Abnormalities of the Teeth
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Steven Chussid D.D.S. |
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Director, Division of Pediatric
Dentistry |
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Abnomalities of teeth
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Environmental alterations |
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Developmental alterations |
Environmental alterations
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Effects on tooth structure
development |
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Localized |
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Systemic |
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Postdevelopmental structure
loss |
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Discoloration of teeth |
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Localized disturbances of
eruption |
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Local factors associated
with enamel defects
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Trauma |
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Local infection |
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Irradiation |
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Enamel hypoplasia
Enamel hypocalcification
Systemic factors associated
with enamel defects
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Infections |
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Medications |
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Inherited diseases |
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Metabolic disorders |
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Malnutrition |
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Birth-related trauma |
Enamel hypoplasia
Enamel hypoplasia
Enamel hypoplasia
Enamel hypoplasia-Rickets
Fluorosis
Fluorosis
Postdevelopmental tooth
loss
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Tooth wear |
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Attrition |
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Caused by tooth to tooth
contact |
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Abrasion |
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Caused by external agent |
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Erosion |
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Caused by chemical process |
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Internal resorption |
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External resorption |
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Attrition
Attrition
Erosion-Bulemia
Internal resorption
Internal resorption
External resorption
External resorption
Environmental discoloration
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Extrinsic |
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Bacteria |
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Iron |
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Tobacco |
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Food and beverage |
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Restorative materials |
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Medications |
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Iron stain
Environmental discoloration
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Intrinsic |
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Erythropoietic porphyria |
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Hyperbilirubinemia |
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Trauma |
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Medications |
Erythropoietic porphyria
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Autosomal recessive disorder of
porphyrin metabolism that results in increased synthesis and excretion of
porphyrins |
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Diffuse discoloration of
dentition results |
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Teeth appear red-brown and
exhibit a red fluorescence when exposed to UV light |
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Prophyrin present in enamel and
dentin of deciduous teeth so discoloration worse |
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Only dentin of permanent teeth
affected |
Erythropoietic porphyria
Hyperbilirubinemia
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Excess levels of bilirubin in
blood |
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Bilirubin can accumulate in
interstitial fluid, mucosa, skin and developing teeth |
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Causes include- |
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Erythroblastosis fetalis |
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A hemolytic anemia of newborns
secondary to blood incompatibility |
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Biliary atresia |
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A sclerosing process of the
biliary tree |
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Premature birth |
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Internal hemorrhage |
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Hyperbilirubinemia
Trauma
Tetracycline stain
Tetracycline stain
Fluorosis
Localized disturbances of
eruption
Ankylosis
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Cessation of eruption after
emergence occuring from an anatomic fusion of tooth cementum or dentin to
alveolar bone |
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Etiology unknown-trauma, local
change of metabolism, thermal irritation, and genetic predisposition have
been suggested |
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Can occur at any age but is
clinically most evident when it develops during first two decades of life |
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Peak prevalence- 8-9 years of
age |
Ankylosis
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Reported prevalence of
clinically detectable ankylosis- 1.5% to 9% |
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Primary molars are most
commonly involved teeth with most cases in mandible |
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Radiographic findings |
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Sound on percussion |
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Treatment considerations |
Ankylosis
Ankylosis
Ankylosis
Ankylosis
Natal teeth
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Usually prematurely erupted
primary teeth |
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Present at birth |
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Prevalence- 1 in 2000 |
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Neonatal teeth erupt within
first month |
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85% are lower incisors, 11%
maxillary incisors |
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Treatment |
Natal teeth
Natal teeth
Natal teeth
Natal teeth
Developmental alterations
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Number |
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Size |
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Shape |
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Structure |
Developmental alterations
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Number |
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Hypodontia |
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Lack of development of one or
more teeth |
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Anodontia |
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Total lack of tooth development |
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Hyperdontia |
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Development of an increased
number of teeth |
Hypodontia
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Common dental anomaly |
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3.5%-8% (excluding third
molars) |
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Female predominance about 1.5:1 |
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Uncommon in primary dentition
(<1%) |
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About 20-23% of population
missing third molars |
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After third molars, second
premolars and laterals most frequent |
Syndromes associated with
hypodontia
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Ectodermal dysplasia |
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Chondroectodermal dysplasia
(Ellis-van Creveld) |
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Incontinentia pigmenti |
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Progeria |
