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The dentin mineral surface is a biological composite primarily composed of carbonated hydroxyapatite crystals integrated within a type I collagen scaffold (Goldberg et al., 2011). It constitutes the bulk of the tooth structure, providing mechanical strength and protecting the underlying dental pulp from external stimuli (Marshall et al., 1997). In dental pathology, the demineralization of this surface by bacterial acids leads to dental caries, while the exposure of dentinal tubules is the primary cause of dentin hypersensitivity (Miglani et al., 2010). Therapeutic interventions target this surface to promote remineralization, where fluoride ions are incorporated into the crystal lattice to form fluorapatite, which is significantly more resistant to acid dissolution (Buzalaf et al., 2011). Additionally, desensitizing treatments aim to occlude exposed tubules on the mineral surface to block the hydrodynamic movement of fluid that triggers nerve pain (Cummins, 2013).
Therapeutic agents interact with the dentin mineral surface through ion exchange, such as the replacement of hydroxyl groups with fluoride to form acid-resistant fluorapatite, or through the precipitation of mineral phases that physically occlude exposed dentinal tubules (Buzalaf et al., 2011; Miglani et al., 2010).
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