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Streptococcus mutans is a primary etiologic agent of dental caries, largely due to its ability to synthesize a robust extracellular polysaccharide (EPS) matrix. This matrix is primarily composed of glucans produced by secreted glucosyltransferases (Gtfs), specifically GtfB, GtfC, and GtfD, which utilize dietary sucrose as a substrate (Bowen & Koo, 2011, Caries Research). The EPS scaffold provides structural integrity to the dental biofilm (plaque), facilitates the stable adhesion of bacteria to the tooth surface, and creates acidic microenvironments that lead to enamel demineralization (Koo et al., 2013, Journal of Dental Research). Because the EPS matrix is essential for the pathogenicity and survival of S. mutans within the oral cavity, it serves as a critical therapeutic target. Drugs and natural compounds targeting this system work by inhibiting Gtf enzymatic activity or disrupting the physical assembly of the biofilm matrix to reduce the virulence of dental plaque (Jeon et al., 2011, Caries Research). This therapeutic approach aims to manage dental disease by modulating the biofilm environment and reducing acid stress rather than employing broad-spectrum antimicrobial action.
Inhibition of glucosyltransferase (Gtf) enzymatic activity to prevent the synthesis of water-insoluble glucans, disruption of the extracellular polysaccharide (EPS) scaffold, and interference with bacterial attachment to the acquired pellicle (Koo et al., 2010, Journal of Bacteriology).
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