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Down |
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Hallermann-Streiff |
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Rieger |
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Crouzons |
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Albright hereditary
osteodystrophy |
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Hypodontia
Hypodontia
Hypodontia
Hypodontia-Ectodermal
dysplasia
Hyperdontia
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Prevalence of supernumerary
teeth is about 1%-3% (higher rate in Asians) |
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Single tooth hyperdontia
represent 75%-85% of cases |
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More common in permanent
dentition |
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Almost 90% in maxilla |
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Maxillary incisor region most
common site then 4th molars,premolars and canines |
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If multiples, usually in
mandibular premolar region |
Syndromes associated with
hyperdontia
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Cleidocranial dysplasia |
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Oral-Facial-Digital |
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Craniometaphyseal dysplasia |
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Apert |
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Hyperdontia
Mesiodens
Hyperdontia
Hyperdontia
Cleidocranial dysplasia
Paramolar
Developmental alterations
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Size |
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Microdontia |
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Macrodontia |
Microdontia
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Teeth are smaller that usual |
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Relative
microdontia=macrognathia |
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Diffuse true microdontia is
uncommon but may occur in Down syndome and pituitary dwarfism |
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Prevalence of isolated
microdontia is between 1% and 8% |
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Maxillary lateral incisor most
frequently affected |
Microdont- peg lateral
Microdont- peg lateral
Microdont
Macrodontia
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Teeth are larger than usual |
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Relative
macrodontia=micrognathia |
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Diffuse involvement very rare |
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Has been noted in association
with pituitary gigantism and hemifacial hyperplasia |
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Macrodontia
Developmental alterations
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Shape |
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Gemination |
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Fusion |
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Concrescence |
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Talon cusp |
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Dens evaginatus |
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Dens invaginatus |
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Taurodontism |
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Dilaceration |
Double teeth
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Gemination and fusion |
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May have very similar clinical
appearance |
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Higher frequency in anterior
and maxillary regions |
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Rate is about 0.1% in permanent
dentition and 0.5% in deciduous |
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Bilateral cases more infrequent |
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Etiology unknown but trauma has
been suggested |
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Treatment considerations |
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Gemination
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Single joined or enlarged tooth
in which tooth count is normal when anomalous tooth is counted as one |
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Result from single tooth
bud???? |
Gemination
Gemination
Gemination
Fusion
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Single joined or enlarged tooth
in which tooth count reveals missing tooth when anomalous tooth is counted as
one |
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Union of two separate tooth
buds? |
Fusion
Fusion
Fusion
Concrescence
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Union of two adjacent teeth by
cementum alone |
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May occur before or after
eruption |
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Seen most commonly posterior
and maxillary regions |
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Etiology believed to be trauma
or overcrowding |
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Treatment considerations |
Concrescence
Talon cusp
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Well-delineated additional cusp
on the surface of an anterior tooth and extends 1/2 the distance from CEJ to
incisal edge |
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Vast majority on lingual
surface |
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Prevalence studies vary from
<1% to 8% |
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3/4 found in permanent
dentition, most commonly maxillary lateral then central |
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In deciduous dentition,
maxillary central most common site |
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Has been associated with other
dental anomalies |
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Treatment considerations |
Talon cusp
Dens evaginatus
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Also known as a central
tubercle |
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A cusplike elevation located in
the central groove |
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Typically occurs in permanent
mandibular premolars |
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Usually bilateral |
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Rare in whites with higher
prevalence in Asians, native Americans and Alaskans |
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Treatment considerations |
Dens evaginatus
Dens invaginatus
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Dens in dente |
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Deep surface invagination of
crown that is lined by enamel |
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Represents an accentuation of
the lingual pit |
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Depth varies |
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Prevalence studies vary from
<1% to 10% |
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Lateral incisors most commonly
affected |
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Bilateral involvement common |
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Treatment considerations |
Dens invaginatus
Taurodontism
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Enlargement of the body and
pulp chamber of a multirooted tooth with apical displacement of the pulpal
floor |
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More commonly seen in permanent
dentition |
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Prevalence is highly variable |
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2%-3% in U.S. |
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Much higher in Eskimos and
Middle Eastern populations |
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Increased frequency in patients
with CL and/or CP, Down, Klinefelter,ectodermal dysplasia,
trich-dento-osseous |
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Taurodontism
Dilaceration
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Abnormal angulation or bend in
the root |
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Thought to be related to trauma
during root development |
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Permanent maxillary incisors
most commonly affected followed by mandibular incisors |
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Rare in primary dentition |
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Treatment depends on severity |
Dilaceration
Amelogenesis imperfecta
