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The salivary proton pool refers to the collective concentration of hydrogen ions and the associated buffering capacity within the oral cavity, primarily maintained by bicarbonate, phosphate, and protein systems (Bardow et al., 2001). It is not a discrete molecular target such as a receptor or enzyme, but rather a physiological chemical environment essential for maintaining the integrity of dental hard tissues. The primary biological function of this pool is to regulate oral pH, preventing it from falling below the critical threshold of approximately 5.5, at which point hydroxyapatite demineralization occurs (Dawes, 2003). In the context of dental caries and erosion, the proton pool becomes a focus for therapeutic intervention; for instance, the use of arginine or urea promotes the production of ammonia by oral bacteria, which neutralizes the proton pool and raises the pH (Burne & Marquis, 2000). The status of this pool is influenced by salivary flow rates, microbial metabolism, and dietary intake, making it a dynamic component of the oral ecosystem (Humphrey & Williamson, 2001). Therapeutic strategies targeting this pool often involve the use of alkalizing agents that leverage the metabolic activity of the oral microbiome to produce neutralizing bases. Monitoring the salivary proton pool through pH and buffering capacity measurements serves as a key biomarker for assessing caries risk and the efficacy of preventive treatments.
Neutralization of hydrogen ions and enhancement of the salivary buffering capacity to maintain oral pH above the critical threshold for enamel demineralization (Dawes, 2003; Burne & Marquis, 2000).
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