On the relative importance of specific and non-specific approaches to oral microbial adhesion

Abstract

In this paper, it is suggested that specificity and non‐specificity in (oral) microbial adhesion are different expressions for the same phenomena. It is argued that the same basic, physico‐chemical forces are responsible for so‐called ‘non‐specific’ and ‘specific’ binding and that from a physico‐chemical point of view the distinction between the two is an artificial one. Non‐specific interactions arise from Van der Waals and electrostatic forces and hydrogen bonding, and originate from the entire cell. A specific bond consists of a combination of the same type of Van der Waals and electrostatic forces and hydrogen bonding, now originating from highly localized chemical groups, which together form a stereo‐chemical combination. The absence or presence of specific receptor sites on microbial cell surfaces must therefore be reflected in the overall, non‐specific surface properties of cells as well. This point is illustrated by showing that glucanbinding lectins on mutans streptococcal strains may determine the pH dependence of the zeta potentials of these cells. When studying microbial adhesion, a non‐specific approach may be better suited to explain adhesion to inert substrata, whereas a specific approach may be preferred in case of adhesion to adsorbed protein films. Adhesion is, however, not as important in plaque formation in the human oral cavity as is retention, because low shear force periods. during which adhesion presumably occurs, are followed by high shear force periods, during which adhering cells must withstand these detachment forces. Evidence is provided that such detachment will be through cohesive failure in the pellicle mass, the properties of which are conditioned by the overall, non‐specific substratum properties. Therefore, in vivo plaque formation may be more readily explained by a non‐specific approach.

Candida biofilm formation on voice prostheses

“…Although VPs will become covered by a conditioning film of adsorbed salivary components prior to adhesion of bacteria or yeasts, experiments in the human oral cavity have demonstrated that the properties of this conditioning film are determined by the material itself (Busscher et al, 1992(Busscher et al, , 1997a. Biofilm formation may therefore be influenced by adjusting the properties of the VPs material, by surface modification, and thus a number of strategies have been employed.…”

Medical biofilms

“…Biofilm formation continues with the transport of cells to the substratum:liquid interface, which is governed by a combination of transport mechanisms (i.e., diffusion, convection, sedimentation, and motility) (Bryers, 2000). Once at a substratum surface, bacterial cells adhere by non-specific and/or specific receptor:ligand adhesion mechanisms (An and Friedman, 1998;Busscher et al, 1992;Glantz et al, 1999). Within minutes of attachment, adherent cells up-regulate the secretion of certain cell signal molecules that orchestrate communitywide phenotypic responses, through a process termed quorum sensing (Bjarnsholt and Givskov, 2007;Camilli and Bassler, 2006;Davies et al, 1998;Harraghy et al, 2007;Hodgkinson et al, 2007;Horswill et al, 2007;Pritchard, 2006;Rumbaugh, 2007).…”

Novel effect of plant lectins on the inhibition ofStreptococcus mutansbiofilm formation on saliva-coated surface

“…Colonization of enamel surfaces by the cariogenic bacteria is thought to be initiated by attachment to a saliva-derived conditioning film, the acquired enamel pellicle (AEP) (Gibbons and Qureshi 1976). The AEP is formed largely by adsorption of many heterogeneous salivary proteins (Mogi et al 1986;Al-Hashimi and Levine 1989) on to dental enamel and promotes the adhesion of S. mutans by specific (Liljemark and Bloomquist 1996;Bowden and Hamilton 1998) and nonspecific mechanisms (Busscher et al 1992). This is followed by multiplication and exopolysaccharide formation by the bacteria to form a biofilm.…”