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The oral biofilm, commonly referred to as dental plaque, is a complex, multi-species microbial community embedded within a self-produced matrix of extracellular polymeric substances (EPS). This matrix, primarily composed of polysaccharides (glucans and fructans), proteins, and extracellular DNA, provides structural stability and serves as a protective barrier against environmental stressors and antimicrobial agents (Flemming & Wingender, 2010; Bowen & Koo, 2011). The formation of this biofilm is initiated by the acquired enamel pellicle, a thin layer of salivary glycoproteins that coats the tooth surface and provides specific receptors for bacterial adhesion (Siqueira et al., 2012). In a pathological state, the maturation of the biofilm leads to the sequestration of acids produced by bacterial metabolism, which demineralizes tooth enamel and triggers inflammatory responses in the surrounding gingival tissues (Marsh, 2006). Therapeutic interventions target this complex by chemically disrupting the EPS matrix, preventing the initial attachment of bacteria to the pellicle, or utilizing antimicrobial agents to penetrate the biofilm and eliminate pathogenic species. Understanding the biochemical interactions within the EPS and the pellicle is essential for the development of effective anti-caries and anti-periodontitis treatments.
Disruption of the extracellular polymeric substance (EPS) matrix, inhibition of bacterial attachment to the acquired pellicle, and direct bactericidal or bacteriostatic action on oral bacterial cell surfaces.
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