骨质疏松中不同炎症因子的研究进展  

Research Progress of Different Inflammatory Factors in Osteoporosis

作　　者：卢锋 陈海啸[2] 

机构地区：[1]浙江大学医学院,浙江 杭州 [2]浙江大学附属台州医院,浙江 临海

出　　处：《临床医学进展》2022年第4期2590-2604,共15页Advances in Clinical Medicine

摘　　要：大量研究表明炎性细胞因子对各种炎性疾病发挥重要作用,但对其具体作用的报道并不总是一致的。它们可用作指示或监测疾病或其进展的生物标志物,也可用作治疗的临床适用参数。免疫系统的各种炎症因子可以上调核因子-κB受体活化因子配体(Receptor Activator for Nuclear Factor-κB Ligand, RANKL)的表达,RANKL与破骨细胞前体细胞的RANK结合促进破骨细胞的分化和活化,最终引起炎症性骨质疏松的发生发展。但迄今为止,炎症因子对骨质疏松的具体影响机制一直没有得到系统地归纳。因此,在这篇综述中,我们筛选总结了炎症因子白介素-1 (Interleukin-1, IL-1)、IL-33、IL-6、IL-8、IL-10和肿瘤坏死因子-α (tumor necrosis factor-α, TNF-α)的生物学信息在炎症和骨质疏松中的作用,为炎症性骨质疏松提供了一个系统的理论基础。A large number of studies have shown that inflammatory cytokines play an important role in various inflammatory diseases, but the reports on their specific effects are not always consistent. They can be used as biomarkers to indicate or monitor the disease or its progress, and can also be used as clinical parameters for treatment. Various inflammatory factors in the immune system can up-regulate the expression of nuclear factor-kappa B receptor activating factor ligand (Receptor Activator for Nuclear Factor-κB Ligand, RANKL). The binding of RANKL to the RANK of osteoclast precursors promotes the differentiation and activation of osteoclasts, resulting in the occurrence and development of inflammatory osteoporosis. But so far, the specific mechanism of inflammatory factors on osteoporosis has not been systematically summarized. Therefore, in this review, we screened and summarized the biological information of inflammatory factors interleukin-1 (Interleukin-1, IL-1), IL-33, IL-6, IL-8, IL-10 and tumor necrosis factor-α (tumor necrosis factor-α, TNF-α) and their roles in inflammation and osteoporosis, which provided a systematic theoretical basis for inflammatory osteoporosis.

关 键 词：骨质疏松 炎症因子 炎症性疾病 破骨细胞 RANKL 

分 类 号：R681[医药卫生—骨科学]