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Streptococcus mutans biofilm formation refers to the assembly and maturation of microbial communities—mainly S. mutans—on tooth surfaces, which produce extracellular polysaccharide (EPS) matrices primarily via glucosyltransferase enzymes (GtfB, GtfC, GtfD)[3][7]. This biofilm, commonly known as dental plaque, is a major virulence factor for S. mutans and plays a central role in the pathogenesis of dental caries by enabling adhesion, protection from host defenses, and acidification of the local environment[1][3]. Mechanisms include both sucrose-dependent and sucrose-independent adhesion, mediated by surface proteins like P1/AgI/II, glucan-binding proteins, and collagen-binding protein[7]. Quorum sensing and signal transduction systems (such as comCDE) regulate biofilm formation and stress responses[1]. Targeting biofilm formation pharmacologically disrupts EPS synthesis, membrane integrity, and bacterial viability, presenting a promising approach for preventing and treating dental caries[2][4][8].
Disruption of cell membrane integrity (farnesol); Inhibition of glucosyltransferase activity (reducing EPS synthesis); Direct killing or inhibition of S. mutans viability (antimicrobial peptides/mutacins); Interference with signal transduction/quorum sensing
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