Abstract

The kinetics of enamel dissolution and mechanism of lesion formation were studied using a simple in vitro chemical method for producing lesions in human dental enamel comparable to natural incipient carious lesions, known as white spots. Enamel was exposed to a decalcification medium consisting of an aqueous solution of an acidic buffer plus a soluble organic polymer, hydroxyethyl cellulose, which protects the surface from acid attack during subsurface dissolution. The extent of the lesion was measured by analysis of the decalcification medium for calcium and phosphate dissolved from enamel and by microscopic examination of sections from the enamel. Enamel dissolution was investigated by a differential method to give the initial rate and by an integral method to give the approach to equilibrium. Five buffer acids (chloroacetic, dichloroacetic, lactic, formic, and acetic) were examined at pH's of 3–6 and buffer concentrations of 0–0.5 M. The initial rate increased with decreasing pH, decreasing acid dissociation constant, and nearly lineraly with increasing buffer concentration. The initial rate of enamel dissolution during white spot formation was expressed quantitatively in a single equation for all these acids in terms of undissociated acid concentration, hydrogen ion concentration, acid dissociation constant, and the dissociation constant of the acid anion complex of calcium ion. This equation is similar to that for surface dissolution demonstrating the interrelation of the two processes. The rate of enamel dissolution is controlled principally by the rate of diffusion of undissociated acid into enamel and to a lesser extent by pH and acid strength. Free calcium ion inhibits dissolution and can affect even the initial dissolution rate. Some acids complex calcium, although weakly, enough to eliminate this inhibition and are somewhat more effective in white spot formation.

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