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Sensory nerve fibers in dentin are specialized peripheral processes of trigeminal neurons that innervate the dental pulp and extend into the inner portion of the dentinal tubules (Magloire et al., 2009). These fibers are primarily categorized as myelinated A-delta fibers, responsible for sharp, localized pain, and unmyelinated C-fibers, which mediate dull, aching pain associated with tissue injury (Fried et al., 2011). According to the widely accepted hydrodynamic theory, external stimuli cause fluid movement within the dentinal tubules, which mechanically distorts and activates these nerve endings (Brännström, 1963). These fibers express a variety of molecular sensors, including mechanosensitive Piezo2 channels and thermosensitive TRP channels like TRPV1 and TRPM8, which translate physical stimuli into electrical signals (Chung et al., 2013). In clinical practice, these fibers are the focus of treatments for dentin hypersensitivity, where agents like potassium nitrate are used to reduce excitability by increasing extracellular potassium levels (Markowitz & Kim, 1990). Understanding the distribution and physiological properties of these fibers is crucial for managing dental pain and developing targeted desensitizing therapies.
Pharmacological agents target these fibers by either inducing prolonged depolarization using potassium ions to prevent action potential generation (Markowitz & Kim, 1990) or by blocking voltage-gated sodium channels to inhibit signal propagation (Becker & Reed, 2012). Additionally, some treatments indirectly affect these fibers by occluding dentinal tubules, thereby reducing the hydrodynamic fluid movement that triggers mechanosensitive receptors on the nerve endings (Brännström, 1963).
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