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Dental caries, commonly known as tooth decay or cavities, is a multifactorial, transmissible infectious disease characterized by the progressive demineralization of the tooth's hard structures, including enamel, dentin, and cementum [5][18]. The condition is primarily driven by the metabolic activity of cariogenic bacteria, most notably Streptococcus mutans, which colonize the tooth surface to form a complex biofilm known as dental plaque [13][18]. These bacteria ferment dietary carbohydrates, particularly sucrose, into organic acids that lower the local pH and dissolve the hydroxyapatite mineral of the tooth [6][20]. Therapeutic interventions aim to disrupt this process by inhibiting bacterial virulence factors like glucosyltransferases (Gtfs), reducing the microbial load with antiseptics, or promoting the remineralization of the tooth surface through the application of fluoride and other mineralizing agents [14][15][19]. Although often discussed in a clinical context, 'Dental caries' describes a pathological state rather than a single molecular receptor or enzyme [1][16].
Inhibition of bacterial enolase and glucosyltransferase enzymes, promotion of enamel remineralization through fluorapatite formation, and disruption of bacterial cell membranes and biofilm architecture [5][14][15].
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