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Dentinal tubule nerve endings are the terminal sensory branches of the trigeminal nerve, primarily A-delta and C-fibers, that reside within the dental pulp and extend into the inner third of the dentinal tubules (StatPearls, 2023). These nerve endings serve as the primary transducers of pain in response to external stimuli, such as thermal changes, osmotic pressure, or mechanical forces, which cause fluid movement within the tubules—a process known as the hydrodynamic theory (Brännström, 1986). In the context of dentin hypersensitivity, these nerves become hyper-excitable due to the exposure of tubules to the oral environment. Therapeutic strategies target these nerve endings either directly, by using potassium salts to induce a depolarization blockade that prevents action potential propagation, or indirectly, by using occluding agents to block the physical stimuli from reaching the nerve terminals (Orchardson & Gillam, 2006). Understanding the physiology of these nerve endings is essential for the development of desensitizing agents and the management of acute dental pain associated with enamel loss or gingival recession (Markowitz & Kim, 1992). Furthermore, molecular targets located on these endings, such as TRP channels and voltage-gated sodium channels, are areas of active research for more specific analgesic interventions (PubMed, 2021).
Desensitizing agents like potassium nitrate increase extracellular potassium concentration, causing a sustained depolarization that prevents nerve repolarization and subsequent action potential generation (StatPearls, 2023). Other agents act by occluding the dentinal tubules to prevent fluid movement (hydrodynamic theory), thereby indirectly preventing the mechanical stimulation of these nerve endings (Brännström, 1986). Silver diamine fluoride acts by both occluding tubules and providing antimicrobial effects (StatPearls, 2023).
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