Bacterial adherence and dental plaque formation.

Abstract

Bacterial masses on the crowns of the teeth, termed dental plaques, are generally separated from the tooth enamel by a pellicle of salivary origin. The initiation of plaque formation entails the firm adherence of bacteria to the pellicle andin situ growth of attached bacteria. Plaque accumulation, after saturation of the pellicle surface, involves adhesive interactions between growing attached bacteria via the interbacterial matrix (host- and bacteria-derived products) and further attachment. Bacterial adherence to the pellicle is a prerequisite for plaque initiation. The attachment of different bacterial species exhibits a great deal of specificity and appears to involve specific receptors on the bacterial and pellicle surfaces. Different salivary glycoproteins, e. g. high M. W. polymers or immunoglubulins in the pellicle, as well as bacterial cell surface appendages (fimbriae) have been implicated, and some evidence suggests involvement of lectin-like interactions. Plaque accumulation may be mediated by bacterial extracellular polysaccharides, salivary components as well as direct cell-to-cell binding. These interactions also exhibit great selectivity, and evidence for a lectinlike nature of some of them has been obtained. Extracellular glucans synthesized from sucrose appear to favor specifically the accumulation ofStreptococcus mutans cells. The role of other homo- and heteropoly-saccharides is much less clear. Salivary components play a dual role in plaque formation. They can mediate bacterial attachment to the pellicle or plaque periphery, but by binding to unattached bacteria they can also diminish the attachment of such bacteria. The bacterial composition of plaque in its early phase of formation appears to be dictated by the relative adherence ability of participating organisms. Shifts in the bacterial composition of plaque in later development stages can also be caused by changes in bacterial growth conditions. In contrast to plaque composition, total plaque mass is governed mainly by growth of attached organisms rather than by continuous new adherence of bacteria to the plaque periphery. Successful practical methods for inhibiting or preventing plaque formation by interfering with bacterial adhesive processes have not yet been developed.