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Dentin tubule mineral surfaces are the hydroxyapatite-based structural components forming the walls of the microscopic channels within the dentin of human teeth [1]. These tubules house odontoblastic processes and dentinal fluid, and their exposure to the oral environment is the primary cause of dentin hypersensitivity [2]. According to the hydrodynamic theory, external stimuli cause fluid movement within these tubules, which triggers mechanoreceptors in the dental pulp, resulting in sharp pain [3]. Therapeutic agents target these mineral surfaces to either physically block (occlude) the tubule orifices or to chemically induce the growth of new mineral layers, such as fluorapatite or hydroxyapatite, to seal the channels [4]. Common treatments include bioactive glasses, arginine-calcium carbonate complexes, and various fluoride salts that react with the tubule mineral to form protective precipitates [5]. These surfaces also serve as a substrate for remineralization therapies aimed at arresting early dental caries by restoring the mineral density of the peritubular dentin [6]. By reducing the diameter of the tubules or sealing them entirely, these drugs effectively decrease dentin permeability and alleviate clinical symptoms [7]. Understanding the chemical interaction between these mineral surfaces and various ions is crucial for developing next-generation desensitizing and restorative dental materials [8].
Physical occlusion of dentinal tubules to inhibit hydrodynamic fluid movement and chemical remineralization of the hydroxyapatite surface to reduce permeability.
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