【摘要】 骨关节炎是一种以软骨磨损为主要病理表现，关节疼痛为主要症状的退行性骨关节疾病。关节的慢性疼痛不仅摧残患者的身心健康，也是患者寻求医疗帮助的主要原因。目前对于骨关节炎疼痛发生机制尚未阐明，研究表明，中枢神经系统突触可塑性改变所致的中枢敏化是骨关节炎疼痛加重的重要因素，而星形胶质细胞恰可在与其他神经细胞的相互作用下，通过改变MAPK、Cx43、TNF-α、CCL2等水平，从而促进突触发生这种可塑性改变，变异和放大外周传入的疼痛信号，使机体对于疼痛信号敏感性增加，是关节之外加剧骨关节炎疼痛的重要原因。故本综述将从探讨星形胶质细胞与其他神经细胞之间的分子机制和相互作用出发，阐释中枢敏化和疼痛产生的机制，以求能为明确骨关节炎疼痛机制提供新的思路。更多还原

【Abstract】 Osteoarthritis is a degenerative bone and joint disease with cartilage wear and tear as the main pathological manifestation and joint pain as the main symptom. Chronic pain in the joints not only destroys the physical and mental health of patients, but is also the main reason for patients to seek medical help. The mechanism of osteoarthritis pain has not been elucidated yet. Studies have shown that central sensitization due to altered synaptic plasticity in the central nervous system is an important factor in the exacerbation of osteoarthritis pain, whereas astrocytes promote such plasticity by altering the levels of MAPK, Cx43, TNF-α, and CCL2 under the interactions with other neuronal cells, amplifying and mutating the peripheral afferent pain signals, leading to a increase in the body sensitivity to pain signals. This is an important cause of exacerbated osteoarthritis pain outside the joint. Therefore, in this review, we explore the molecular mechanisms and interactions between astrocytes and other nerve cells to elucidate the mechanisms of central sensitization and pain generation, in order to provide new ideas to clarify the mechanism of osteoarthritis pain.更多还原