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The Oral bacteria and tooth mineral surfaces target refers to the dynamic interface between the polymicrobial biofilm (dental plaque) and the crystalline hydroxyapatite structure of the tooth (StatPearls, 2023). This system is the primary site of dental caries pathogenesis, where acidogenic bacteria like Streptococcus mutans ferment dietary sugars to produce organic acids, lowering the local pH and causing mineral dissolution (NIH, 2022). Therapeutic interventions targeting this interface involve either the use of antimicrobials to disrupt the biofilm or the application of remineralizing agents like fluoride (Journal of Dental Research, 2019). Fluoride acts by inhibiting bacterial enzymes such as enolase and by substituting hydroxyl groups in the tooth mineral to form fluorapatite, which is significantly more resistant to acid-induced demineralization than the original hydroxyapatite (PubChem, 2024). This interface is also the site of action for antiseptic agents like chlorhexidine, which binds to both bacterial cell walls and the tooth surface to provide long-lasting antimicrobial activity (StatPearls, 2023).
Inhibition of bacterial enolase, disruption of microbial cell membranes, formation of acid-resistant fluorapatite, and reduction of hydroxyapatite solubility (NIH, 2022; PubChem, 2024).
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