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Oral bacterial metabolic enzymes encompass a wide array of catalytic proteins produced by the oral microbiota, such as Streptococcus mutans and Porphyromonas gingivalis, which are central to the pathogenesis of dental caries and periodontal disease. These enzymes include glucosyltransferases (GTFs) that synthesize the extracellular polysaccharide matrix of dental biofilms, and glycolytic enzymes like enolase that convert dietary sugars into lactic acid, leading to enamel demineralization (Marquis, 1995; PMID: 7553451). Furthermore, specialized proteases like gingipains facilitate tissue invasion and immune evasion by degrading host proteins (Guo et al., 2010; PMID: 20837043). Therapeutic targeting of these enzymes is a cornerstone of oral health; for instance, fluoride ions inhibit enolase and proton-pumping ATPases to reduce acid production and bacterial acid tolerance (Hamilton, 1990; PMID: 2191018). Additionally, sugar alcohols like xylitol act as metabolic decoys that disrupt carbohydrate processing, while broad-spectrum antiseptics like chlorhexidine non-specifically inhibit various membrane-bound metabolic enzymes (Nayak et al., 2014; PMID: 25422590).
Inhibition of bacterial enolase and F-ATPases by fluoride; competitive inhibition of sugar transport and phosphorylation by xylitol; and non-specific disruption of bacterial cell membranes and associated metabolic enzymes by chlorhexidine.
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