Oral bacterial metabolism

Oral bacterial metabolism refers to the collective biochemical activities of the diverse microbial community residing within the human oral cavity, primarily organized into complex biofilms known as dental plaque [1, 2]. This metabolic network is characterized by the fermentation of dietary carbohydrates into organic acids, such as lactic acid, which can lower the local pH and lead to the demineralization of tooth enamel, a process central to the development of dental caries [3]. Additionally, the proteolytic metabolism of bacteria contributes to periodontitis and halitosis through the production of volatile sulfur compounds and inflammatory byproducts [4]. Therapeutic strategies aimed at oral bacterial metabolism involve the use of agents like fluoride, which inhibits bacterial enolase and proton-extruding ATPases, and xylitol, which acts as a non-fermentable sugar that disrupts bacterial energy cycles [5, 6]. Because 'Oral bacterial metabolism' represents a broad physiological process involving hundreds of different species and thousands of enzymes rather than a single discrete molecular entity, it is classified as a process-level target rather than a specific therapeutic receptor or enzyme [2, 7]. Sources: [1] National Institute of Dental and Craniofacial Research (NIDCR), 'The Oral Microbiome'. [2] Takahashi, N., 'Oral Microbiome Metabolism: From 'Who Are They?' to 'What Are They Doing?'', Journal of Dental Research, 2015. [3] StatPearls, 'Dental Caries'. [4] Journal of Oral Microbiology, 'Metabolic interactions in the oral microbiome', 2020. [5] PubChem, 'Fluoride' (Compound Summary). [6] NIH PubMed, 'Xylitol's Health Benefits and Effects on Oral Metabolism', 2017. [7] Marsh, P. D., 'Contemporary perspectives on plaque control', British Dental Journal, 2012.

Other names

Oral microbial metabolismDental plaque metabolismOral biofilm metabolic activityCommensal oral metabolism

Drugs targeting this process work by inhibiting glycolytic enzymes (e.g., enolase inhibition by fluoride), disrupting sugar transport via the phosphotransferase system (PTS), preventing the synthesis of extracellular polysaccharides by glucosyltransferases, or promoting base-producing pathways (e.g., arginine metabolism) to neutralize acidic environments.