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Peripheral nerve endings in the dental pulp are the terminal sensory branches of the trigeminal nerve, primarily consisting of myelinated A-delta fibers and unmyelinated C-fibers. These nerve endings are responsible for the transduction of various stimuli—including thermal, mechanical, and chemical changes—into electrical signals that the brain perceives as pain. They express a high density of specific molecular targets such as voltage-gated sodium channels (notably Nav1.7, Nav1.8, and Nav1.9) and transient receptor potential (TRP) channels like TRPV1 and TRPA1, which are critical for pain signaling (Hargreaves & Byers, 2011; PMID: 21600595). In pathological states like pulpitis, inflammatory mediators sensitize these endings, leading to hyperalgesia and spontaneous pain (Kim & Anderson, 2007; PMID: 17716311). Pharmacologically, these nerve endings are the primary site of action for local anesthetics, which bind to and inhibit sodium channels to prevent the transmission of pain signals during dental procedures. While 'Peripheral nerve endings in dental pulp' is a functional therapeutic target site, it is considered an anatomical structure containing multiple specific molecular targets rather than a single receptor or molecule.
Voltage-gated sodium channel blockade; Transient receptor potential (TRP) channel modulation; Inhibition of action potential propagation
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