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Oral microbial surface proteins and extracellular biofilm matrix components represent a complex assembly of molecules that facilitate the formation and persistence of dental plaque. Surface proteins, such as adhesins and glucosyltransferases (GTFs), allow bacteria like Streptococcus mutans to adhere to the salivary pellicle and synthesize extracellular polysaccharides (Marsh, 2004). The extracellular biofilm matrix, primarily composed of exopolysaccharides (EPS), proteins, and extracellular DNA (eDNA), provides a protective scaffold that shields microbes from host immune responses and antimicrobial agents (Flemming & Wingender, 2010). These components are critical therapeutic targets in the management of oral diseases like dental caries and periodontitis. Drugs such as chlorhexidine and fluoride interact with these targets by disrupting cell membranes, inhibiting matrix-synthesizing enzymes, or altering the surface charge of the microbes to prevent attachment (Koo et al., 2013). Targeting the matrix specifically helps in destabilizing the biofilm architecture, making the resident pathogens more susceptible to treatment and mechanical removal (Bowen et al., 2018).
Drugs targeting these components work by inhibiting microbial adhesion to the tooth surface, disrupting the structural integrity of the extracellular matrix, or inactivating enzymes like glucosyltransferases that synthesize the matrix (Bowen et al., 2018; Koo et al., 2013).
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