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Fluoride retention refers to the physiological and pharmacokinetic maintenance of fluoride ions within biological systems, specifically in the oral cavity and mineralized tissues (Duckworth et al., 1991, PubMed: 2110467; Wieringa, 2015). It is not a discrete molecular target such as a receptor or enzyme but rather a therapeutic parameter or physiological state defining the persistence of fluoride at its biological sites of action (NIH, PMC9569062). In dentistry, maximizing oral fluoride retention in saliva and dental plaque is the primary goal for preventing dental caries, as it ensures a sustained presence of fluoride ions to inhibit enamel demineralization and promote remineralization (ClinicalTrials.gov, NCT04620252; Caries Research, 1993). Systemically, approximately 99% of retained fluoride is sequestered in the skeleton, where it integrates into the hydroxyapatite crystal lattice to form fluorapatite (ResearchGate, Fluoride Metabolism). While therapeutic levels of retention enhance bone density and tooth resistance, excessive accumulation can lead to adverse effects such as dental or skeletal fluorosis (WHO Guidelines; Int J Environ Res Public Health, 2022). The degree of retention is influenced by the fluoride delivery vehicle, salivary flow rate, and renal clearance efficiency (Sjögren & Birkhed, 1993).
Fluoride retention is a pharmacological process where fluoride ions are incorporated into mineralized tissues or held in oral fluid reservoirs. In the teeth, fluoride replaces the hydroxyl group in hydroxyapatite to form fluorapatite, which is more resistant to acid dissolution (Wieringa, 2015). Topical fluoride applications promote the formation of 'loosely bound' calcium fluoride (CaF2) reservoirs on enamel surfaces and in plaque, which release fluoride ions during acid challenge to facilitate remineralization (Duckworth et al., 1991). Systemic retention is regulated by the balance of skeletal uptake and renal excretion, primarily through glomerular filtration (ResearchGate, Fluoride Metabolism).
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