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Exposed dentinal tubinal mineral surfaces are the primary structural target for treating dentin hypersensitivity (DH). Dentin is a calcified tissue composed of approximately 70% hydroxyapatite, characterized by thousands of microscopic channels called dentinal tubules that extend from the pulp to the dentinoenamel junction [Miglani, S., et al. (2010). Journal of Conservative Dentistry]. When enamel or cementum is lost, these tubules become exposed to the oral environment, allowing stimuli to induce fluid flow that triggers pulpal nociceptors, a process described by the hydrodynamic theory [Brännström, M. (1963). Sensory Mechanisms in Dentine]. Therapeutic agents target these mineral surfaces to either occlude the tubule openings or desensitize the nerves within. For instance, bioactive glasses like calcium sodium phosphosilicate (NovaMin) react with saliva to form a hydroxyapatite-like layer on the mineral surface, effectively sealing the tubules [Burwell, A. K., et al. (2009). Journal of Clinical Dentistry]. Other treatments, such as arginine-calcium carbonate technology, utilize the affinity of amino acids for the mineralized dentin to deposit protective plugs [Cummins, D. (2009). Journal of Clinical Dentistry].
The primary mechanism involves the physical occlusion of exposed dentinal tubules to block the hydrodynamic flow of fluid, thereby preventing the stimulation of mechanoreceptors in the pulp [Miglani, S., et al. (2010). Journal of Conservative Dentistry]. Additionally, certain agents like potassium nitrate work by increasing the extracellular potassium ion concentration, which depolarizes the nerve membranes and prevents the transmission of pain signals [Poulsen, S., et al. (2006). Cochrane Database of Systematic Reviews]. Other mechanisms include the precipitation of proteins (e.g., glutaraldehyde) or the formation of insoluble mineral complexes (e.g., stannous fluoride or strontium salts) on the mineralized tubule walls to reduce permeability [West, N. X., et al. (2013). Journal of Dentistry].
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