate (40% have supernumeries)

clinical presentation: mesiodens, paramolar, distomolar forms- conical, supplemental, tuberculate

management: 35-50% primaries will lead to supernumerary permanents, monitor path of eruption of permanent teeth, resorption of roots of adjacent teeth, cyst
removal- before root of permanent tooth >1/2 formed but after enamel formation
extract in coincidence with eruption of perm tooth
can wait and see, but might need to remove when ortho
space maintainer

Question 2

hypodontia= congenital absence of teeth
types
prevalence : male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 2

prevalence:
primary teeth <1%, permanent teeth 3.5%-6.5%
female>male
3rd molars (9-37%)
caucasians- lower 5s followed by upper 2s
mongoloids- lower incisors
<10% of cases have >2 missing teeth

hypodontia, oligodontia= 6 or more missing, anodontia= bogay completely

etiology:
ectodermal dysplasia (brows, hair, frontal bossing, ears sticking out, conical teeth), Ellis van creveld syndrome, down's, clefts

clinical presentation: often occurs with microdontia

management:
hypodontia in primary teeth, 75% perm dentition will be affected
clinical and radiographic assessment, preventive care cos need to save whatever you have, restore aesthetics

Question 3

root number increase
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 3

prevelance:
male>female
lower 6s, canines, premolars
lower canines and premolars likely have a distal lingual root

clinical presentation:
large cusps of carabelli, paramolar tubercles
management: complicate extractions/ortho/endo

Question 4

root number reduction
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 4

prevalence:
female>male
single pyramidal root in <1% of 1st molars, 15-40% of 2nd and 3rd molars

Question 5

double teeth
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 5

prevalence:
no sexual predilection
primary teeth: 1-2%, perm teeth: 0.7% mongoloids
incisors
if primary double teeth, succedaneous tooth may be double or exhibit hyper/hypodontia

management:
difficult plaque control, deep groove present place FS
monitor root resorption of primary double tooth to prevent delay eruption of perm successor, divide tooth for aesthetic/ortho reasons

Question 6

accessory cusp: talon's, cusp of carabelli, paramolar cusp
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 6

talons:
cusp projecting from cingulum of incisors, enamel/dentine/pulp horn
if unaesthetic or interfere w occlusion drill w LA
cusp of carabelli:
extra cusp on mesial-palatal of 6s, usually bilateral
paramolar cusp:
extra cusp on buccal of molars

Question 7

dens invaginatus
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 7

prevalence:
males>females
severe form in 0.25%
1-5% in perm teeth

clinical presentation: deep pits in normal looking teeth, grossly distorted tooth w orifice of invagination at incisal edge
enamel lined cavity within tooth
incomplete enamel lining/dentine deficiency gives communication with pulp and acute dento-alveolar infection

management: prophylactic sealing soon after eruption

Question 8

dens evaginatus
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 8

enamel covered tubercle projecting from tooth surface
prevalence:
mongoloids 1-4%
usually premolars, less often canine and molars
size of tubercle & pulpal extension varies

clinical presentation: fracture and pulpal infection

management: preventive resin restoration with pulpal protection soon after eruption
direct pulp cap if occlusion is in the way

Question 9

dilaceration
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 9

abrupt deviation of long axis of tooth, crown/root affected
trauma to primary incisors @ 4-5 yrs old

management:
mild cases eruption then reshaped for aesthetics
if fail to eruption, orthodontic track down or surgical removal (remove surgically)

Question 10

Hutchinson's incisors
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 10

dental changes in 40-70% of patients with congenital syphilis

hutchinson's incisors:
barrel shaped (incisal edge

Question 11

globodontia
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 11

etiology: otodental syndrome

clinical presentation: high frequency deafness from childhood, globular deformity of crown of premolars & molars

Question 12

taurodontism
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 12

apical extension of trunks of teeth
etiology: ectodermal dysplasia, klinefelter’s syndrome (XXY), 20% of AI cases

clinical presentation: radiograph showing enlarged pulp chamber and short roots

management:
endo treatment complications

Question 13

megadontia
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 13

teeth larger than range of normal distribution
not double tooth by lack of incisal notching & pulpal bifurcation
etiology: pituitary gigantism, hypertrichosis, heriditory gingial hyperplasa, hemifacial hypertrophy

Question 14

microdontia
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 14

prevalence: rare in primary dentition and rare in generalised microdontia
usually perm upper laterals and 8s
etiology: associated with hypodontia, common in ectodermal dysplasia, down’s syndrome
clinical presentation: can have normal form or tapering

Question 15

bigger root
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 15

prevalence: upper canines
males 5x> females

etiology: megadontia

Question 16

smaller root
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 16

etiology: dentine & pulp dysplasia, hypoparathyroidism, excessive irradiation of jaw during root formation

Question 17

arrest of tooth germ development

etiology: syndromes

Answer 17

etiology: osteomyelitis, irradiation of jaw in childhood, severe trauma, chronic untreated chronic pulpal infection of primary teeth, fracture of jaw

