Antimicrobial actions of fluoride for oral bacteria.

Fluoride is widely used as a highly effective anticaries agent. Although it is felt that its anticaries action is related mainly to effects on mineral phases of teeth and on the process of remineralization, fluoride also has important effects on the bacteria of dental plaque, which are responsible for the acidification of plaque that results in demineralization. The results of recent studies have shown that fluoride can affect bacterial metabolism through a set of actions with fundamentally different mechanisms. It can act directly as an enzyme inhibitor, for example for the glycolytic enzyme enolase, which is inhibited in a quasi-irreversible manner. Direct action seems also to occur in inhibition of heme-based peroxidases with binding of fluoride to heme. The flavin-based peroxidases of many oral bacteria are insensitive to fluoride. Another mode of action involves formation of metal-fluoride complexes, most commonly AlF4-. These complexes are responsible for fluoride inhibition of proton-translocating F-ATPases and are thought to act by mimicking phosphate to form complexes with ADP at reaction centers of the enzymes. However, the actions of fluoride that are most pertinent to reducing the cariogenicity of dental plaque are those related to its weak-acid character. Fluoride acts to enhance membrane permeabilities to protons and compromises the functioning of F-ATPases in exporting protons, thereby inducing cytoplasmic acidification and acid inhibition of glycolytic enzymes. Basically, fluoride acts to reduce the acid tolerance of the bacteria. It is most effective at acid pH values. In the acidic conditions of cariogenic plaque, fluoride at levels as low as 0.1 mM can cause complete arrest of glycolysis by intact cells of Streptococcus mutans. Overall, the anticaries actions of fluoride appear to be complex, involving effects both on bacteria and on mineral phases. The antibacterial actions of fluoride appear themselves to be complex but to be dominated by weak-acid effects.