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Tooth enamel remineralization via fluoride ion incorporation describes a physicochemical process, not a canonical molecular target. Fluoride ions (F⁻) become incorporated into the crystalline structure of tooth enamel by replacing hydroxide (OH⁻) in hydroxyapatite (Ca₁₀(PO₄)₆(OH)₂), forming fluorapatite (Ca₁₀(PO₄)₆F₂)[2][3][7]. Fluorapatite is significantly more resistant to acid dissolution, making the enamel less susceptible to demineralization from cariogenic bacterial acids[7][1][3]. Topical fluoride applied via toothpaste, rinses, or water fluoridation enhances this process, accelerating the remineralization of early carious lesions and inhibiting future mineral loss[2][7][9]. This is a process of mineral exchange and not a specific molecule, receptor, enzyme, or transporter, thus it does not meet criteria for a canonical druggable target[1][2][7][9]. Excessive fluoride exposure may cause enamel mottling (dental fluorosis) or, rarely, skeletal fluorosis[8]. Note: This entry refers to a biological and chemical process, not a single molecular entity, protein, or receptor. It is thus not a canonical therapeutic target in the sense of a druggable protein, receptor, enzyme, or transporter, but rather a well-characterized process in dental biology and cariology.
Incorporation of fluoride ions into hydroxyapatite forming fluorapatite, which has lower solubility and greater acid resistance[2][3][7][9] Acceleration of remineralization of partially demineralized enamel crystals by promoting crystal growth of fluorapatite[1][7] Inhibition of bacterial metabolism and acid production in dental plaque[7][8]
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