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A heterogeneous group of
hereditary disorders that demonstrate developmental alterations in the
structure of enamel in the absence of a systemic disorder |
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Many subtypes |
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Numerous patterns of
inheritance |
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Wide variety of clinical
manifestations |
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Frequency varies between 1:718
and 1:14,000 |
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Both dentitions involved |
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Amelogenesis imperfecta
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Formation of enamel a multistep
process |
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Formation of enamel matrix |
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Mineralization of matrix |
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Maturation of matrix |
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Hereditary defects of enamel
formation usually classified as: |
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Hypoplastic |
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Hypocalcified |
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Hypomaturative |
Amelogenesis
imperfecta
Witkop classification
Amelogenesis imperfecta
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Hypoplastic |
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Teeth erupt with insufficient
amounts of enamel |
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Amount of enamel varies greatly |
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Enamel present is mineralized
appropriately and contrasts well with dentin on radiographs |
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Teeth may have abnormal shape
and open contacts |
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Open bite may be present |
AI-Hypoplastic smooth
AI-Hypoplastic pitted
AI-Hypoplastic pitted
AI-Hypoplastic rough
Amelogenesis imperfecta
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Hypocalcified |
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Proper amount of enamel matrix
is formed but but it doesn’t mineralize properly |
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Teeth shaped normally upon
eruption but enamel is soft and easily lost |
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Enamel yellow-brown upon
eruption but quickly becomes brown to black |
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Accumulate calculus |
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Enamel and dentin have similar
density on radiographs |
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AI-Hypocalcified
AI-Hypocalcified
Amelogenesis imperfecta
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Hypomaturative |
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Enamel matrix is laid down
properly and begins to mineralize but there is a defect in maturation of
enamel’s crystal structure |
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Affected teeth normal in shape |
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Mottled appearance-white, brown
or yellow |
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Enamel soft and chips away from
dentin |
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Enamel has similar radiodensity
to dentin |
AI-Hypomaturative
AI-Hypomaturative,
snowcapped
Dentinogenesis imperfecta
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Hereditary developmental
disturbance of dentin |
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Autosomal dominant |
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Also known as hereditary
opalescent dentin |
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Shields classification |
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Prevalence is about 1:8000 |
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Most cases in whites of English
or French ancestry from communities near English Channel |
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Dentinogenesis imperfecta
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All teeth in both dentitions
affected |
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Deciduous teeth affected most
severely followed by permanent incisors and first molars |
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Yellow-brown to blue-gray
translucent, opalescent appearance |
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Enamel frequently separates
easily from dentin |
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Once exposed, dentin exhibits
rapid attrition |
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Bulbous crowns with cervical
constriction |
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Thin roots |
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Early obliteration of pulp
chambers and root canals |
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Dentinogenesis imperfecta
Dentinogenesis imperfecta
Dentinogenesis imperfecta
Dentinogenesis imperfecta
Dentinogenesis imperfecta
Dentin dysplasia
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Rare autosomal-dominant
condition that affects dentin |
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Prevalence about 1:100,000 |
Dentin dysplasia
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Type I |
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Radicular type or ‘rootless
teeth’ |
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Roots short and pulps almost
obliterated |
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Periapical radiolucencies |
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More common type |
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Enamel and coronal dentin are
normal |
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Wide variation in root
formation because dentinal disorganization may occur at different stages of
tooth development |
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Color is normal in both
dentitions |
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Radiographically, deciduous
teeth more severly affected |
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Dentin dysplasia type I
Dentin dysplasia type I
Dentin dysplasia
Dentin dysplasia
Dentin dysplasia
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Type II |
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Coronal type |
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Root length normal in both
dentitions |
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Primary teeth |
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Clinically resemble
dentinogenesis imperfecta |
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Radiographically have similar
appearance to Type I |
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Permanent teeth |
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Normal coloration |
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Pulp chambers enlarged with
apical extension-thistle-tube-shaped or flame-shaped |
Dentin dyplasia type II
Dentin dyplasia type II
Regional odontodysplasia
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‘Ghost teeth’ |
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Localized, non-hereditary
developmental abnormality of teeth with extensive adverse effects on
formation of enamel, dentin and pulp |
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Occurs in region or quadrant |
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Etiology unknown |
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Occurs in both dentitions and
if present in primary dentition,permanent teeth in area usually affected |
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Maxillary predominance- 2.5:1 |
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Many affected teeth fail to
erupt |
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Erupted teeth have small
irregular yellow-brown crowns |
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Short roots, enlarged pulp and
open apical foramina |
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Regional odontodysplasia
Regional odontodysplasia
Regional odontodysplasia
References
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Oral & Maxillofacial
Pathology-Second Edition |
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Neville, Damm, Allen and
Bouquot |
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Oral Pathology-Clinical
Pathologic Correlations |
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Regezi, Sciubba and Jordan |
Thank you!