摘要Objective To examine whether CpG ODN could modulate osteoclastogenesis. Methods Bone marrow mononuclear cells (BMMs) were plated in 96-well plates, there was 0.2mL of the cell culture medium in each well. All the wells were divided into 3 groups, Group 1: in the presence of mouse M-CSF (30ng*mL-1) and RANKL (20ng*mL-1), and either different concentration of ODN-1826 or ODN-1982 for 5 days; Group 2: ODN-1826 or ODN-1982 (100nmol*L-1) was added to BMMs [incubated with M-CSF (30ng*mL-1) and RANKL (20ng*mL-1)] at different times after the start of the BMM culture (total incubation time 102 hours). Group 3: BMMs were grown for 72 hours with M-CSF(30ng*mL-1)and for another 72 hours with M-CSF and RANKL(20ng*mL-1) in the absence or presence of either ODN-l826 or ODN-1982.On day 3, medium was changed and osteoclast formation was evaluated on day 4 or 5, then TRAP staining and analysis. Results ODN-1826 could inhibit RANKL-induced osteoclastogenesis in a dose-dependent manner, the inhibition becomes less pronounced when ODN-l826 was added later. Addition of ODN-1826 10 and 24 hours after the start of the experiment results in inhibition by 95%(P<0.001) and 40% (P<0.001). When ODN-1826 was added 72 hours after the start of the experiment, a significant enhancement of RANKL osteoclastogenic activity was obtained (>90%, P<0.001). The enhancement obtained in the presence of ODN-1826 during the last 30 hours of the experiment was evident at 20nmol*L-1of the ODN (P<0.001 ). Conclusion ODN-1826 could promote osteoclastogenesis only under conditions with prior exposure of BMMs to RANKL (in the absence of the ODN), suggesting the need for a priming phase dependent on RANKL-RANK interaction.