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The tooth surface hydroxyapatite, dental pellicle, and oral biofilm represent the primary interfaces for therapeutic intervention in oral health. Hydroxyapatite is the crystalline calcium phosphate mineral that constitutes the bulk of dental enamel and dentin, serving as the structural foundation of the tooth (StatPearls, 2023). Immediately upon exposure to saliva, this mineral surface is coated by the acquired enamel pellicle, a thin layer of adsorbed salivary proteins and glycoproteins that modulates mineral homeostasis and provides binding sites for microbial colonization (Siqueira et al., 2012). The subsequent accumulation of bacteria leads to the formation of dental plaque, a complex multi-species biofilm (Marsh, 2004). Drugs targeting these surfaces typically aim to enhance mineral resistance to acid, inhibit bacterial adhesion to the pellicle, or disrupt the structural integrity of the biofilm to prevent dental caries and periodontal disease. These interactions are critical for maintaining the balance between demineralization and remineralization and for controlling the pathogenic potential of the oral microbiome.
Mechanisms include the substitution of hydroxyl groups in hydroxyapatite with fluoride to form acid-resistant fluorapatite, the use of cationic antimicrobials to bind and disrupt negatively charged bacterial membranes and pellicle proteins, and the application of surfactants to destabilize the extracellular polymeric matrix of the oral biofilm (StatPearls, 2023; PubMed, 2017).
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