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Oral bacteria and dental biofilm constitute a complex, multi-species community of microorganisms organized within a self-produced matrix of extracellular polymeric substances (EPS) on oral surfaces (Marsh, 2004, Caries Research) [1]. This biofilm is a highly structured ecosystem where bacteria communicate via quorum sensing and engage in metabolic cross-feeding, providing them with enhanced resistance to host immune responses and antimicrobial agents (Lamont et al., 2018, Nature Reviews Microbiology) [2]. In a healthy state, the oral microbiota maintains a symbiotic relationship with the host; however, shifts in environmental conditions, such as frequent sugar consumption or poor hygiene, can lead to dysbiosis (Kilian et al., 2016, British Dental Journal) [3]. This shift favors acidogenic species like Streptococcus mutans or proteolytic pathogens like Porphyromonas gingivalis, which are the primary drivers of dental caries and periodontal disease, respectively (Hajishengallis, 2015, Nature Reviews Immunology) [4]. Therapeutic strategies focus on the mechanical disruption of the biofilm and the use of chemical agents, such as fluoride and chlorhexidine, which inhibit bacterial metabolism and membrane integrity (Walsh et al., 2019, Cochrane Database of Systematic Reviews) [5]. Effective management of the dental biofilm is essential for preventing localized oral infections and reducing the risk of systemic complications, including endocarditis and cardiovascular disease (Lockhart et al., 2012, Circulation) [6].
Disruption of bacterial cell membranes, inhibition of glycolytic enzymes (e.g., enolase), interference with bacterial adhesion/co-aggregation, and inhibition of cell wall synthesis.
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