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The bacterial cell membrane and oral biofilm matrix are fundamental structural components that facilitate the survival and pathogenicity of oral bacteria. The cell membrane serves as a vital semi-permeable barrier, maintaining ion gradients and protecting the cytoplasm; its disruption by surfactants or cationic agents leads to rapid bacterial lysis [1]. The oral biofilm matrix, or extracellular polymeric substances (EPS), consists of a complex network of polysaccharides, proteins, and DNA that anchors bacteria to tooth surfaces and provides a protective microenvironment [2]. This matrix acts as a physical shield against the host immune system and limits the diffusion of therapeutic agents, contributing to the high antibiotic tolerance of dental plaque [3]. Targeting these structures is a cornerstone of oral hygiene, utilizing agents that either compromise membrane integrity or enzymatically dissolve the matrix scaffold [4]. Such interventions are essential for preventing and treating biofilm-mediated diseases, including dental caries and periodontitis [5]. By destabilizing the physical architecture of the biofilm, these treatments allow for more effective mechanical removal of plaque and better penetration of other antimicrobial agents [6]. However, the non-specific nature of these targets can sometimes lead to the disruption of beneficial commensal bacteria within the oral cavity [7].
Antimicrobials like chlorhexidine bind to the negatively charged bacterial cell membrane, causing leakage of low molecular weight components and eventual precipitation of cytoplasmic contents [1]. Matrix-targeting agents, such as enzymes or chelators, degrade the extracellular polymeric substances (EPS), thereby reducing the structural integrity of the biofilm and facilitating the removal of dental plaque [2].
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