Question 18

odontodysplasia
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 18

ghost teeth
etiology: unknown, rare development condition, affected either dentition

clinical presentation: small brown teeth with rough soft surface (mistaken for caries)
pain, swelling, delayed eruption
mild- root formation almost normal, develops later than other teeth
severe- ghost like little differentiation of dental tissues

histo: markedly irregular enamel & amorphous coronal dentine

Question 19

amelogenesis imperfecta
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 19

prevalence: uncommon

etiology: inheritance by autosomal dominant- enamelin gene on chromosome 4
recessive- gene chromosome 2, associated with ocular defects
x-linked inheritance- males more severe, females show vertical bands
associated with taurodontism

clinical presentation:
hypoplastic- looks normal but soft and breaks off in chuncks (enamel not enough), genelralised spacing if enamel uniformly thin, delay in eruption & unerupted teeth may undergo replacement resorption, AOB in 60% of cases
hypomineralised- normal thickness of enamel initially, dark yellow to brown to chalky white depending on degree, enamel wear away to expose rough sensitve dentine, xray difficult to distinguish enamel & dentine, may appear moth eaten

clinical:
SSC/overdentures to maintain VD, Veneers, ortho for AOB, definitive crowns/veneers deferred till late teens

Question 20

tricho-dento-osseous syndrome

clinical presentation: forms

Answer 20

clinical presentation: tight curly hair, cortical osteosclerosis, thick & cornified nails, teeth in mixed AI

Question 21

epidermolysis bullosa dystrophica

clinical presentation: forms

Answer 21

clinical presentation: multiple bullae of mucus membrane & skin
dystrophic nails
fine pittig hypoplasia (honeycomb)

Question 22

Molar-incisor hypomineralisation
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 22

clinical presentation: cheese molars (firable enamel), defects well demarcated with asymmetric distribution, incisors irregular distributed mottling
etiology: uncertain

management:
SCC for molars if not suitable for CR/GIC, CR veneers for incisors, analyse occlusion, KIV extraction

Question 23

environmental enamel defects

Answer 23

localised: infection trauma of primary teeth
generalised: changes during tooth development, prematurity, malnutrition, exanthemathous fevers, excessive F

Question 24

dentinogenesis imperfecta
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 24

prevalence: rare,
etiology: genetic, autosomal dominant
clinical presentation: varying severity, primamry teeth usually worse, opalescent bluish/brownish colour, enamel chips away at ADJ exposing soft dentine which wears away rapidly
xrays show bulbous vrowns, short roots, obliteration of pulp chamber & root canal by abnormal dentine
histo: hypomineralised enamel also, flat ADJ, dentine matrix amorphous, tubules abnormal size & shape

management: difficult cos dentine base suckz

Question 25

coronal dentine dysplasia

clinical presentation:

Answer 25

clinical presentation: primary teeth amber and translucent, perm teeth normal colour, xrays show flame shaped pulp chambers, multiple pulp stones, thin root canal

Question 26

radicular dentine dysplasia

Answer 26

clinical presentation: all teeth affected, rootless teeth/ non opalescent dentine
teeth normal colour or light brown to bluish
xrays show normal crown, roots short, pulp chamber small

Question 27

osteogenesis imperfecta

clinical presentation

Answer 27

clinical presentation:

impaired hearing, brittle bones, blue sclera, 50% have DI, but not all permanent teeth equally affected

Question 28

dentine defects due to environment

etiology

Answer 28

localised: trauma to primary cause change in succedaneous teeth
generalised: tetracycline, irradiation/hypothyroidism

Question 29

genetic defects of cementum
cleidocranial dysostosis
hypophosphatasia
clinical presentation

Answer 29

cleidocranial dysostosis: hypoplasia cementum, may be related to delay
hypophosphatasia: aplasia of cementum, lack of perio attachment, early loss of primary teeth

Question 30

environmental defects of cementum

Answer 30

from chronic infection or traumatic occlusion

Question 31

premature eruption
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 31

prevalence: 1:2000/3000 births
clinical presentation: natal teeth (at birth), neonatal teeth (within 1st month of birth), may be supernumeraries but usually primary teeth, mobile inflamed gingiva

management: may cause trauma to feeding or danger of aspiration, leave to firm up/extract

Question 32

ectopic eruption
prevalence: male/female, 
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene

Answer 32

etiology: presence of supernumerary, odontomes, ectopic crypt position

Question 33

generalised delayed eruption

etiology: syndromes

Answer 33

etiology:
premature low birth wt babies
down's and turner's
cleidocranial dysostosis
malnutrition
reduced growth hormones

Question 34

localised delayed eruption

etiology

Answer 34

etiology: early loss of primary molars delay eruption of premolars, supernumerary, odontomes, fibrous tissue overlying erupting tooth

Question 35

localised premature exfoliation

etiology

Answer 35

pulpal infection spreading to periradicular tissue, ectopic eruption of 6 cause resorption of distal root and early loss of E

Question 36

generalised premature exfoliation

etiology

Answer 36

hypophosphatasia

histiocytosis X

Question 37

generalised delayed exfoliation

etiology

Answer 37

down’s turner’s

Question 38

localised delayed exfoliation

etiology

Answer 38

primary double teeth, congenital absence of perm successor, infraocclusion

Question 39

physiological root resorption when and how?

Answer 39

begins soon after root formation completed after 3-4 yrs

intermitten process with period of repair

Question 40

pathological root resorption etiology

Answer 40

trauma, infection, excessive ortho, impacted/supernumerary teeth