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2023 Fiscal Year Final Research Report

Orofacial pain mechanism due to infant stress

Research Project

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Project/Area Number 21K10123
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 57060:Surgical dentistry-related
Research InstitutionNihon University

Principal Investigator

SHIBUTA Ikuko (鈴木郁子)  日本大学, 歯学部, 専修研究員 (60459906)

Co-Investigator(Kenkyū-buntansha) 篠田 雅路  日本大学, 歯学部, 教授 (20362238)
三枝 禎  日本大学, 松戸歯学部, 教授 (50277456)
人見 涼露  日本大学, 歯学部, 講師 (70548924)
林 良憲  日本大学, 歯学部, 准教授 (80582717)
Project Period (FY) 2021-04-01 – 2024-03-31
Keywords幼少期ストレス / 一次侵害受容ニューロン / 三叉神経節
Outline of Final Research Achievements

The involvement of the Nav1.8 and the CCL2/CCR2 signaling in the trigeminal ganglion (TG) in facial skin incisional pain hypersensitivity was examined. The whisker pad skin was incised on postnatal day 4 and week 7. Mechanical hypersensitivity was enhanced in Incision-Incision group. The number of Nav1.8-immunoreactive TG neurons and the amount of CCL2 expressed in the macrophages and satellite glial cells in the TG were increased on day 14 after re-incision in the Incision-Incision group. Blockages of Nav1.8 and CCR2 suppressed the enhancement of mechanical hypersensitivity in the Incision-Incision group. CCL2 enhanced mechanical hypersensitivity. Our results suggest that neonatal facial injury accelerates the TG neuronal hyperexcitability following orofacial skin injury in adult in association with Nav1.8 overexpression via CCL2 signaling, resulting in the enhancement of orofacial incisional pain hypersensitivity in the adulthood.

Free Research Field

口腔生理学

Academic Significance and Societal Importance of the Research Achievements

本研究は、これまで注目されてこなかった幼少期ストレス負荷による免疫細胞-侵害受容ニューロン間コミュニケーションの可塑的変化によって発症する頭頸部疼痛の分子基盤を解明したことであり,学術的独自性が高い研究であると確信する。本研究の成果は,幼少期ストレス負荷に起因した成熟期に発症する顎顔面部領域の異常疼痛発症のメカニズム解明に留まらず,臨床応用を念頭においてEBMに基づいた異常疼痛治療に対するターゲット分子の同定に寄与し,新規治療法の創造に繋げることができる。

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Published: 2025-01-30  

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