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The dental plaque biofilm matrix is a complex, three-dimensional scaffold composed of extracellular polymeric substances (EPS) such as polysaccharides, proteins, lipids, and extracellular DNA (eDNA) [3, 6]. This matrix is primarily synthesized by resident oral microorganisms, such as Streptococcus mutans, and is further augmented by host-derived components from saliva and gingival crevicular fluid [6, 16]. Its primary biological functions include providing structural integrity to the biofilm, facilitating bacterial adhesion to the tooth surface, and creating a protective microenvironment that shields microbes from host immune responses and antimicrobial agents [3, 10]. The matrix also plays a critical role in disease pathogenesis by trapping metabolic acids, leading to localized demineralization of tooth enamel (caries) and promoting inflammatory responses in the gingiva (periodontitis) [9, 12]. Therapeutic strategies targeting the matrix aim to disrupt its structural stability or inhibit its synthesis using enzymes like dextranase and DNase, or specialized drug delivery systems like pH-responsive nanoparticles [5, 8, 12]. By degrading the matrix, these treatments enhance the penetration of traditional antimicrobials and facilitate the restoration of a healthy oral microbiome [5, 11].
Enzymatic degradation of extracellular polymeric substances; inhibition of glucosyltransferase and fructosyltransferase enzymes; pH-responsive drug release within the matrix; disruption of extracellular DNA-mediated structural integrity; enhancement of antimicrobial penetration through matrix channels [5, 6, 8, 12].
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