1. Growth (eruption) of teeth
1.1. Premature eruption (Natal / Neonatal teeth)
1.1.1. Natal
1.1.1.1. Deciduous teeth that have erupted into the oral cavity in infants at birth
1.1.2. Neonatal teeth
1.1.2.1. erupts prematurely within the first 30 days of life
1.1.3. teeth are often well formed, normal in all aspects but may exhibit mobility.
1.1.4. Seen when only a single deciduous teeth is lost w/t subsequent eruption of the succedaneous tooth.
1.2. Delayed eruption
1.2.1. Causes
1.2.1.1. Systemic
1.2.1.1.1. rickets, cretinism, cleidocranial dysplasia.
1.2.1.2. Local
1.2.1.2.1. fibromatosis gingivae.
1.3. Multiple unerupted teeth
1.3.1. Uncommon condition
1.3.2. Deciduous teeth may be retained
1.3.2.1. Or Deciduous teeth would be shed
1.3.2.1.1. but the permanent teeth would have failed to erupt (Pseudo-anodontia).
1.3.3. Radiographs may be normal
1.3.3.1. but the eruptive forces would be lacking.
1.4. Embedded and Impacted teeth
1.4.1. individual teeth which are unerupted usually because of a lack of eruptive force.
1.4.2. Impacted teeth are prevented from eruption by some physical barrier in the eruption path
1.4.2.1. Lack of space – crowding, premature loss of deciduous teeth.
1.4.2.2. Rotation of tooth buds.
1.4.3. C/F
1.4.3.1. Any tooth may be impacted
1.4.3.1.1. usually mandibular third molars (22%)
1.4.3.1.2. maxillary third molars (18%)
1.4.3.1.3. maxillary cuspids (0.9%)
1.4.3.2. Mandibular teeth are more severely impacted than maxillary teeth.
1.4.4. Complications
1.4.4.1. Infection
1.4.4.2. Resorption of adjacent roots.
1.4.4.3. Periodic pain and even trismus.
1.4.4.4. Referred pain from impacted tooth.
1.4.4.5. Dentigerous cyst and ameloblastomatous change.
1.5. Ankylosed deciduous teeth
1.5.1. called Submerged teeth, Infraocclusion, Secondary retention, Submergence, Reimpaction and Reinclusion.
1.5.2. Submerged appearance may be due to
1.5.2.1. Continued growth of the alveolar process
1.5.2.2. Crown height of deciduous tooth is less than that of adjacent permanent teeth.
1.5.3. Solid sound on percussion when compared to the dull, cushioned sound of normal teeth.
1.5.4. Diagnosis is suspected clinically and confirmed with radiographs.
1.5.5. Complications
1.5.5.1. Development of malocclusion
1.5.5.2. Local periodontal disturbance
1.5.5.3. Dental caries of both the ankylosed tooth + adjacent teeth.
2. structure of teeth
2.1. Enamel hypoplasia
2.1.1. Ameloblasts – extremely sensitive to to external stimuli
2.1.1.1. many factors can result in enamel abnormalities
2.1.2. types of enamel abnormalities
2.1.2.1. Caused by environmental factors
2.1.2.1.1. occurs only when the injury occurs during the development or more specifically
2.1.2.1.2. Once the enamel is calcified
2.1.2.2. Hereditary – Amelogenesis imperfecta (AI)
2.1.3. C/F
2.1.3.1. 3 types of defects seen
2.1.3.1.1. Hypoplasia
2.1.3.1.2. Diffuse opacities
2.1.3.1.3. Demarcated opacities
2.2. Amelogenesis imperfecta
2.2.1. called hereditary enamel dysplasia, hereditary brown enamel
2.2.2. Entirely an ectodermal disturbance
2.2.3. Classification
2.2.3.1. Hypoplastic
2.2.3.1.1. enamel is not formed to full
2.2.3.1.2. normal thickness
2.2.3.2. Hypocalcified
2.2.3.2.1. enamel is so soft + it can be removed by prophylaxis instrument.
2.2.3.3. Hypomaturation
2.2.3.3.1. enamel can be pierced by an explorer
2.2.3.4. Hypomaturation-hypoplastic
2.2.3.4.1. associated with Taurodontism
2.2.4. C/F
2.2.4.1. All teeth of both dentitions affected to some degree.
2.2.4.2. Crowns may show discoloration(dark)
2.2.4.3. Enamel may be totally lost
2.2.4.4. have chalky texture or cheesy consistency or relatively hard.
2.2.5. Radiographic features
2.2.5.1. Enamel may be totally absent
2.2.5.2. or seen only on the cusp tips and inter-proximal surfaces.
2.2.5.3. similar radiodensity to dentin.
2.2.6. Histologic features
2.2.6.1. Disturbance in the differentiation of ameloblast
2.2.6.1.1. seen as defective matrix formation
2.2.6.2. Hypocalcification
2.2.6.2.1. shows defects in matrix structure and mineral deposition.
