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The oral bacterial cells and biofilm matrix, commonly known as dental plaque, is a highly organized microbial community attached to oral surfaces and encased in a self-produced extracellular polymeric substance (EPS) matrix. This matrix, consisting of polysaccharides, proteins, and extracellular DNA, serves as a protective barrier against host defenses and antimicrobial penetration while facilitating nutrient exchange and horizontal gene transfer (Flemming, H. C., & Wingender, J., 2010, 'The biofilm matrix', Nature Reviews Microbiology). In a healthy oral environment, these biofilms exist in a symbiotic state, but ecological shifts—often driven by high sugar intake or poor hygiene—can lead to the overgrowth of acidogenic or proteolytic pathogens. These shifts result in the development of dental caries and periodontal diseases, which are among the most prevalent chronic conditions globally (NIDCR, 2023, 'Periodontal (Gum) Disease'). Therapeutic interventions target the biofilm by mechanically disrupting the matrix, chemically inhibiting bacterial metabolism, or using agents that degrade the EPS to enhance drug penetration. Effective management of the oral biofilm is critical for preventing localized tissue destruction and reducing the risk of systemic complications associated with chronic oral infections.
Drugs targeting this complex act through multiple pathways: disrupting bacterial cell membranes to cause lysis, inhibiting metabolic enzymes (such as enolase in glycolysis), degrading the extracellular polymeric substance (EPS) scaffold via enzymatic action, preventing initial bacterial adhesion to the pellicle, and interfering with quorum sensing signaling to prevent biofilm maturation (Marsh, P. D., 2004, 'Dental plaque as a biofilm and a microbial community - implications for health and disease', BMC Oral Health; Bowen, W. H., et al., 2018, 'The extracellular glycans of dental plaque biofilms', Journal of Dental Research).
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