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Oral plaque bacteria constitute a complex, multi-species microbial biofilm that adheres to oral surfaces, primarily the teeth [1]. This biofilm is composed of a diverse array of bacteria embedded in a self-produced matrix of extracellular polymeric substances (EPS) [1]. Biologically, these microorganisms perform essential roles in niche colonization, interspecies communication via quorum sensing, and metabolic activities such as the fermentation of dietary carbohydrates [2]. When the microbial balance shifts—often due to high sugar intake or poor oral hygiene—pathogenic species like Streptococcus mutans and Porphyromonas gingivalis become dominant [3]. This dysbiosis leads to the production of organic acids that demineralize tooth enamel (caries) or trigger inflammatory responses in the gingiva (periodontitis) [4]. As a therapeutic target, oral plaque is managed through mechanical disruption and pharmacological agents like chlorhexidine, which disrupts bacterial cell membranes, and fluoride, which inhibits bacterial enzymes and promotes enamel remineralization [5]. Beyond local oral diseases, these bacteria are increasingly recognized for their role in systemic inflammation and conditions such as infective endocarditis and cardiovascular disease [6]. [1] Marsh, P. D. (2004). Dental plaque as a microbial biofilm. Caries Research. [2] Kolenbrander, P. E., et al. (2010). Communication among oral bacteria. Microbiology and Molecular Biology Reviews. [3] Takahashi, N., & Nyvad, B. (2011). The role of bacteria in the caries process: ecological perspectives. Journal of Dental Research. [4] Hajishengallis, G. (2015). Periodontitis: from microbial immune subversion to systemic inflammation. Nature Reviews Immunology. [5] Walsh, T., et al. (2019). Fluoride toothpastes for preventing dental caries. Cochrane Database of Systematic Reviews. [6] Lockhart, P. B., et al. (2012). Periodontal disease and atherosclerotic vascular disease. Circulation.
Antimicrobial agents target oral plaque bacteria through several mechanisms: chlorhexidine and cetylpyridinium chloride disrupt the bacterial cytoplasmic membrane causing leakage of cellular contents [1]; fluoride ions inhibit bacterial enolase and proton-extruding ATPase, thereby reducing acid production and interfering with bacterial metabolism [5]; and antibiotics like metronidazole inhibit DNA synthesis in anaerobic pathogens [4].
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