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Bacterial adhesion to dental enamel is the foundational biological process for the formation of dental plaque, a complex multispecies biofilm (Rosan and Lamont, 2000). This process is initiated by the deposition of the acquired enamel pellicle (AEP), a protective layer of salivary proteins and glycoproteins, onto the tooth surface (Siqueira et al., 2012). Early bacterial colonizers, such as Streptococcus mutans and Streptococcus sanguinis, utilize specific surface proteins known as adhesins to bind to complementary receptors within the AEP (Nobbs et al., 2011). This adhesion involves a transition from reversible, long-range physical interactions to irreversible, short-range stereochemical binding. In the context of oral health, this process is a primary driver of dental caries and periodontal disease, as the resulting biofilm facilitates acid production and inflammatory responses (StatPearls, 2023). Pharmacological strategies to combat this include the use of anti-adhesive agents like delmopinol, which reduces the surface tension of the enamel, and competitive inhibitors that block bacterial binding sites (Simonsson et al., 1991).
Inhibition of bacterial attachment to the acquired enamel pellicle through chemical modification of the tooth surface, competitive binding to bacterial adhesins, or disruption of the salivary protein layer.
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