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Tooth mineral surfaces are primarily composed of hydroxyapatite, a crystalline calcium phosphate that provides the essential hardness and structural integrity to enamel and dentin [1]. These surfaces act as a protective barrier for the inner tooth structures and are the site of critical ion exchange processes with saliva and the oral biofilm [2]. In a healthy oral environment, the mineral surface undergoes continuous cycles of demineralization and remineralization; however, an imbalance caused by acidic challenges or bacterial activity leads to dental caries and erosion [3]. Therapeutic agents target these surfaces to either inhibit mineral loss or promote the deposition of new mineral phases. Fluoride, for instance, interacts with the surface to form fluorapatite, which is more resistant to acid dissolution than the original hydroxyapatite [2]. Other treatments, such as synthetic hydroxyapatite or CPP-ACP, aim to physically repair surface defects or occlude dentinal tubules to alleviate hypersensitivity [4].
Promotion of remineralization through the provision of calcium and phosphate ions, conversion of hydroxyapatite to acid-resistant fluorapatite, and physical occlusion of exposed dentinal tubules to block external stimuli.
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