Dental Anomalies I Flashcards
Ameloblasts:
extremely sensitive to external stimuli
Enamel defects
Enamel defects may be caused by
Enamel — does not occur after initial formation
Abnormalities
local or systemic factors
remodeling
etched permanently on tooth surface
Stages of enamel development:
(3)
(1) Matrix formation: enamel proteins laid down
(2) Mineralization: minerals deposited, original proteins removed
(3) Maturation: final mineralization, remaining original proteins removed
Hard, translucent enamel
Timing of injury:
Final enamel:
affects location and appearance of defect
record of all significant insults received during tooth
development
Enamel defects
Clinical features:
(2)
Enamel hypoplasia:
Enamel opacities:
Clinical features:
Enamel hypoplasia:
(2)
large areas of missing enamel
Pits, fissures, grooves
Enamel opacities:
(3)
areas of enamel hypomaturation
diffuse or demarcated
White, yellow, brown
Turner hypoplasia
Periapical inflammatory disease or trauma of overlying deciduous tooth
Turner hypoplasia
Clinical and Radiographic features:
Observed in
Traumatic cases –
Focal areas of
Extensive hypoplasia –
RG: (2)
permanent teeth – MC premolar
max central incisors
white, yellow, brown discoloration
may involve entire crown
lack of enamel, irregular surface dentin
Antineoplastic therapy
Developmental abnormalities secondary to use of
Severity dependent on (4)
— therapy – more severe alterations
radiation or chemotherapy
age of treatment, form of therapy, dose and field of radiation
Radiation
Antineoplastic therapy
Clinical features:
Radiation: (4)
Chemotherapy: (3)
enamel hypoplasia, microdontia, radicular hypoplasia, Hypodontia
enamel hypoplasia, microdontia, occasionally radicular hypoplasia
Dental Fluorosis
(3)
Ingestion of excessive FL → significant enamel defects
Retention of amelogenin proteins in enamel → hypomineralized enamel
Dose dependent
Dental fluorosis
Clinical features:
(3)
White, opaque enamel, with areas of brown/yellow discoloration
Affected teeth are caries resistant
Bilateral, symmetrical distribution
Treatment: enamel defects
(3)
Most defects are cosmetic
Focal loss of enamel – increased prevalence of caries
Composite restorations, veneers, full crowns
Tooth wear
Considered pathologic when the degree of destruction creates
functional,
aesthetic, or dental sensitivity problems
Attrition
(2)
Loss of tooth structure due to tooth-to-tooth contact
Poor-quality/absent enamel can accelerate process
Attrition
Clinical features:
(3)
Incisal and occlusal surfaces
Large, flat, smooth and shiny wear facets
Slow loss of tooth structure, reparative secondary dentin forms
Abrasion
(2)
Pathologic wearing of tooth structure secondary to an external agent
Toothbrushing MC
Abrasion
Clinical features:
Dependent on —
Toothbrushing:
Tobacco pipe, bobby pins:
cause
horizontal cervical notches on buccal surface
V-shaped notches on incisal edge
Erosion
(2)
Loss of tooth structure caused by a non-bacterial chemical process
Exposure to acidic source, reduced salivary flow
Erosion
Clinical features:
(2)
Cupped lesion, central depression of dentin surrounded by elevated enamel
May create concave sloping areas on palatal surfaces
Tooth wear treatment
— cause
Detailed —, — measures
Erosion:
Restorative treatment:
Multifactorial
diagnosis, preventative
may consider limiting toothbrushing 1x daily
composite, veneers, full crown
Extrinsic stains
Arises from the surface accumulation of
Usually can be removed with
Ex (6)
exogenous pigment
surface treatment
Tobacco, bacterial stains, food + beverages, iron, restorative materials, medications
Intrinsic stains
Arises from
Cannot be removed by —
Ex (6)
endogenous materials that are incorporated into enamel and dentin
prophylaxis
Amelogenesis imperfecta, dentinogenesis imperfecta, dental fluorosis, hyperbilirubinemia, trauma, medications
Internal Resorption
Loss of tooth structure on the
Commonly arises secondary to
Continues if
dentinal walls of the pulp
inflammatory reaction
vital pulp tissue remains
Internal Resorption
Clinical and Radiographic features:
Inflammatory resorption:
Replacement resorption:
Coronal pulp affected →
resorbed dentin replaced by inflamed granulation tissue
pulpal dentinal wall is resorbed with bone and cementum-like bone
pink tooth of Mummery
Inflammatory resorption:
RG:
resorbed dentin replaced by inflamed granulation
tissue
well-circumscribed radiolucent enlargement of pulp chamber
External resorption
Loss of tooth structure along
Exposure of
Common causes: (4)
Common!
external surface of root
adjacent mineralized cementum to cemetoclasts
localized pressure (ie: orthodontic therapy), excessive
occlusal forces, cysts, tumors
External resorption
Clinical and Radiographic findings:
(2)
“moth-eaten” loss of tooth structure
Over pulp chamber, radiolucency superimposed
Ankylosis
(2)
Anatomic fusion of tooth cementum with the alveolar bone
May be caused by trauma, chemical/thermal irritation, genetically
decreased PDL
Ankylosis
Clinical features:
(5)
MC 1st-2nd decade
MC mandibular primary first molar
Mandible 10:1
Ankylosis of permanent teeth uncommon
Sharp, solid sound upon percussion
Ankylosis
Radiographic features:
(3)
Absence of PDL space (difficult to detect)
Adjacent teeth inclined towards affected tooth
Supraeruption of opposing tooth
Ankylosis
Treatment:
For primary teeth (lack of exfoliation) → extraction
Anodontia:
total lack of development of teeth
Hypodontia:
lack of development of one or more teeth
Oligodontia:
lack of development of 6 or more teeth
Hyperdontia:
development of an increased # of teeth – supernumerary
Tooth number anomalies
(3)
More than 200 genes associated with odontogenesis
Syndromic and non syndromic
MC genes implicated: PAX9, MSX1, AXIN2 genes (hypodontia)
Hypodontia
Prevalence of
Absence of
Syndrome associated:
3-10% in permanent teeth
primary teeth correlates strongly with missing successor
Ectodermal dysplasia
Hypodontia
Clinical features:
(2)
After 3rd molars, MC in 2nd premolar and lateral incisor
MC in females
Hyperdontia
Most cases represent
Syndromes: (2)
Positively correlated with —
single-tooth supernumerary
Cleidocranial dysplasia, Gardner
macrodontia
Hyperdontia
Clinical features:
(3)
Single tooth hyperdontia: MC in anterior maxilla – mesiodens
Accessory 4th molar: distomolar/distodens
2: 1 male
Microdontia
(4)
Presence of unusually small teeth
Genetic and environmental factors play a role
Conditions: Down syndrome, pituitary dwarfism
Isolated cases more common than diffuse cases
Microdontia
Clinical features:
(2)
Isolated microdontia: MC in max lateral – peg lateral
MC in females
Macrodontia
(4)
Teeth larger than average
Genetic and environmental factors play a role
Conditions: pituitary gigantism, XYY males, pineal hyperplasia,
hyperinsulinism
Isolated cases more common than diffuse cases
Macrodontia
Clinical features:
(2)
Isolated macrodontia: MC in incisors or canines
MC in males
