中文摘要：

为了探讨肿瘤坏死因子α（TNF-α）/鼠重组白介素-1α（IL-1α）是否能独立于RANKL/RANK/OPG机制之外直接刺激破骨细胞（OC）的形成和活化。提取4周龄C57雌性小鼠脾细胞,加入鼠巨噬细胞集落刺激因子（M-CSF）TNF-α（±IL-1α）进行体外培养,同时加入骨保护素（OPG）和可溶性NF-κB受体活化子配体（sRANKL）以区别RANKL/RANK/OPG机制。通过OC形态学观察、抗酒石酸酸性磷酸酶（TRAP）染色、骨吸收陷窝方法鉴定OC的形成和活化水平。结果显示：TNF-α（±IL-1α）能诱导脾细胞融合产生TRAP阳性的多核细胞并在象牙片上产生吸收陷窝,加入OPG不能阻断其诱导破骨细胞形成和产生骨吸收陷窝。结果表明：在M-CSF存在的情况下,TNF-α以一种独立于RANKL/RANK/OPG之外的机制诱导破骨细胞的形成和活化,而且IL-1α能显著促进TNF-α的诱导作用（P〈0.05）。

英文摘要：

M-CSF and TNF-a （-＋-IL-la） were added to spleen cells obtained from C57 female rat, meanwhile, OPG and sRANKL were also added to these cultures to distinguish the pathway of os- teoclastogenesis. The formation and activation of oste0clasts were detected by ways of morphologic observation,histochemical staining for tartrate-resistant acid phosphatase （TRAP） and lacunar re- sorption through scanning electron microscopy. The results indicated that osteoclast differentiated from spleen cells in the presence of M-CSF and TNF-a,and that lacunar resorption was stimulated by adding IL-la significantly. The process of M-CSF and TNF-a is distinct from the RANKL/ RANK/OPG signaling pathway.