Survival of Oral Bacteria

Abstract

The global distribution of individual species of oral bacteria demonstrates their ability to survive among their human hosts. Such an ubiquitous existence is the result of efficient transmission of strains and their persistence in the oral environment. Genetic analysis has identified specific clones of pathogenic bacteria causing infection. Presumably, these express virulence-associated characteristics enhancing colonization and survival in their hosts. A similar situation may occur with the oral resident flora, where genetic variants may express specific phenotypic characteristics related to survival. Survival in the mouth is enhanced by dental plaque formation, where persistence is associated with the bacteria's capacity not only to adhere and grow, but also to withstand oxygen, wide fluctuations in pH and carbohydrate concentration, and a diverse array of microbial interactions. Streptococcus mutans has been discussed as a 'model' organism possessing the biochemical flexibility that permits it to persist and dominate the indigenous microflora under conditions of stress.

Humoral immunity to commensal oral bacteria in human infants: evidence that Streptococcus mitis biovar 1 colonization induces strain-specific salivary immunoglobulin A antibodies

“…However, despite the formidable commitment of the human immune system to SIgA synthesis, the mucosal surfaces are permanently colonized by complex microbiotas that appear to be unaffected by it (Bowden and Hamilton, 1998). It is not that the mucosal immune system fails to recognize commensal bacteria, as we and others have demonstrated salivary SIgA antibodies react with them (Smith et al, 1985(Smith et al, , 1990Gregory et al, 1990;Widerstrom et al, 1992;Cole et al, 1998Cole et al, , 1999Cole et al, , 2004, and commensal bacteria are known to be coated with SIgA (Brandtzaeg et al, 1968).…”

Dental Caries: A Microbiological Approach

“…Changes in the phenotypes in plaque could influence bacterial selection and survival [52,53] and the overall activities of the plaque community. In addition to generation of diversity through changes in their genomic DNA strains of species of oral bacteria colonizing a mouth may be influenced by 'clonal replacement' where new clones replace the existing clones in a habitat and contribute to strain diversity [53].…”

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.…”