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Nerve fibers in the dental pulp are not a single molecule or receptor, but rather a complex network of myelinated (A-delta and A-beta) and unmyelinated (C) sensory and autonomic (sympathetic) nerve fibers that innervate the connective tissue core of the tooth. These fibers originate largely from branches of the trigeminal nerve, with sensory neurons forming a plexus (the plexus of Raschkow) beneath the odontoblast layer. The main functions of these fibers include transmitting pain signals (especially in response to stimuli that move dentinal fluid, in line with the hydrodynamic theory), mediating responses to thermal/mechanical/noxious stress, regulating blood flow through release of neuropeptides, and potentially participating in tissue regeneration after injury or infection. Key molecular markers include neuropeptides such as substance P and CGRP, as well as mechanotransduction and nociception-related proteins (TRPV1, TRPA1, PIEZO2). Although nerve fibers themselves are not therapeutic targets, their molecular components (e.g., sodium channels, TRP channels, neuropeptides) are emerging targets for the management of dental pain and inflammation[1][2][3][4][6][7]. Please note that "nerve fibers in dental pulp" refers to a population of structures rather than a molecular target (such as a receptor or enzyme), so there is a classification mismatch if you are seeking information on a druggable entity. Individual components within these fibers (ion channels, receptors, neuropeptides) may serve as therapeutic targets in the context of dental pain and disease.
Blockade of voltage-gated sodium channels (local anesthetics) - Inhibition of neuropeptide release (CGRP antagonists, experimental) - Modulation of TRP channel activity (e.g., TRPV1/TRPA1 antagonists/agonists)
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