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Tooth enamel and dentin are primarily composed of hydroxyapatite [Ca10(PO4)6(OH)2], a crystalline calcium phosphate mineral that provides the structural hardness necessary for mastication (PubChem CID 14781). In the oral environment, this mineral undergoes constant cycles of demineralization and remineralization influenced by bacterial acids and salivary buffers (NIH/NIDCR). When demineralization exceeds remineralization, dental caries and erosion occur, leading to the loss of tooth structure. Therapeutic interventions target this mineral substrate to promote the deposition of new mineral or the conversion of hydroxyapatite into fluorapatite [Ca10(PO4)6F2] (Journal of Dental Research). Fluorapatite is significantly more resistant to acid-induced dissolution than the original hydroxyapatite, thereby enhancing the tooth's defense against decay (StatPearls). Modern treatments utilize fluoride, nano-hydroxyapatite, and calcium-phosphate complexes to stabilize the mineral surface and occlude exposed dentinal tubules (PubMed). This target is unique in that it involves the chemical modification of a biological crystal rather than the modulation of a protein or signaling pathway.
Promotion of remineralization through ion deposition and the substitution of hydroxyl groups with fluoride ions to form acid-resistant fluorapatite.
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