抄録
Objectives: This study aimed to elucidate the role of macrophages in the trigeminal ganglia (TG) in developing pulpitis-associated ectopic orofacial pain. Methods: Rats underwent maxillary pulp exposure, and Fluoro-Gold (FG) was administered in the ipsilateral whisker pad (WP). Head withdrawal threshold (HWT) upon mechanical stimulation of the WP was recorded, and liposomal clodronate clophosome-A (LCCA; macrophage depletion agent) was administered to the TG at three and four days after pulp exposure. Immunohistochemically, TG sections were stained with anti-Iba1 (a macrophage marker) and anti-Nav1.7 antibodies. Results: Pulp exposure decreased HWT and increased the number of Iba1-IR cells near FG-labelled TG neurons. LCCA inhibited the decrease in HWT and stopped the increase of FG-labelled Nav1.7-IR TG neurons in the pulpitis group. Conclusions: Activation of macrophages by pulpitis induces the overexpression of Nav1.7 in TG neurons receiving inputs from WP, resulting in pulpitis-induced ectopic facial mechanical allodynia.
本文言語 | 英語 |
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ページ(範囲) | 145-150 |
ページ数 | 6 |
ジャーナル | Journal of Oral Biosciences |
巻 | 66 |
号 | 1 |
DOI | |
出版ステータス | 出版済み - 3月 2024 |