Abstract：
OBJECTIVE: Synovitis is a widely accepted sign of osteoarthritis (OA), characterised by tissue hyperplasia, where increased infiltration of immune cells and proliferation of resident fibroblasts adopt a pro-inflammatory phenotype, and increased the production of pro-inflammatory mediators that are capable of sensitising and activating sensory nociceptors, which innervate the joint tissues. As such, it is important to understand the cellular composition of synovium and their involvement in pain sensitisation to better inform the development of effective analgesics.
METHODS: Studies investigating pain sensitisation in OA with a focus on immune cells and fibroblasts were identified using PubMed, Web of Science and SCOPUS.
RESULTS: In this review, we comprehensively assess the evidence that cellular crosstalk between resident immune cells or synovial fibroblasts with joint nociceptors in inflamed OA synovium contributes to peripheral pain sensitisation. Moreover, we explore whether the elucidation of common mechanisms identified in similar joint conditions may inform the development of more effective analgesics specifically targeting OA joint pain.
CONCLUSIONS: The concept of local environment and cellular crosstalk within the inflammatory synovium as a driver of nociceptive joint pain presents a compelling opportunity for future research and therapeutic advancements.
METHODS: Studies investigating pain sensitisation in OA with a focus on immune cells and fibroblasts were identified using PubMed, Web of Science and SCOPUS.
RESULTS: In this review, we comprehensively assess the evidence that cellular crosstalk between resident immune cells or synovial fibroblasts with joint nociceptors in inflamed OA synovium contributes to peripheral pain sensitisation. Moreover, we explore whether the elucidation of common mechanisms identified in similar joint conditions may inform the development of more effective analgesics specifically targeting OA joint pain.
CONCLUSIONS: The concept of local environment and cellular crosstalk within the inflammatory synovium as a driver of nociceptive joint pain presents a compelling opportunity for future research and therapeutic advancements.
摘要：
目的：滑膜炎是广泛接受的骨关节炎（OA）的体征，以组织增生为特征，其中免疫细胞的浸润增加和常驻成纤维细胞的增殖采用促炎表型，并增加了能够敏感和激活感觉伤害感受器的促炎介质的产生，支配关节组织。因此，重要的是了解滑膜的细胞组成及其在疼痛致敏中的参与，以更好地指导有效镇痛药的开发。
方法：使用PubMed鉴定了以免疫细胞和成纤维细胞为重点的研究，WebofScience和SCOPUS。
结果：在这篇综述中，我们全面评估了炎症OA滑膜中固有免疫细胞或滑膜成纤维细胞与关节伤害感受器之间的细胞串扰导致外周疼痛致敏的证据.此外，我们探讨了在类似关节疾病中确定的常见机制的阐明是否可以为开发更有效的针对OA关节痛的镇痛药提供信息.
结论：作为伤害性关节痛的驱动因素，炎性滑膜内的局部环境和细胞串扰的概念为未来的研究和治疗进展提供了令人信服的机会。
方法：使用PubMed鉴定了以免疫细胞和成纤维细胞为重点的研究，WebofScience和SCOPUS。
结果：在这篇综述中，我们全面评估了炎症OA滑膜中固有免疫细胞或滑膜成纤维细胞与关节伤害感受器之间的细胞串扰导致外周疼痛致敏的证据.此外，我们探讨了在类似关节疾病中确定的常见机制的阐明是否可以为开发更有效的针对OA关节痛的镇痛药提供信息.
结论：作为伤害性关节痛的驱动因素，炎性滑膜内的局部环境和细胞串扰的概念为未来的研究和治疗进展提供了令人信服的机会。
