Abstract

There are reports on hypoesthesia and anesthesia in taste sensation persisting for several months or even years after dental anesthesia, pulpectomy and tooth extraction. Taste disorders following dental treatments are usually attributed to peripheral injury of taste (the chorda tympani) nerve fibers running with the lingual nerve fibers near the mandibular molars. 2 However, taste impairment in patients who received treatment of the maxillary anterior teeth cannot be explained by peripheral nerve injury, because the chorda tympani nerve fibers neither innervate nor run through the anterior surgical site. The inferior alveolar nerve, a branch of the trigeminal nerve, innervates dental pulp and periodontal tissue. Peripheral fibers of the inferior alveolar nerve are injured upon dental treatments such as pulpectomy and tooth extraction. In particular, there is a risk that the nerve trunk is crushed or torn upon extraction of mandibular third molars, because the IAN runs in the mandibular canal in close proximity to the molar root tips. Following peripheral nerve injury, glial cells respond at the primary nerve terminals in the central nervous system. In animal models of inferior alveolar nerve injury, microglia appear in the trigeminal spinal subnucleus caudalis and spinal dorsal horn and release substances that affect neuronal excitability. Inhibition of microglial activation suppresses development of pain hypersensitivity, suggesting that active microglia cause abnormal pain sensation by alteration of excitability in neurons processing somatosensory information. The inferior alveolar nerve also terminates in synapses with neurons of the rostral nucleus of the solitary tract where taste afferents terminate. In light of these observations, inferior alveolar nerve injury may activate microglia in the rostral nucleus of the solitary tract and the active microglia may alter neuronal excitability of the NST neurons that process taste information conveyed by taste afferents resulting in Activation of microglia in the nucleus of the solitary tract by inferior alveolar nerve injury

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