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This target refers to the non-specific physicochemical adhesion process between oral microbiota and the dental enamel surface, which serves as the foundational step in dental plaque (biofilm) development. The interaction is mediated by a combination of long-range van der Waals forces and electrostatic forces, alongside short-range hydrophobic interactions, as described by the DLVO theory of microbial adhesion (Busscher et al., 1984, 'Physicochemical surface properties of oral streptococci'). The enamel surface is typically coated by an acquired salivary pellicle, which modulates these forces and provides a substrate for bacterial docking (Marsh, 2004, 'Dental plaque as a biofilm and a microbial community'). Disruption of this initial attachment is a primary strategy in preventing oral infectious diseases, including dental caries and periodontitis (StatPearls, 'Dental Caries'). While not a discrete molecular receptor, this interaction is targeted by various oral care agents like chlorhexidine and surfactants that alter surface free energy or disrupt bacterial cell membranes (An & Friedman, 1998, 'Concise review of bacterial adhesion'). Understanding these non-specific forces is crucial for developing anti-adhesive coatings and therapeutic rinses that prevent the transition from a healthy oral state to a pathogenic biofilm.
Interference with electrostatic and van der Waals forces, alteration of surface free energy, and disruption of the acquired salivary pellicle to prevent bacterial attachment.
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