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Oral microbial enzymes represent a heterogeneous group of catalytic proteins produced by the diverse microbiota of the human oral cavity, including bacteria such as Streptococcus mutans and Porphyromonas gingivalis (Bowen & Koo, 2011, Caries Res). These enzymes are central to the pathogenesis of dental caries and periodontal disease by facilitating biofilm formation, acid production, and tissue degradation (Marquis et al., 2003, Monogr Oral Sci). For instance, glucosyltransferases (GTFs) synthesize extracellular polysaccharides that allow bacteria to adhere to tooth enamel, while gingipains (cysteine proteases) disrupt host immune responses and degrade periodontal tissues (Potempa et al., 2000, Periodontol 2000). Therapeutic strategies targeting these enzymes range from broad-spectrum inhibitors like fluoride, which affects glycolytic enzymes, to highly specific small molecules like atuzaginstat designed to block virulence factors associated with systemic conditions like Alzheimer's disease (Dominy et al., 2019, Sci Adv). Because this target encompasses a vast array of enzymes across different species, drug development often focuses on specific high-virulence enzymes rather than the collective group.
Inhibition of bacterial enolase, glucosyltransferase, and cysteine proteases (gingipains) to disrupt biofilm integrity, metabolic acid production, and host tissue degradation.
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