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The bacterial cell membrane and the oral surface pellicle represent a dual-target system critical in oral pharmacology and infection control. The bacterial cell membrane is a phospholipid bilayer essential for maintaining cellular homeostasis and osmotic balance; its disruption by cationic agents leads to cytoplasmic leakage and cell death (StatPearls, 2023). The oral surface pellicle, or acquired enamel pellicle (AEP), is a thin, acellular film composed of salivary proteins, glycoproteins, and lipids that forms on tooth surfaces within minutes of exposure to saliva (Journal of Dentistry, 2015). While the pellicle protects enamel from acid erosion, it also serves as the primary substrate for the attachment of pioneer colonizing bacteria, leading to the formation of dental plaque and subsequent diseases like caries and periodontitis (NCBI, 2020). Therapeutic agents such as chlorhexidine exhibit high substantivity by binding to both the negatively charged bacterial membranes and the proteinaceous pellicle, providing prolonged antimicrobial activity and inhibiting biofilm development (Cochrane Database, 2017). This composite target is considered 'incorrect' in a strict molecular sense because it combines a bacterial structural component with a host-derived salivary film, though they are often addressed together in dental therapeutics.
Drugs targeting these structures typically act by disrupting the phospholipid bilayer of bacterial membranes to cause cytoplasmic leakage or by binding to the oral pellicle to prevent bacterial adhesion and biofilm maturation.
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