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The oral bacterial surface and dental biofilm matrix constitute a highly organized microbial community encased in a self-secreted scaffold of extracellular polymeric substances (EPS) [Bowen et al., 2018; Flemming & Wingender, 2010]. This matrix, primarily composed of glucans, fructans, proteins, and extracellular DNA, serves as a protective barrier against mechanical shear, host immune defenses, and antimicrobial penetration [Flemming & Wingender, 2010; Marsh, 2004]. It facilitates the initial attachment of pioneer species like Streptococcus mutans to the salivary pellicle and enables subsequent co-aggregation of diverse microbial taxa [Marsh, 2004; Hajishengallis et al., 2012]. Pathological shifts in the biofilm composition or metabolic activity lead to the localized production of acids that demineralize tooth enamel (caries) or trigger chronic inflammatory responses in the gingival tissues (periodontitis) [Hajishengallis et al., 2012; Pitts et al., 2017]. Pharmacological interventions aim to destabilize this matrix, inhibit the enzymes responsible for EPS synthesis (such as glucosyltransferases), or disrupt the bacterial cell surfaces to prevent colonization and promote biofilm clearance [Koo et al., 2017; Pitts et al., 2017].
Drugs targeting this complex act by disrupting bacterial cell membranes, inhibiting enzymes like glucosyltransferases that synthesize the matrix, preventing bacterial adhesion to the dental pellicle, and promoting the oxidative degradation of the extracellular polymeric substance (EPS) [Koo et al., 2017; Pitts et al., 2017].
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