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Enamel and dentin demineralization is the loss of mineral ions (primarily calcium and phosphate) from the hydroxyapatite crystals of enamel and dentin due to acid exposure, most commonly from bacterial metabolism of dietary carbohydrates. This process begins when acid lowers the pH in the dental biofilm, causing dissolution of the highly organized hydroxyapatite structure in enamel and dentin, leading to subsurface mineral loss, white spot lesions, and, if unchecked, progression to caries lesions[3][4][5][6]. Remineralization is the natural and therapeutic process of restoring those minerals, frequently aided by fluoride and other agents, which enhance formation of fluorapatite—a mineral more resistant to acid dissolution[6]. Enamel and dentin demineralization is a pathological process rather than a molecular target, and references to it are about tissue-level phenomena, not a discrete molecule or receptor to which drugs directly bind. This is not a canonical molecular target (such as a receptor, enzyme, or transporter) but a process affecting dental tissue structure; thus, it is not considered a valid standalone therapeutic target for structured molecular information databases[4][6].
Inhibition of demineralization by fluoride and remineralization-promoting agents; remineralization through ion deposition; neutralization of acid by buffering agents[2][5][6]
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