锝［99Tc］亚甲基二膦酸盐抑制类风湿关节炎患者外周血单核细胞向破骨样细胞转分化

目的：研究锝［99Tc］亚甲基二膦酸盐（technetium［99Tc］ methylenediphosphonate，99Tc-MDP）对核因子κB受体活化子配体（receptor activator of NF-κB ligand，RANKL）和巨噬细胞集落刺激因子（macrophage-colony stimulating factor，M-CSF）诱导类风湿关节炎(rheumatoid arthritis，RA)患者外周血单核细胞 (peripheral blood mononuclear cells，PBMCs)向破骨样细胞转分化的影响。方法：从6例RA患者外周血中分离单核细胞，于RPMI-1640培养液中培养，RANKL（25 μg/L）和 M-CSF（25 μg/L）诱导转分化，用不同浓度99Tc-MDP干预（5,10,20,50 mg/L），在不同时间点（4,12,20 d）终止培养并行HE染色，抗酒石酸酸性磷酸酶(tartrate resistant acid phosphatase,TRAP)染色。结果：RA患者外周血单核细胞培养至第12～16天，可见大量TRAP染色强阳性多核巨细胞，99Tc-MDP可显著抑制上述变化，且其抑制作用随浓度的增加而增强（P＜0.05）。结论：99Tc-MDP可通过抑制破骨样细胞转分化而达到延缓RA骨质破坏的作用。

Technetium [99Tc] methylenediphosphonate inhibits osteoclast formation from PBMCs in patients with rheumatoid arthritis

Objective To observe the influence of technetium [99Tc] methylenedipho-honate (99Tc-MDP) on osteoclastogenesis induced by receptor activator of NF-κB ligand (RANKL) and macrophage-colony stimulating factor (M-CSF)in peripheral blood mononuclear cells in patients with rheumatoid arthritis, and to study the mechanism of 99Tc-MDP in osteoclast differentiation. Methods The monocytes/macrophages were isolated from peripheral blood in patients with rheumatoid arthri-tis, incubated in RPMI-1640 with receptor activator of NF-κB ligand (RANKL, 25 μg/L), macro-phage-colony stimulating factor (M-CSF, 25μg/L ) and different concentrations of 99Tc-MDP (5, 10, 20,and 50 mg/L) for 4,12, and 20 days. Tartrate resistant acid phosphatase staining was used to observe the formation of osteoclasts. Results After 12 or 16 days culture of peripheral blood mononuclear cells, plenty of large nultinuclear cells could be found on the coverslips. 99Tc-MDP markedly inhibited those changes and the inhibitory effects were increased as the concentration of 99Tc-MDP increased (P<0.05). Conclusion 99Tc-MDP probably has some protective effect on rheumatoid arthritis by inhibiting osteoclast formation.