pedo abnormalities Flashcards
Hyperdontia: presence of supernumerary teeth prevalence : male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
hypodontia= congenital absence of teeth types prevalence : male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
root number increase prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
root number reduction prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
prevalence:
female>male
single pyramidal root in <1% of 1st molars, 15-40% of 2nd and 3rd molars
double teeth prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
accessory cusp: talon's, cusp of carabelli, paramolar cusp prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
dens invaginatus prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
dens evaginatus prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
dilaceration prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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)
Hutchinson's incisors prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
dental changes in 40-70% of patients with congenital syphilis
hutchinson's incisors: barrel shaped (incisal edge
globodontia prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
etiology: otodental syndrome
clinical presentation: high frequency deafness from childhood, globular deformity of crown of premolars & molars
taurodontism prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
megadontia prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
microdontia prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
bigger root prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
prevalence: upper canines
males 5x> females
etiology: megadontia
smaller root prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
etiology: dentine & pulp dysplasia, hypoparathyroidism, excessive irradiation of jaw during root formation
arrest of tooth germ development
etiology: syndromes
etiology: osteomyelitis, irradiation of jaw in childhood, severe trauma, chronic untreated chronic pulpal infection of primary teeth, fracture of jaw
odontodysplasia prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
amelogenesis imperfecta prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
tricho-dento-osseous syndrome
clinical presentation: forms
clinical presentation: tight curly hair, cortical osteosclerosis, thick & cornified nails, teeth in mixed AI
epidermolysis bullosa dystrophica
clinical presentation: forms
clinical presentation: multiple bullae of mucus membrane & skin
dystrophic nails
fine pittig hypoplasia (honeycomb)
Molar-incisor hypomineralisation
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene
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
environmental enamel defects
localised: infection trauma of primary teeth
generalised: changes during tooth development, prematurity, malnutrition, exanthemathous fevers, excessive F
dentinogenesis imperfecta
etiology: syndromes
clinical presentation: forms
management: if/when/how to intervene
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
coronal dentine dysplasia
clinical presentation:
clinical presentation: primary teeth amber and translucent, perm teeth normal colour, xrays show flame shaped pulp chambers, multiple pulp stones, thin root canal
radicular dentine dysplasia
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
osteogenesis imperfecta
clinical presentation
clinical presentation:
impaired hearing, brittle bones, blue sclera, 50% have DI, but not all permanent teeth equally affected
dentine defects due to environment
etiology
localised: trauma to primary cause change in succedaneous teeth
generalised: tetracycline, irradiation/hypothyroidism
genetic defects of cementum
cleidocranial dysostosis
hypophosphatasia
clinical presentation
cleidocranial dysostosis: hypoplasia cementum, may be related to delay
hypophosphatasia: aplasia of cementum, lack of perio attachment, early loss of primary teeth
environmental defects of cementum
from chronic infection or traumatic occlusion
premature eruption prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
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
ectopic eruption prevalence: male/female, etiology: syndromes clinical presentation: forms management: if/when/how to intervene
etiology: presence of supernumerary, odontomes, ectopic crypt position
generalised delayed eruption
etiology: syndromes
etiology: premature low birth wt babies down's and turner's cleidocranial dysostosis malnutrition reduced growth hormones
localised delayed eruption
etiology
etiology: early loss of primary molars delay eruption of premolars, supernumerary, odontomes, fibrous tissue overlying erupting tooth
localised premature exfoliation
etiology
pulpal infection spreading to periradicular tissue, ectopic eruption of 6 cause resorption of distal root and early loss of E
generalised premature exfoliation
etiology
hypophosphatasia
histiocytosis X
generalised delayed exfoliation
etiology
down’s turner’s
localised delayed exfoliation
etiology
primary double teeth, congenital absence of perm successor, infraocclusion
physiological root resorption when and how?
begins soon after root formation completed after 3-4 yrs
intermitten process with period of repair
pathological root resorption etiology
trauma, infection, excessive ortho, impacted/supernumerary teeth
