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Dental plaque is the diverse microbial community, embedded in a matrix of host and bacterial polymers, growing on teeth as a biofilm. Dental plaque develops naturally, and contributes to the host defences by preventing colonization by exogenous species. The composition of dental plaque varies at distinct surfaces as a result of the inherent biological and physical properties at these sites; the balance of the predominant bacterial populations shifts in disease. Plaque has an open architecture, with channels traversing from the biofilm surface through to the enamel. This structure affects the movement of molecules within plaque, and gradients in key determinants develop. Bacteria growing on a surface display a novel phenotype; one consequence of which is an increased resistance to antimicrobial agents. Resistance can result from restricted inhibitor penetration (diffusion-reaction theory), slower bacterial growth rates, transfer of resistance genes, suboptimal environmental conditions for inhibitor activity, and the expression of a resistant phenotype. Such biofilm-associated traits, coupled with the pharmacokinetic profile of orally delivered antimicrobial agents (high concentrations for short periods/lower concentrations for longer periods), affect the mode of action and efficacy of antimicrobials. Agents with a broad spectrum of activity in laboratory studies may display a far narrower inhibitory profile under the conditions prevailing in the mouth. This may result in a selective inhibition of species implicated in disease, or reduced production of virulence factors, while preserving the benefits associated with a resident oral microflora. [ABSTRACT FROM AUTHOR]

Dental plaque is the diverse microbial community, embedded in a matrix of host and bacterial polymers, growing on teeth as a biofilm. Dental plaque develops naturally, and contributes to the host defences by preventing colonization by exogenous species. The composition of dental plaque varies at distinct surfaces as a result of the inherent biological and physical properties at these sites; the balance of the predominant bacterial populations shifts in disease. Plaque has an open architecture, with channels traversing from the biofilm surface through to the enamel. This structure affects the movement of molecules within plaque, and gradients in key determinants develop. Bacteria growing on a surface display a novel phenotype; one consequence of which is an increased resistance to antimicrobial agents. Resistance can result from restricted inhibitor penetration (diffusion-reaction theory), slower bacterial growth rates, transfer of resistance genes, suboptimal environmental conditions for inhibitor activity, and the expression of a resistant phenotype. Such biofilm-associated traits, coupled with the pharmacokinetic profile of orally delivered antimicrobial agents (high concentrations for short periods/lower concentrations for longer periods), affect the mode of action and efficacy of antimicrobials. Agents with a broad spectrum of activity in laboratory studies may display a far narrower inhibitory profile under the conditions prevailing in the mouth. This may result in a selective inhibition of species implicated in disease, or reduced production of virulence factors, while preserving the benefits associated with a resident oral microflora. [ABSTRACT FROM AUTHOR]