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The oral pathogenic microbiota refers to the diverse community of microorganisms, including bacteria, fungi, and viruses, that inhabit the oral cavity and contribute to disease when the ecological balance is shifted toward a dysbiotic state [1]. Key pathogens such as Streptococcus mutans are primarily responsible for dental caries through the fermentation of dietary sugars into organic acids, while organisms like Porphyromonas gingivalis act as keystone pathogens in the development of periodontitis [2, 3]. These microbes typically reside within complex, multi-species biofilms known as dental plaque, which protect them from host immune responses and increase their resistance to antimicrobial agents [1]. Beyond localized oral diseases, the pathogenic microbiota is linked to systemic conditions, including cardiovascular disease and diabetes, via the translocation of bacteria and inflammatory mediators into the systemic circulation [4]. Therapeutic strategies involve the use of broad-spectrum antiseptics, targeted antibiotics, and fluoride to reduce pathogen load and inhibit metabolic activity [5]. Modern research is also exploring the use of probiotics and narrow-spectrum antimicrobials to selectively target pathogens while preserving the beneficial commensal flora.
Drugs targeting the oral pathogenic microbiota act through various mechanisms, including the inhibition of bacterial cell wall synthesis (e.g., penicillins), disruption of protein synthesis (e.g., tetracyclines), interference with DNA replication (e.g., metronidazole), and the physical disruption of microbial cell membranes by antiseptic agents [5]. Fluoride specifically inhibits the enzyme enolase in the glycolytic pathway of cariogenic bacteria, reducing acid production [3].
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