Department of Physiology, Nihon University School of Dentistry, Tokyo, Japan.
Department of Physiology, Nihon University School of Dentistry, Tokyo, Japan.
J Oral Biosci. 2024 Mar;66(1):145-150. doi: 10.1016/j.job.2024.02.001. Epub 2024 Feb 10.
This study aimed to elucidate the role of macrophages in the trigeminal ganglia (TG) in developing pulpitis-associated ectopic orofacial pain.
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.
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.
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.
本研究旨在阐明三叉神经节（TG）中巨噬细胞在发展与牙髓炎相关的异位口面痛中的作用。
大鼠上颌牙髓暴露，同侧触须垫（WP）给予氟金（FG）。记录 WP 机械刺激时的头部退缩阈值（HWT），牙髓暴露后 3 天和 4 天向 TG 给予脂质体氯膦酸盐 clophosome-A（LCCA；巨噬细胞耗竭剂）。免疫组织化学染色，TG 切片用抗 Iba1（一种巨噬细胞标志物）和抗 Nav1.7 抗体染色。
牙髓暴露降低 HWT，并增加 FG 标记的 TG 神经元附近的 Iba1-IR 细胞数量。LCCA 抑制 HWT 的降低，并阻止牙髓炎组中 FG 标记的 Nav1.7-IR TG 神经元的增加。
牙髓炎激活巨噬细胞导致从 WP 接收输入的 TG 神经元中 Nav1.7 的过度表达，导致牙髓炎引起的异位面部机械性痛觉过敏。
