Kinetics of enamel demineralization in vitro

Previously, we reported that the rate (R) of hydroxyapatite dissolution in acetic, lactic, and phosphoric acid solutions is a function of the degree o f saturation with respect to the dissolving mineral, DS (defined as the rat io of the mean ionic activity product for hydroxyapatite [Ca5OH(PO4)(3)] in solution to its solubility product constant), and the sum of the acid acti vities (Sigma BiH) in solution: R = K(1-DS)(m)(Sigma BiH)(n). The present s tudy was undertaken to explore the general validity of this model in descri bing the kinetics of enamel demineralization. Thin sections of human enamel were exposed to partially saturated 0.1 mol/L lactic acid solutions, at tw o different DS levels, and at pH values of 4.3 to 6.0. Thin sections of hum an enamel were also exposed to solutions with four different concentrations of acetic and lactic acids (pH 4.3) with three different DS values and, at one DS value, to solutions of propionic acid. Mineral loss was monitored b y quantitative microradiography. In solutions with pH values of 4.3 and 5.0 , "lesions" were formed with well-defined surface layers, whereas, in solut ions with pH 6.0, "lesions" were produced with no apparent surface layers. The formation of relatively intact surface layers was consistent with predi cted phase transformations. Rates of mineral loss were found to be inversel y proportional to both the degree of saturation with respect to enamel mine ral, DSEn, and the pH of the solution and increased with increased activiti es of each organic acid, consistent with the proposed model. However, at th e same DSEn and acid activity, rates of demineralization were the same in t he acetic and propionic acid solutions, whereas rates of demineralization i n lactic acid were greater. It is suggested that specific interactions of a cid species with enamel mineral may modify the rate of enamel demineralizat ion. These in vitro findings suggest that relatively small differences in D SEn values found in plaque fluid may result in very significant differences in the rate of enamel demineralization in vivo.