2.2.6.3. Hypomaturation
2.2.6.3.1. shows alterations in enamel rods and rod sheath structures.
2.3. Dentinogenesis imperfecta
2.3.1. called Hereditary opalescent dentin, Capdepont’s teeth.
2.3.2. Only the mesodermal portion of the odontogenic apparatus is affected.
2.3.3. Dentin is defective.
2.3.4. Can be seen in association with Osteogenesis Imperfecta(OI)
2.3.5. Classification
2.3.5.1. Type I
2.3.5.1.1. DI that always occur with OI
2.3.5.2. Type II
2.3.5.2.1. DI that never occurs with OI
2.3.5.3. Type III
2.3.5.3.1. Brandy wine type – similar to I and II along with multiple pulp exposures in deciduous teeth
2.3.6. C/F
2.3.6.1. Deciduous teeth are more severely affected in Type I.
2.3.6.2. Both the dentitions are equally affected in Type II and III.
2.3.6.3. characteristic translucent or opalescent hue. .
2.3.6.4. Dentin is attrided rapidly.
2.3.6.5. Enamel may be lost early
2.3.7. Radiographic features
2.3.7.1. Type I&II
2.3.7.1.1. Total or partial obliteration of the pulp chambers and root canals
2.3.7.1.2. Roots may be short and blunted.
2.3.7.1.3. Seen in both dentitions.
2.3.7.2. Type III
2.3.7.2.1. marked variation.
2.3.7.2.2. describes it as Shell teeth.
2.3.7.2.3. extremely thin dentin and enormous pulp chambers.
2.3.7.2.4. Roots are extremely short.
2.3.8. Histologic features
2.3.8.1. Normal enamel
2.3.8.2. irregular tubules with large areas of uncalcified matrix in dentin
2.3.8.3. Tubules are larger in diameter and lesser in number.
2.3.8.4. Pulp chamber is obliterated by dentin deposition
2.4. Dentin dysplasia
2.4.1. Called Rootless teeth.
2.4.2. disturbance in dentin formation characterized by normal enamel but atypical dentin formation with abnormal pulp morphology.
2.4.3. Classification
2.4.3.1. Shields
2.4.3.1.1. Type I
2.4.3.1.2. Type II
2.4.3.2. Witkops
2.4.3.2.1. Type I
2.4.3.2.2. Type II
2.4.4. Etiology
2.4.4.1. Hereditary disease.
2.4.4.2. Autosomal dominant inheritance.
2.4.5. C/F
2.4.5.1. Radicular
2.4.5.1.1. Both dentitions are affected.
2.4.5.1.2. clinically normal in morphology and color.
2.4.5.1.3. Slight amber translucency.
2.4.5.1.4. Extreme mobility of teeth and premature exfoliation due to abnormally short roots.
2.4.5.2. Coronal
2.4.5.2.1. Both dentitions are affected.
2.4.5.2.2. Permanent dentition is normal.
2.4.6. Radiographic features
2.4.6.1. Radicular
2.4.6.1.1. Pulp chambers +root canals are completely obliterated in deciduous
2.4.6.1.2. Crescent shaped pulpal remnant
2.4.6.1.3. Obliteration of permanent teeth
2.4.6.1.4. Periapical radiolucencies
2.4.6.2. Coronal
2.4.6.2.1. Pulp chambers of deciduous teeth are obliterated.
2.4.6.2.2. Periapical radiolucencies do not occur.
2.4.6.2.3. Obliteration does not occur befor eruption.
2.4.7. Histologic features
2.4.7.1. Radicular
2.4.7.1.1. portion of coronal dentin is usually normal.
2.4.7.1.2. Normal dentinal tubule formation appears to be blocked
2.4.7.2. Coronal
2.4.7.2.1. Coronal dentin is relatively normal.
2.4.7.2.2. Permanent teeth has multiple pulp stones or denticles.
2.5. Regional odontodysplasia
2.5.1. called odontodysplsia, odontogenic dysplasi ,Ghost teeth and Odontogenesis imperfecta.
2.5.2. Unusual dental anomaly in which one / several teeth in a localized area are affected.
2.5.3. Causes
2.5.3.1. Somatic mutation , Latent virus , Local vascular defects, Hyperpyrexia
2.5.4. C/F
2.5.4.1. Maxillary teeth are frequently involved
2.5.4.1.1. permanent incisors and cuspids.
2.5.4.2. Mandibular anteriors may be affected.
2.5.4.3. Both the dentitions are affected.
2.5.4.4. delayed or total failure of eruption.
2.5.4.5. Irregular in shape
2.5.5. Radiographic feature
2.5.5.1. reduction in radiodensity
2.5.5.1.1. ghost appearance.
2.5.6. Histologic features
2.5.6.1. reduction in the amount of dentin.
2.5.6.2. Widening of predentin layer.
2.5.6.3. Large areas of interglobular dentin.
2.5.6.4. calcified bodies