The role of glial cells in trigeminal ganglion for orofacial neuropathic pain.

2018 Fiscal Year Final Research Report

• Project/Area Number: 15K20520
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Surgical dentistry
• Research Institution: Osaka University
• Principal Investigator: KAWANO AKIYO 大阪大学, 歯学研究科, 助教 (10570294)
• Research Collaborator: Kadono Kohki
• Project Period (FY): 2015-04-01 – 2019-03-31
• Keywords: 口腔顔面痛 / 神経因性疼痛 / Iba1 / 三叉神経節

Outline of Final Research Achievements

In this study, we used the neuropathic pain model rat which mental nerve was loosely ligated and the hypoalgesia model rat which mental nerve was transected. The behavior of Iba1 immunoreactive cells and satellite cells and ED1 immunoreactive cells in the trigeminal ganglion was observed. In both models, the number of Iba1 immunoreactive cells was increased. In addition, double staining with Iba1 antibody using SK3 antibody which is a marker of satellite cells and ED1 which is a marker of monocyte lineage cells shows that Iba1 positive cells do not co-express with SK3 cells, On the other hand, Iba1 positive cells co-expressed with ED1, and expression increased after nerve injury in both models, and in particular significantly increased 2 weeks after injured.

Free Research Field

口腔顔面痛、神経因性疼痛

Academic Significance and Societal Importance of the Research Achievements

歯科領域においては、抜歯や顎骨内腫瘍、顎変形症に対する骨切り術などの外科処置の偶発症として三叉神経の損傷が発生することはまれではない。しかし、神経損傷後の神経因性疼痛の発症メカニズムは完全には解明されていない。本研究では口腔顔面領域の神経因性疼痛発症時の三叉神経節におけるIba1（脳内ミクログリアのマーカー）陽性細胞の働きを一部解明した。このことによって、将来的に口腔顔面領域における神経因性疼痛発症の機序が明らかとなり、治療薬開発の一助になると考える。