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The oral bacterial biofilm matrix and cell surfaces represent a complex, multi-species structural target essential for the development of dental diseases such as caries and periodontitis (Bowen et al., 2018). The matrix is primarily composed of extracellular polymeric substances (EPS), including glucans, fructans, proteins, and extracellular DNA, which provide a protective scaffold for embedded microorganisms (Koo et al., 2013). Bacterial cell surfaces within this biofilm feature various adhesins and receptors that facilitate initial attachment to the tooth pellicle and subsequent inter-species co-aggregation (Marsh & Zaura, 2017). Therapeutic strategies targeting this assembly aim to disrupt the structural integrity of the matrix, inhibit the enzymatic production of EPS, or directly compromise the bacterial cell membranes (StatPearls, 2023). By destabilizing the biofilm, these agents enhance the penetration of antimicrobials and promote the mechanical removal of plaque (NIH, 2022). However, targeting the oral biofilm presents challenges, including the need to maintain a healthy microbiome balance and overcome the inherent resistance of sessile bacteria compared to planktonic cells (Nature Reviews Microbiology, 2018). Common agents like chlorhexidine and fluoride interact with these surfaces to reduce bacterial load and metabolic activity (PubChem).
Disruption of the extracellular polymeric substance (EPS) matrix, inhibition of bacterial adhesion to the acquired pellicle, and lysis of bacterial cell membranes.
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