2021 Fiscal Year Final Research Report

Macrophages in trigeminal ganglion contributes to the ectopic orofacial pain following inferior alveolar nerve injury

Research Project

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Project/Area Number	19K10049
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Review Section	Basic Section 57010:Oral biological science-related
Research Institution	Nihon University
Principal Investigator	SHINODA Masamichi 日本大学, 歯学部, 教授 (20362238)
Co-Investigator(Kenkyū-buntansha)	林良憲日本大学, 歯学部, 准教授 (80582717) 人見涼露日本大学, 歯学部, 講師 (70548924) 岩田幸一日本大学, 歯学部, 特任教授 (60160115) 久保亜抄子日本大学, 歯学部, ポスト・ドクトラル・フェロー (70733202)
Project Period (FY)	2019-04-01 – 2022-03-31
Keywords	異所性疼痛 / 下歯槽神経損傷 / 一酸化窒素 / 三叉神経節
Outline of Final Research Achievements	Orofacial ectopic mechanical allodynia was developed following inferior alveolar nerve injury (IANI). The amount of nitric oxide (NO) in the trigeminal ganglion increased after IANI. The number of nitric oxide synthase (nNOS)-positive trigeminal ganglion neurons projected into the facial skin was increased. Inhibition of nNOS attenuated the ectopic mechanical allodynia. Following administration of NO substrate to the trigeminal ganglion in naive rats, activation of satellite cells which are non-neuronal cells in the trigeminal ganglion and the ectopic mechanical allodynia were induced. In addition, inhibition of satellite cell activation after IANI attenuated the ectopic mechanical allodynia. These results indicate that NO is a key molecule involved in neuron-satellite glial cell communication and associated with mechanical allodynia in the broad orofacial area following trigeminal nerve injury.
Free Research Field	口腔生理学
Academic Significance and Societal Importance of the Research Achievements	口腔顔面領域における異所性異常疼痛は，二次侵害受容ニューロンの興奮性増強により発症することが知られている。現在、口腔顔面領域における異所性異常疼痛に対して使用されている治療薬は，いずれも二次侵害受容ニューロンの興奮性増強を抑制することにより異常疼痛発症を抑制している。しかし、このような薬物が奏功しない口腔顔面痛患者は多い。本研究によって異所性異常疼痛発症に対する三叉神経節内の非神経細胞活性化の役割が解明できれば，従来の薬物では奏功しない難治性疼痛発症を抑制できる新規治療法の創造につながる。