Dental Abnormalities The teeth exhibit many structural abnormalities, which may occur as a result of developmental or genetic alterations or as a result of a systemic process, such as gastroesophageal reflux disease, medications, or environmental and mechanical influences. Amelogenesis imperfecta is a developmental disorder of the dentition. It is a rare inherited disorder that results in abnormal formation of tooth enamel on the external layer of the crown of the tooth. The teeth become yellow, brown, or gray and are associated with temperature hypersen-sitivity, increased calcium deposition, gingival hyperplasia, and an increased risk of dental caries. Restorative dental work with crowns and implants is frequently required. Hypoplasia of the enamel is produced by defective amelogenesis in the deciduous and permanent teeth and persists unchanged after the enamel is formed. It, there-fore, differs fundamentally from caries, erosion, and other acquired lesions. Enamel formation begins in the fifth intrauterine month for deciduous teeth and in the fourth postnatal month for some of the permanent teeth, being completed between 4 and 7 years of age. There are two types of enamel hypoplasia, an inherited form that results from a disturbance in the ectodermal layer during embryogenesis, and an environmental form, which results from systemic infections, disease, and metabolic or nutritional abnormalities. Hypoplastic tooth enamel has abnormalities ranging from shallow grooves on the smooth enamel to a number of deep grooves or areas in which the underlying dentinal junction is completely exposed, revealing a hard but thin surface. The irregular outline and texture of the lesion distinguish it from a smooth abrasion or erosion, which is more indicative of dental caries. The mechanism of hypoplasia is believed to be either a temporary delay in calcification, resulting in distortion and collapse of an uncalcified matrix, or an actual degeneration of ameloblastic cells. In contrast to enamel hypoplasia, in which enamel opacities may be white, yellow, or brown, white spots (hypomineralization or hypocalcification) are opaque white well-demarcated round to oval patches on the enamel surface without loss of substance. The cementing substance between the enamel rods is lacking, altering the refractive property of the enamel layer without causing further alterations of the teeth. This condition should not be confused with fluorosis, or “mottled” enamel, which is a hypomineralization of tooth enamel caused by excessive fluoride ingestion. Unlike enamel hypoplasia, fluorosis does not increase the risk for caries, but similar to enamel hypoplasia, it does have aesthetic implications. Amelogenesis imperfecta is a very rare hereditary hypoplasia of enamel. In one of the two types described, enamel is completely missing (agenesis), and in the other, the enamel matrix is laid down but fails to calcify. Both deciduous and permanent teeth are affected. Such enamel is soft and may be easily broken away from the dentin by normal wear or by an instrument. Consequently, there are intact crowns on recently erupted teeth but progressive deterioration of the enamel on previously erupted teeth. With aging, very little enamel is left, being only visible at the cervical line. The soft dentin is whitish gray and rapidly discolors further, and is worn down to stumps from years of mastication. Consequently, teeth are typically small, with multiple pits and grooves causing rapid deterioration of the teeth and significant tooth loss. Dentinogenesis imperfecta (opalescent dentin), represents a group of hereditary disorders that result in abnormal dentin formation in both deciduous and permanent teeth. The crowns of the teeth are of normal dimension with stunted roots. The pulp canals are markedly reduced in size or completely obliterated. The color of the teeth as they erupt ranges from slightly pink to darker bluish or brownish gray. There is a tendency of the enamel to fracture and peel away owing to defective dentin, leaving an atypical, amber-brown dentin that is translucent or opalescent. The teeth show rapid wear. Sensitivity is lacking because of continual deposition of secondary dentin in the pulp. A dystrophic arrangement of dentinal tubules and abnormal blood supply via canals that penetrate the dentinal substance and impart the brownish color are characteristic. This condition may be part of a generalized osteogenesis imperfecta, characterized by brittle bones and blue sclerae. Gemination is the production of twin teeth from one enamel organ. The epithelium of the enamel organ invaginates as though to produce two separate teeth. If this abortive fission is symmetric, the result is a bifid tooth, with fully developed crowns and confluent roots. Asymmetric division gives rise to a smaller accessory tooth or component. When the gemination process is multiple, the designation odontoma should apply. A fused tooth is more common in the deciduous dentition, differing from twin teeth in that some physical pressure has caused a joining of young tooth germs (both enamel organ and dental papilla). If the fusion is late, only the roots may be joined, because the crowns have already developed. Supernumerary teeth, which are wholly formed, are usually due to hyperplasia of the dental lamina, forming extra tooth germs. Such a tooth may be normal in shape, peg shaped, or of rudimentary size, lying between the roots of a normal molar. A supernumerary cusp or root, including the enamel pearl, on the other hand, is formed by local hyperplasia of the tooth germ, or, in some cases, of invagination of the dental epithelium as in geminated teeth. Destruction of the tooth surface by mechanical forces, whether from coarse abrasive foods, bruxism (teeth grinding), tooth brushing, or certain occupations, such as holding nails between the teeth, is referred to as abrasion. The term attrition is used for the natural wear of incisal and occlusal surfaces, whereas abrasion from tooth brushing primarily affects the cervical parts of cuspid and bicuspid teeth. Erosion is a chemical process that may, at times, produce lesions that are indistinguishable from abrasive lesions. Affected individuals, typically in their thirties or older, develop wedge-or spoon-shaped erosions on the labial and buccal surfaces, primarily on the gingival margins, from alterations of saliva presumably acting in an enzymatic fashion. The lesions are usually smooth, similar to abrasions, but rough pitted lesions have also been seen. Gastroesophageal reflux with proximal extension to the oral cavity can displace saliva, leaving the surfaces of the tooth bare and thereby permitting pepsin, a proteolytic enzyme, to act on and remove the protective dental pellicle. Once this protective layer is destroyed, the acid is permitted to interact with enamel and the hydrogen ion can begin to dissolve the enamel. The degree and rate of dissolution are affected by the ratio of acidity to buffering near the tooth. Erosive disease affects tooth sensitivity, tooth stability, and aesthetics. Similar damage can be seen with the excessive ingestion of acidic foods and liquids. Fluorosis, or mottled enamel, is an endemic lesion in geographic areas where the content of fluoride ion in the drinking water exceeds 2 parts per million. It occurs only in individuals exposed to high concentrations of fluorine during enamel formation prior to tooth eruption (young children and early adolescents). Affected teeth range in appearance from a hard and glazed surface with small chalky spots, to wider paper-white areas or striations, to pitted and irregularly marred or excoriated and mottled color changes of chalky white and shades of brown from yellow to almost black. Dentition is almost universally affected by aging; the teeth begin to yellow or darken in color owing to thinning of the dentin that lies under the surface enamel. Dental caries, commonly referred to as tooth decay, is a bacterial infection resulting in demineralization and destruction of the hard surfaces of the teeth, specifically the enamel, dentin, and cementum. The bacteria produce acidity through the fermentation of food debris on the teeth. Streptococcus mutans has been identified in the plaque and saliva in teeth laden with dental caries; its presence in this environment sugge ts a causative role in the pathogenesis of dental caries.
