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Dental plaque formation is a complex, multi-stage biological process resulting in the development of a resilient microbial biofilm on tooth surfaces [4, 8]. The sequence begins with the adsorption of a salivary pellicle—a thin film of host-derived proteins and glycoproteins—onto the enamel, followed by the reversible and then irreversible attachment of primary bacterial colonizers like Streptococcus and Actinomyces species [9, 12, 17]. These microorganisms utilize dietary sugars, particularly sucrose, to synthesize an extracellular polymeric substance (EPS) matrix that provides structural stability and shields the community from antimicrobial agents and host defenses [5, 14, 15]. As the biofilm matures, it undergoes co-aggregation, recruiting secondary colonizers and transitioning into a more diverse microbial community capable of producing acidic byproducts that lead to enamel demineralization [12, 17]. Clinically, the uncontrolled progression of this process is the primary etiological factor for dental caries, gingivitis, and periodontitis [1, 15, 17]. Therapeutic interventions focus on mechanical removal or the use of chemical agents that inhibit bacterial adhesion, disrupt the biofilm matrix, or interfere with cariogenic metabolism [1, 7, 11].
Interruption of bacterial adhesion to the salivary pellicle, inhibition of extracellular polysaccharide synthesis (e.g., by targeting bacterial glucosyltransferases), and disruption of bacterial cell membrane integrity.
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