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Bacterial enzymes involved in metabolism and plaque formation represent a functional group of proteins, primarily from species like Streptococcus mutans, that drive the development of dental biofilms and caries (Bowen & Koo, 2011, Caries Research). Central to this process are glucosyltransferases (GTFs), which convert dietary sucrose into insoluble glucans, forming the structural scaffold of dental plaque and enabling bacterial adhesion to tooth enamel (Kuramitsu, 1993, Critical Reviews in Oral Biology & Medicine). Other critical enzymes include fructosyltransferases (FTFs) and various glycolytic enzymes, such as enolase, which facilitate the production of lactic acid, leading to enamel demineralization (Marquis, 1995, Antonie Van Leeuwenhoek). Therapeutic intervention often involves the use of agents like fluoride, which inhibits enolase and other metabolic steps, or antiseptic compounds like chlorhexidine that disrupt bacterial membranes and enzymatic activity (Walsh et al., 2019, Cochrane Database). Targeting these enzymes is a primary strategy for preventing oral diseases by reducing the virulence of the oral microbiome without necessarily eliminating all commensal bacteria (Jeon et al., 2011, Journal of Dental Research).
Inhibition of glucosyltransferases (GTFs) to prevent extracellular polysaccharide synthesis, inhibition of enolase to reduce glycolytic acid production, and disruption of bacterial metabolic homeostasis through competitive inhibition or membrane disruption.
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