论文部分内容阅读
目的:检测RANKL在成釉细胞瘤(ameloblastoma,AM)组织中的表达情况及探讨RANKL在AM骨吸收机制中的作用。方法:通过免疫组化方法检测RANKL在AM组织中的表达情况;通过建立AM细胞/新生大鼠骨细胞共培养体系,观察AM细胞诱导破骨细胞形成的活性,再以OPG(RANKL的抑制剂)进行干预,观察OPG对AM细胞诱导破骨细胞形成活性的影响。结果: RANKL在AM组织中有恒定的表达;AM细胞能够诱导新生大鼠骨细胞分化为成熟的破骨细胞,但此活性可被OPG明显抑制结论:AM细胞诱导破骨细胞形成可能是AM骨吸收过程中局部破骨细胞形成的重要来源和机制,而RANKL在此过程中发挥重要作用。
Objective: To detect the expression of RANKL in ameloblastoma (AM) and to explore the role of RANKL in AM bone resorption. Methods: The expression of RANKL in AM tissues was detected by immunohistochemistry. The osteoblast-forming activity induced by AM cells was observed by establishing a co-culture system of AM cells / neonatal rat osteoblasts. Then, OPG (inhibitor of RANKL ) To observe the effect of OPG on the osteoclastogenesis induced by AM cells. RESULTS: RANKL was constitutively expressed in AM tissues. AM cells induced the differentiation of newborn rat osteoblasts into mature osteoclasts. However, this activity was inhibited by OPG. Conclusion: AM cells induce the formation of osteoclasts probably by AM bone Absorption of local osteoclasts during the formation of an important source and mechanism, and RANKL play an important role in this process.