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The oral bacteria and dental plaque biofilm matrix is a complex, multi-species microbial community organized within a self-produced scaffold of extracellular polymeric substances (EPS), including polysaccharides, proteins, and extracellular DNA [1][2]. This biofilm adheres tenaciously to tooth surfaces and mucosal tissues, creating a highly regulated microenvironment that protects constituent pathogens from host immune clearance and increases their tolerance to antimicrobial agents by up to 1,000-fold compared to free-floating cells [2][3]. The matrix serves as both a structural framework and a metabolic reservoir, facilitating nutrient cycling, horizontal gene transfer, and cell-to-cell signaling (quorum sensing) among diverse bacterial species [3]. When the ecological balance of the biofilm is disrupted—often by high sugar intake—acidogenic and aciduric bacteria proliferate, leading to the demineralization of tooth enamel (caries) or the triggering of chronic inflammatory responses in the periodontium (gingivitis and periodontitis) [4]. Therapeutic strategies targeting this matrix focus on mechanical disruption, chemical inhibition of bacterial adhesion, and the use of antimicrobial agents that either penetrate the biofilm to kill bacteria or degrade the EPS components to destabilize the entire structure [5].
Disruption of bacterial cell membranes, inhibition of bacterial glycolysis and acid production, inhibition of glucosyltransferase enzymes responsible for matrix synthesis, and physical or chemical destabilization of the extracellular polymeric scaffold [2][5].
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