癌症引起的疼痛是头颈癌最常见的并发症。小胶质细胞集落刺激因子受体 1 (CSF1R) 在炎症和神经性疼痛中发挥着至关重要的作用。然而，CSF1R 对口面部癌引起的疼痛的影响尚不清楚。在这里，我们的目的是确定CSF1R在癌症引起的口面部疼痛中的作用。我们用Walker 256B细胞建立了癌症引起的口面部疼痛的动物模型。冯弗雷丝试验和激光强度疼痛测试仪用于评估肿瘤引起的机械和热超敏反应。米诺环素和 PLX3397 用于改变肿瘤诱导的机械和热痛觉过敏。此外，我们评估了 PLX3397 对三叉神经脊髓尾核亚核 (Vc) 内免疫炎症介质和神经元激活的影响。Walker 256B 细胞诱导的肿瘤生长导致机械和热痛觉过敏，并伴有小胶质细胞激活和 CSF1R 上调。使用米诺环素或 PLX3397 治疗可逆转肿瘤引发的相关伤害行为和小胶质细胞激活。 PLX3397 治疗的结果是，肿瘤诱导的促炎细胞因子表达增加和 Vc 神经元激活受到显着抑制。我们的研究结果表明，通过 CSF1R 阻断小胶质细胞激活可能有助于预防癌症引起的口面部疼痛。© 2024约翰·威利

Cancer-induced pain is the most common complication of the head and neck cancer. The microglia colony-stimulating factor receptor 1 (CSF1R) plays a crucial role in the inflammation and neuropathic pain. However, the effect of CSF1R on orofacial cancer-induced pain is unclear. Here, we aimed to determine the role of CSF1R in orofacial pain caused by cancer.We established an animal model of cancer-induced orofacial pain with Walker 256B cells. Von Frey filament test and laser-intensity pain tester were used to evaluate tumor-induced mechanical and thermal hypersensitivity. Minocycline and PLX3397 were used to alter tumor-induced mechanical and thermal hyperalgesia. Additionally, we evaluated the effect of PLX3397 on immunoinflammatory mediators and neuronal activation within the trigeminal spinal subnucleus caudalis (Vc).Walker 256B cell-induced tumor growth resulted in mechanical and thermal hyperalgesia, accompanying by microglia activation and CSF1R upregulation. Treatment with minocycline or PLX3397 reversed the associated nocifensive behaviors and microglia activation triggered by tumor. As a result of PLX3397 treatment, tumor-induced increases in pro-inflammatory cytokine expression and neuronal activation of the Vc were significantly inhibited.The results of our study showed that blocking microglial activation via CSF1R may help prevent cancer-induced orofacial pain.© 2024 John Wiley & Sons Ltd.