Light诱导类风湿关节炎滑膜细胞向破骨细胞转化

目的 观察Light在类风湿关节炎(RA)滑膜细胞向破骨细胞转化过程中的作用.方法 取8例RA患者滑膜组织,胶原酶消化获取滑膜细胞,每例滑膜细胞分成5份培养,第1组加入巨噬细胞集落刺激因子(MCSF)作阴性对照,第2组加入MCSF和LIGHT,第3组加入MCSF和核因子(NF)-κB受体激动剂配体(RANKL),第4组加入MCSF、LIGHT和RANKL,第5组加入LIGHT.体外培养2周后,行抗酒石酸酸性磷酸酶(TRAP)染色,F肌动蛋白(F-actin)染色以及象牙片上骨吸收陷窝观察破骨细胞的形成和活性.结果 第1组和第5组TRAP(-),F-actin(-),象牙片上无骨吸收陷窝形成;第2组TRAP(+),F-actin(+),骨陷窝形成(+),多核破骨细胞呈圆形和椭圆形,体积较小,骨陷窝分散,体积较小;第3组TRAP(++).F-actin(++),骨陷窝形成(++),多核破骨细胞体积大,骨陷窝较多,体积大,形态不规则;第4组TRAP(+++),F-actin(+++),骨陷窝形成(++++),多核破骨细胞更多,骨陷窝大且有融合趋势.结论 Light能诱导RA滑膜细胞向破骨细胞转化,并能促进RANKL诱导滑膜细胞向破骨细胞转化的能力.

Light induced synovial macrophage-osteoclast differentiation in rheumatoid arthritis

Objective To observe the effect of LIGHT on synovial macrophage-osteoclast difier entiation in rheumatoid arthritis.Methods Synovial macrophages were collected from 8 synovial tissues har vested from RA patients by digestion with conagenase.The macrophages from each patient were divided into 5 subgroups:group 1 was co-cultured with Macrophage Colony Stimulating Factor(MCSF).group 2 was co cultured with MCSF and LIGHT.group 3 was co-cultured with MCSF and Receptor activator for Nuclear Fac tor kB ligand(RANKL),group 4 was co-cultured with MCSF and LIGHT and RANKL group 5 was co-cul tared with LIGHT.After two weeks of culture.tartrate resistant acid phosphatase(TRAP)and F-actin staining were used to detect the formation of osteoclast on cover slip(CS).Functional evidence of osteoclasts was as sessed by the formation of resorption pits ou dentine slice(DS).Results TRAP and F-actin were both nega tive in group 1 and group 5 and no pit on dentine slice could be observed.In group 2.there were some small round and ovoid osteoclasts with TRAP(+)and F-actin(+).Pits on DS were small and discrete.In group 3. there were many large irregular osteoclasts with TRAP(++)and F-actin(++).The number and volume of pits were both increased.In group 4.there were even more and larger osteoclasts with TRAP(+++)and F-actin (+++).The pits were even larger and became confluent,ie,pits(++++).Conclusion LIGHT can promote RANKL-mediated osteoclastogenesis in RA synovial macrophages.and it can induce osteoclast formation through a mechanism independent of RANKL.