Pathogenic oral biofilm matrix and bacterial cell surface

The pathogenic oral biofilm matrix and bacterial cell surfaces constitute a complex, three-dimensional environment where microorganisms are encased in a self-produced matrix of extracellular polymeric substances (EPS) (Flemming & Wingender, 2010). This matrix is primarily composed of polysaccharides like glucans and fructans, proteins, and extracellular DNA (eDNA), which provide structural stability and act as a barrier against antimicrobial penetration (Koo et al., 2013). Bacterial cell surfaces within the biofilm display specific adhesins that facilitate attachment to the acquired enamel pellicle and promote inter-species co-aggregation (Marsh, 2004). This structural assembly is a major therapeutic target in dentistry, as it mediates the localized acidification that leads to dental caries and the inflammatory response in periodontitis (Bowden & Hamilton, 1998). Drugs such as chlorhexidine and fluoride interact with these surfaces to disrupt membrane integrity or inhibit the enzymatic production of the matrix (Koo et al., 2017). Effective treatment requires agents that can either degrade the EPS scaffold or interfere with the initial adhesion of bacteria to oral surfaces. Furthermore, the matrix serves as a reservoir for signaling molecules, facilitating quorum sensing and the coordinated expression of virulence factors (Flemming & Wingender, 2010). Targeting the biochemical components of the matrix, such as glucosyltransferases, offers a way to reduce biofilm pathogenicity without necessarily killing all oral bacteria (Koo et al., 2013).

Other names

Dental plaqueOral biofilmExtracellular polymeric substances (EPS)Dental biofilm matrix

Therapeutic agents targeting the oral biofilm matrix and cell surfaces work through several pathways: physical disruption of the EPS scaffold, enzymatic degradation of matrix polysaccharides (e.g., via dextranases), inhibition of glucosyltransferase enzymes that synthesize the matrix, and the alteration of bacterial cell surface properties to prevent adhesion or induce membrane lysis (Koo et al., 2017; Marsh, 2004).