Thus far, we have assumed that the cariostatic effects of fluoride are mediated through a chemical reaction between this ion and the outermost portion of the enamel surface. The preponderance of data supports this view. A growing body of information suggests, however, that the caries-preventive action of fluoride may also include an inhibitory effect on the oral flora involved in the initiation of caries. The ability of fluoride to inhibit glycolysis by interfering with the enzyme enolase has long been known; concentrations of fluoride as low as 50 ppm have been shown to interfere with bacterial metabolism. Moreover, fluoride may accumulate in dental plaque in concentrations above 100 ppm. Although the fluoride normally present in plaque is largely bound (and thus unavailable for antibacterial action), it dissociates to ionic fluoride when the pH of plaque decreases (i.e., when acids are formed). Thus, when the carious process starts and acids are formed, plaque fluoride in ionic form may serve to interfere with further acid production by plaque microorganisms. In addition, it may react with the underlying layer of dissolving enamel, promoting its remineralization as fluorhydroxyapatite. The end result of this process is a “physiologic” restoration of the initial lesion (by remineralization of enamel) and the formation of a more resistant enamel surface. The ability of fluoride to promote the reprecipitation of calcium phosphate solutions in apatitic forms has been repeatedly demonstrated.
In addition to these possible effects of fluoride, several investigators have reported that the presence of tin, especially as provided by stannous fluoride, is associated with significant antibacterial activity, which has been reported to decrease both the amount of dental plaque and gingivitis in both animals and adult humans. Existing evidence suggests that these antibacterial effects of fluoride and tin may also contribute to the observed cariostatic activity of topically applied fluorides.