| Project/Area Number |
18K17157
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 57050:Prosthodontics-related
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| Research Institution | Nihon University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 加齢 / ミクログリア / M1 / M2 / サイトカイン / 口腔粘膜 / 機械痛覚過敏 / SAMP8 / ＳＡＭＰ８ / ＳＡＭＲ１ / 口腔内 / 炎症性ミクログリア / 抗炎症性ミクログリア / 炎症 / 疼痛 |
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| Outline of Final Research Achievements |
The effect of aging on intra-oral mucosal pain acceptance mechanism are not clear. Microglia regulate neuronal excitability and are involved in orofacial pain development. The effects of aging on mechanical allodynia in the intra oral focusing on the microglial pain regulation mechanism were investigated by behavioral observation experiments, immunohistochemistry experiments, and behavioral pharmacochemical experiments using aged mice. From these experimental results, it was revealed that aging effects property changes to inflammatory or anti-inflammatory microglia and expression of cytokines TNF-α and IL-10 released from each microglia, and as a result, it was suggested that mechanical hyperalgesia developed after oral mucosal injury was enhanced and sustained.
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| Academic Significance and Societal Importance of the Research Achievements |
口腔粘膜の疼痛は患者の苦痛を招く。加齢が疼痛受容機構へ及ぼす影響の検索において、口腔粘膜損傷後に機械痛覚過敏が加齢により増強及び持続するという成果は、高齢者補綴臨床に有用な疼痛治療ガイドラインの作成や、損傷部が治癒したかに見える粘膜に対する疼痛の有無の診査診断に役立つ可能性を学術的意義に持ち、加齢はミクログリア性の疼痛調節に変化を及ぼすという成果は、鎮痛薬の開発に寄与するという学術的意義を持つ。超高齢社会となった現在、健康寿命の延長の為に口腔内に生じる問題の改善が求められており、口腔内の異常な疼痛により咀嚼や嚥下が困難となった患者に対する、その改善の一助となる事を本研究の社会的意義と考える。
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