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Exposed dentin surface and dentinal tubules represent a critical clinical target in the management of dentin hypersensitivity. Dentinal tubules are microscopic, fluid-filled channels that traverse the dentin from the pulp to the dentino-enamel or cemento-enamel junction (PubMed, PMID: 10856166). When protective layers like enamel or cementum are lost due to attrition, erosion, or gingival recession, these tubules become exposed to the oral environment (StatPearls, 2023). According to the hydrodynamic theory, external stimuli such as cold, heat, or pressure cause rapid fluid movement within the tubules, which stimulates pulpal mechanoreceptors and triggers sharp, transient pain (NIH, 2021). Pharmacological and mechanical treatments aim to either occlude these tubules to stop fluid flow or alter the excitability of the underlying nerves (Journal of Dentistry, 2013). Effective management of this target is essential for improving patient quality of life and preventing further dental complications such as pulpitis.
Therapeutic agents act via two primary mechanisms: tubule occlusion and nerve desensitization. Occluding agents (e.g., stannous fluoride, calcium sodium phosphosilicate, oxalates) physically block the tubule orifices to prevent fluid movement, while desensitizing agents (e.g., potassium nitrate) increase the extracellular potassium concentration to depolarize and inhibit the transmission of nerve impulses (StatPearls, 2023; PubMed, PMID: 10856166).
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