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Teeth, their removal is usually indicated. The resulting edentulous zone can then be restored with prosthesis.

ABNORMALITIES OF DENTAL PULP Pulp Calcification This is rather common phenomenon that occurs with increasing age for no apparent reason. There appears to be no relation to inflammation, trauma, or systemic disease. Pulp calcification may be microscopic in size, or it may be large enough to be detected radiographically (Fig. 16 !"#. $alcifications may be either diffuse (linear# or nodular (pulp stones#. The diffuse or linear deposits are typically found in the root canals and generally are parallel to the blood vessels. Pulp stones are usually found in the pulp chamber. %hen they are composed predominantly of dentin, they are reffered to as true denticles& when they represent foci of dystrophic calcification, they are reffered to as false denticles. Pulp stones are occasionally subdivided into attached and free types, depending on whether they are incorporated into the dentin wall or are surrounded by pulpal tissue. Pulp stones appear to have no clinical significance. They are not believed to be a source of pain and are not associated with any forms of pulpitis. They may, however, be problematic during endodontic therapy of non vital teeth. Internal Resorption 'esorption of the dentin of the pulpal walls may be seen as part of an inflammatory response to pulpal in(ury, or it may be seen in cases in which no apparent trigger can be identified (Fig, 16 !)#. The resorption occurs as a result of the activation of osteoclasts or dentinoclasts on internal surfaces of the root or crown. 'esorption lacunae are seen, containing these cells and chronic inflammatory cells. 'eversal lines may also be found in the ad(acent hard tissue indicating attempts at repair. *n time, the root or crown will be perforated by the process, ma+ing the tooth useless. ,ny tooth may be involved, and usually only a single tooth is effected, although cases in which more than one tooth is involved have been described. *n advanced cases, teeth may appear pin+ owing to the pro-imity of pulp tissue to the tooth surface. .ntil root fracture or communication with a periodontal poc+et occurs, patients generally have no symptoms. The treatment of choice is root canal therapy before perforation. /nce there is communication between pulp and periodontal ligament, the prognosis of saving the tooth is very poor. /ccasionally, the process may spontaneously arrest for no apparent reason. External Resorption 'esorption of teeth from e-ternal surfaces may have one of several causes. This change may be the result of an ad(acent pathologic process, such as (1# chronic inflammatory lesions, (0# cysts, (!# benign tumors, and (1# malignant neoplasms. The pathogenesis of e-ternal resorption from these causes has been related to release of chemical mediators, increased vascularity, and pressure. 2-ternal resorption of teeth may also be seen in association with (1# trauma, (0# reimplantation or transplantation of teeth, and (!# impactions (Fig. 16 !3#. Trauma that causes in(ury to or necrosis of the periodontal ligament may initiate resorption of tooth roots. This trauma may be from a single event, from malocclusion, or from e-cessive orthodontic forces. 4ecause reimplanted and transplanted teeth are non vital and have no surrounding

viable periodontal ligament, they are eventually resorbed and replaced by bone. This is basically a natural physiologic process in which the calcified collagen matri- of the tooth serves as a framewor+ for the deposition of new viable bone. *mpacted teeth, when they impinge or e-ert pressure on ad(acent teeth, may cause root resorption of the otherwise normally erupted tooth. /ccasionally, impacted teeth themselves may undergo resorption. The cause of this phenomenon is un+nown, although it is believed to be related to a partial loss of the protective effect of the periodontal ligament or reduced enamel epithelium. Finally, e-ternal resorption of erupted teeth may be idiopathic. ,ny tooth may be involved, although molars are least li+ely to be effected. /ne of two patterns may be seen. *n one, resorption occurs immediately apical to the cementoenamel (unction, mimic+ing a pattern of caries associated with -erostomia (Fig. 16 15#. *n e-ternal resorption, however, the lesions occur on root surfaces below the gingival epithelial attachment. *n the other pattern of e-ternal resorption, the process starts at the tooth ape- and progresses occlusally (Fig. 16 11#. 2-ternal resorption is a particularly frustrating type of dental abnormality for both patient and practitioner, because there is no plausible or evident e-planation for the condition and no effective treatment. /ver an e-tended clinical course, resorption eventually causes loss of the affected tooth. ALTERATIONS IN COLOR Exo enous Stains 6tains on the surface of teeth that cam be removed with abrasives are +nown as e-ogenous or e-trinsic stains. The color change may be caused by pigments in dietary substances (e.g., coffee, tobacco# or by the colored by products of chromogenic bacteria in dental pla7ue. $hromogenic bacteria are believed to be responsible for brown, blac+, green, and orange stains seen predominantly in children. 4rown and blac+ stains are typically seen in the cervical zone of teeth, either as a thin line along the gingival margin or as a wide band (Fig. 16 10#. This type of stain is also often found on teeth ad(acent to salivary duct orifices. 8reen stain is tenacious and is usually found as a band on the labial surfaces of the ma-illary anterior teeth (Fig. 16 1!#. 4lood pigments are thought to contribute to the green color. /range or yellow orange stains appear on the gingival third of teeth in a small percentage of children. These are generally easily removed. En!o enous Stains 9iscoloration of teeth resulting from deposits its of systemically circulating substances during tooth development is defined as endogenous or intrinsic staining. 6ystemic ingestion of tetracycline during tooth development is a well +nown cause of endogenous staining of teeth. Tetracycline has an affinity for teeth and bones and will be deposited in these sites during metabolic activity. The drug:s bright yellow color is reflected in the subse7uently erupted teeth (Fig. 16 11#. The fluorescent property of tetracycline can be demonstrated with an ultraviolet light in clinically erupted teeth. %ith time, the tetracycline o-idizes, resulting in a color change from yellow to gray or brown with the loss of its fluorescent 7uality. 4ecause tetracycline can cross the placenta, it may stain primary teeth if ta+en during pregnancy. *f administered between birth and age 6 or " years, permanent teeth may be affected. /nly