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Streptococcus mutans is a primary causative agent of dental caries, largely due to its ability to form robust biofilms on tooth surfaces [1]. The biofilm matrix is a complex assembly of extracellular polymeric substances (EPS), primarily glucans synthesized by glucosyltransferases (Gtfs), which provide structural integrity and create protected acidic microenvironments [2]. Surface-associated processes, including initial adhesion via Antigen I/II (SpaP) and sucrose-dependent binding, facilitate the colonization and accumulation of the bacteria on the enamel [3]. Therapeutic strategies targeting these processes aim to disrupt the matrix scaffold or inhibit the enzymes and adhesins involved, thereby reducing the pathogenicity of the biofilm [4]. This approach is distinct from traditional antibiotics as it focuses on modulating the environment and bacterial behavior rather than simple bactericidal action [5]. By interfering with EPS synthesis and adhesion, these agents prevent the localized acidification that leads to enamel demineralization and subsequent tooth decay [1, 2].
Inhibition of glucosyltransferases (GtfB, GtfC, GtfD) to prevent EPS synthesis, disruption of cell-surface adhesins such as Antigen I/II (SpaP) to block initial attachment, and modulation of quorum sensing pathways to inhibit biofilm maturation.
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