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Oral and denture biofilms are complex, multi-species microbial communities embedded within a self-produced matrix of extracellular polymeric substances (EPS) that adhere to both natural tooth surfaces and prosthetic materials (Marsh, 2004, PubMed). These biofilms serve as a protective environment for pathogens such as Streptococcus mutans and Candida albicans, facilitating their survival against host immune responses and antimicrobial agents (Bowen et al., 2018, NIH). In a disease state, the shift from a commensal to a pathogenic biofilm leads to conditions like dental caries, periodontitis, and denture stomatitis (Gendreau & Loewy, 2011, PubMed). Therapeutic strategies targeting these biofilms focus on physical disruption, inhibition of microbial adhesion, and the use of antimicrobial agents to reduce pathogen load or alter metabolic activity (Zero, 2006, PubMed). Understanding the interface between the biofilm and the underlying tooth or denture surface is critical for developing effective preventive and curative dental treatments. Furthermore, these biofilms can act as reservoirs for systemic infections, particularly in vulnerable populations (Seneviratne et al., 2011, PubMed).
Drugs targeting oral and denture biofilms primarily act through the disruption of microbial cell membranes, inhibition of essential metabolic enzymes such as those involved in glycolysis, and interference with the adhesion of primary colonizers to the pellicle or prosthetic surface (Marsh, 2010, PubMed). For instance, fluoride inhibits enolase to reduce acid production, while chlorhexidine increases membrane permeability, leading to cytoplasmic leakage (NIH, PubChem).
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