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Streptococcus mutans dental biofilm, commonly known as dental plaque, is a complex, structured community of microorganisms embedded in a self-produced matrix of extracellular polymeric substances (EPS) on the tooth surface. S. mutans is the primary etiologic agent of dental caries due to its ability to synthesize glucans from dietary sucrose via glucosyltransferases, which facilitates firm adherence to the teeth and provides a scaffold for other microbes (Bowen et al., 2018). Within this protected biofilm environment, S. mutans ferments carbohydrates to produce lactic acid, leading to a localized drop in pH that demineralizes tooth enamel (Loesche, 1986). Therapeutic strategies targeting this biofilm aim to disrupt its formation, neutralize acid production, or eliminate the bacteria using antimicrobial agents like chlorhexidine and fluoride. However, the dense EPS matrix often limits drug penetration, making the biofilm significantly more resistant to treatment than planktonic cells (Koo et al., 2017). Furthermore, S. mutans can enter the bloodstream during dental procedures, potentially leading to infective endocarditis, where it forms biofilms on heart valves (Lemos et al., 2019).
Therapeutic agents target the S. mutans dental biofilm through various mechanisms: chlorhexidine acts as a broad-spectrum antiseptic by disrupting bacterial cell membranes; fluoride inhibits the glycolytic enzyme enolase to reduce acid production and promotes enamel remineralization; xylitol interferes with the transport and metabolism of sucrose, reducing the production of sticky extracellular polysaccharides; and other agents may inhibit glucosyltransferases (GTFs) to prevent the assembly of the biofilm matrix (Koo et al., 2013; Marquis, 1995; Jones, 1997).
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