Anomalies Dentin

DENTINOGENESIS IMPERFECTA •A hereditary developmental disturbance of the dentin •Similar dental changes may be seen in conjunction with the systemic hereditary disorder of bone osteogenesis imperfecta•Morphologically:

oThe dentitions have a blue-to-brown discoloration often with a distinctive translucence o The enamel frequently separates easily fro m the underlying defective dentin. Once exposed, the dentin often demonstrates significantly accelerate d attrition

•Radiographically:o the teeth have bulbous crownsoCervicalconstrictionothin roo tsoobli teration of the root canals and pulp chambe rs oSome teeth may show normal sized pulps or pulpal enlargement

•Histologically:oShort misshapen tubules course through an atypical granular dentin matrix which often demonstrates interglobular calcification

• Treatment– Overlay dentures placed on teeth that are covered

with fluoride-releasing glass-ionomer cement– Additional therapeutic approaches

VITAMIN D-RESISTANT RICKETS• Inherited as an X- linked(male) dominant trait• The disorder is caused by mutations in a zinc metalloproteina

se gene known as PHEX (phosphate regulating gene)• Radiographically :

– large pulp chambers with pulp horns extending almost to the dentinoenamel junction

• In some cases ,the cuspal enamel may be worn down by attrition to the level of the pulp horn causing pulpal exposure and pulp death

• Morphologically:– The tooth appear dead

• Histologically:– The dentin appears abnormal and is characterized by the deposition

of globular dentin , which often exhibits clefting.

• Treatment– early treatment with calcitriol and multiple daily

doses of phosphate.– Endodontic therapy is necessary for the pulpally

involved teeth.

Dentin Dysplasia• Thereare two major pattern s: type I and type II• Caused by genetic disorder• Dentine dysplasia type I– Normal shape, form and consistency.– radiographically :little or no detectable pulp and

roots that are markedly short or absent.

• Dentin Dysplasia Type II– exhibits numerous features of dentinogenesis

imperfecta– Radiographically:bulbous crowns, cervical

constriction, thin roots, and obliteration of the pulp.

• Treatment:– Excessive care of oral hygiene must be established

and maintained– If periapical inflammato ry lesions develop the

therapeutic choice is use and is guided by the root length.

Regional odontodysplasia • localized nonhereditary developmental abnormality of teeth with extensive

adverse effects on the formation of enamel, dentin ,and pulp. • Most cases are idiopathic, but a number have been related to various

syndromes,Growth abnormalities, Neural disorders. and vascular malformations

• Morphology:Many of the affected teeth fail to erupt. Erupted teeth demonstrate small irregular crowns that are yellow to brown

• Radiographically:the altered teeth demonstrate extremely thin enamel and dentin surrounding an enlarged radiolucent pulp(ghost teeth)

• Histologically:– structure of the enamel is irregular or lacking with a laminated appearance– dentin contains clefts scattered through a mixture of interglobular dentin and

amorphous material– pulp tissue contains free or attached stones that may exhibit tubules or consist of

laminated calcification

• Treatment:– Endodontic therapy on non vital teeth that have

sufficient hard tissue – Erupted teeth can be covered with etched-

retained restorations or stainless steel crowns

SEGMENTAL ODONTOMAXILLARY DYSPLASIA

• developmental disorder that affects the jaw and (sometimes) the overlying facial tissues

• Etiology:unknown• Morphology:

– unilateral enlargement of the maxillary bone, along with fibrous hyperplasia of the overlying gingival soft tissues .

– maxillary premolars frequently are missing and the primary teeth in the affected area may be hypoplastic or show enamel defects

• Histologically: – The affected maxillary bone consists of irregular trabeculae with a

woven appearance. This bone shows numerous resting and reversal lines but it lacks significant osteoblastic and osteoclastic activity.

• Treatment:– not much is known about its natural evolution.

Once diagnosed, the condition seems to remain stable and may not require surgical intervention. However, orthodontic therapy and orthognathic surgery may be considered in some cases.

DENS EVAGINATUS• an abnormal proliferation and folding of a portion the IEE and

subjacent ectomesenchymal cells of the dental papilla into the stellate reticulum during the bell stage of tooth formation

• Morphology:– cusp-like elevation of enamel located in the central groove or

lingual ridge of the buccal cusp of permanent premolar or molar teeth

• Radiographically– the occlusal surface exhibits a tuberculated appearance. and often

a pulpal extension is seen in the cusp• Etiology:

– Unknown,can result from many factors, including genetic and environmental ones .

• Treatment:• Type I: Normal pulp, mature apex • Type II: Normal pulp, immature apex• Type III: Inflamed pulp, mature apex • Type IV: Inflamed pulp, immature apex• Type V: Necrotic pulp, mature apex• Type VI: Necrotic pulp, immature apex