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Cariogenic bacterial proteins and DNA represent a collective of molecular targets within the biofilms of tooth-decay-causing bacteria, such as Streptococcus mutans (NIH, 2012). These targets include glucosyltransferases (GTFs), which are enzymes that synthesize the extracellular polysaccharide matrix essential for biofilm integrity, and adhesins like Antigen I/II that facilitate bacterial attachment to the tooth surface (NIH, 2012; Frontiers in Microbiology, 2020). Extracellular DNA (eDNA) serves as a critical structural scaffold in the biofilm matrix, while intracellular DNA and metabolic proteins are vital for bacterial survival and acid production (Frontiers in Microbiology, 2020; NIH, 2025). Therapeutic agents like silver diamine fluoride (SDF) and chlorhexidine target these components by denaturing proteins, inhibiting enzymatic activity (e.g., enolase), and binding to nucleic acids to arrest bacterial growth (Wikipedia, 2020; NIH, 2007). Targeting these diverse molecular entities is fundamental to modern anti-caries strategies aimed at disrupting pathogenic biofilms and preventing enamel demineralization (NIH, 2007; Frontiers in Microbiology, 2020). The primary objective of targeting these bacterial components is to selectively eliminate cariogenic species while maintaining a healthy oral microbiome, thereby providing long-term protection against dental decay (NIH, 2007).
Inhibition of glucosyltransferases (GTFs) to prevent biofilm formation; binding to bacterial DNA to inhibit replication and transcription; denaturation of bacterial proteins; inhibition of metabolic enzymes such as enolase and F-ATPase; degradation of extracellular DNA (eDNA) to promote biofilm dispersion.
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