Oral bacterial cells and biofilm matrix components

Oral bacterial cells and biofilm matrix components constitute the complex, multi-species microbial community known as dental plaque, which adheres to tooth surfaces and oral mucosa. This biological assembly is characterized by a self-produced matrix of extracellular polymeric substances (EPS)—including polysaccharides, proteins, and extracellular DNA—that provides structural stability and protection against environmental stressors (Flemming & Wingender, 2010). The biofilm serves as a reservoir for pathogens and a site for intense metabolic activity, where the fermentation of dietary sugars by bacteria like Streptococcus mutans leads to acid production and subsequent tooth demineralization (Marsh, 2006). In the context of periodontal disease, the biofilm triggers inflammatory responses that can lead to tissue destruction and systemic complications (Marsh, 2006). Therapeutic interventions aim to disrupt the matrix, reduce the bacterial load, or modulate the microbial composition to maintain a health-associated oral environment (StatPearls, 2023). Common agents like chlorhexidine and fluoride target the viability and metabolic output of the constituent cells, while mechanical disruption remains a primary method for managing the biofilm's structural integrity (NIH, 2023; Donlan, 2002).

Other names

Dental plaqueOral biofilmExtracellular polymeric substances (EPS)Oral microbiotaDental biofilmSubgingival plaqueSupragingival plaque

Drugs targeting this assembly act by disrupting bacterial cell membranes (e.g., chlorhexidine), inhibiting essential metabolic enzymes like enolase to prevent acid production (e.g., fluoride), or mechanically and chemically destabilizing the extracellular polymeric substance (EPS) matrix to facilitate biofilm removal (StatPearls, 2023; NIH, 2023). Some agents also interfere with bacterial adhesion to the acquired pellicle or inhibit the synthesis of glucans by glucosyltransferases, which are critical for matrix structural integrity (Marsh, 2006).