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Tooth hydroxyapatite and collagen represent the primary inorganic and organic components of dental hard tissues, including enamel, dentin, and cementum [1]. Hydroxyapatite, a crystalline calcium phosphate (Ca10(PO4)6(OH)2), provides the hardness and structural integrity of the tooth, while Type I collagen forms a scaffold in dentin that supports mineralization and provides toughness [2]. In the context of dental disease, the demineralization of hydroxyapatite by bacterial acids leads to dental caries, and the subsequent exposure and degradation of the collagen matrix result in structural failure [3]. Therapeutic interventions often target these components to promote remineralization, such as through the application of fluoride or bioactive glasses, or to stabilize the organic matrix using cross-linking agents or protease inhibitors [4]. Fluoride ions specifically substitute hydroxyl groups in hydroxyapatite to form fluorapatite, which is significantly more resistant to acid dissolution [5]. Understanding the interaction between these two phases is critical for developing restorative materials and preventive treatments that mimic the natural tooth structure [6].
The mechanism of action involves the chemical modification of the hydroxyapatite crystal lattice and the preservation of the collagenous organic matrix [1, 2]. Fluoride-containing agents promote the formation of fluorapatite, which has a lower solubility product than hydroxyapatite, thereby resisting acid-induced demineralization [5]. Other agents, such as CPP-ACP, maintain a supersaturated state of calcium and phosphate at the tooth surface to drive remineralization [6]. In dentin, drugs may also target the organic phase by inhibiting matrix metalloproteinases (MMPs) and cysteine cathepsins, which prevents the degradation of the collagen scaffold that is necessary for mineral deposition [3, 4].
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