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The bacterial cell membrane and cell envelope of oral plaque bacteria constitute the primary protective barrier and structural framework for microorganisms within the dental biofilm [1]. This target is a complex assembly comprising the inner cytoplasmic membrane, a peptidoglycan layer, and, in Gram-negative species, an outer membrane containing lipopolysaccharides and porins [2]. These structures are essential for maintaining cellular homeostasis, facilitating adherence to oral surfaces, and protecting the bacteria from environmental stressors [3]. In clinical practice, this envelope is the primary site of action for many antiseptic agents found in mouthwashes and toothpastes, such as chlorhexidine and cetylpyridinium chloride, which disrupt the membrane's integrity [4]. Additionally, beta-lactam antibiotics target the synthesis of the peptidoglycan component within this envelope to induce cell lysis [5]. Effective targeting of the cell envelope is crucial for the management of oral infections like dental caries and periodontitis, though the protective nature of the biofilm matrix often limits drug penetration [6]. Disruption of these structures leads to the leakage of intracellular components and eventual cell death, which is the goal of most topical oral antimicrobials [4]. [1] Marsh, P. D. (2006). BMC Oral Health. [2] Silhavy, T. J., et al. (2010). Cold Spring Harb Perspect Biol. [3] Nobbs, A. H., et al. (2009). Microbiol Mol Biol Rev. [4] McDonnell, G., & Russell, A. D. (1999). Clin Microbiol Rev. [5] Kohanski, M. A., et al. (2010). Nat Rev Microbiol. [6] Seneviratne, C. J., et al. (2011). J R Soc Med.
Disruption of lipid bilayer integrity, inhibition of peptidoglycan synthesis, and alteration of membrane permeability leading to cytoplasmic leakage.
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