Abstract

Dental caries is caused by acids generated by the dental plaque adhering to the tooth surface. This paper gives the definition of dental caries, its importance, and introductory remarks on enamel structure and composition. Four different approaches on the mechanisms of the acid interaction with dental enamel are discussed: a) the semipermeable membrane mechanism, in which a pH drop in the enamel is thought to be due to large positively charged mucine cations and small penetrable anions in the enamel. In this mechanism the acid is acting indirectly through salivary mucins on the enamel. The practical importance is most likely minor; b) dissolution mechanism, based on a direct attack of H+ and undissociated acid (HA) on the enamel. This mechanism, giving a reasonable empirical description of experimentally obtained data, assumes that caries is mainly determined by the kinetics of the acid-enamel interaction and that second phases (DCPD) make the enamel crystallites partly insoluble; c) dissolution-precipitation mechanism(s). In these mechanism(s) the surface layer covering the lesion is crucial. During lesion formation (assuming quasi equilibrium), the rate of dissolution and rate of precipitation of the surface layer are equal (or nearly equal). Lesion depth progresses proportional to the square root of time; the apparent diffusion constant ≈ 10-12 cm2.sec-1; and d) inhibitor controlled mechanism. In this approach, caries is considered (as in b) a kinetic phenomenon in which mainly the inhibitor penetration determines the process. Lesion depth progresses with t1/3 and the apparent diffusion constants are ≈ 10-5 cm2.sec-1.

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