OPG和RANKL在创伤后异位骨化模型中的表达及作用

目的研究创伤后异位骨化模型中护骨素（OPG）和核因子-κB受体活化因子配体（R．ANKL）的表达变化，探讨OPG／RANKL系统在异住骨化发病机制中的作用。方法将30只健康的成年雄性新西兰实验兔随机分为两组：模型组（20只）：诱导新西兰实验兔产生异位骨化；对照组（10只），作为空白对照。在造模后第8周处死新西兰实验兔，收集模型组新西兰实验兔形成的异位骨标本作为异位骨化组和对照组实验兔相同部位组织进行对照并行免疫组化染色。结果对照组10只实验兔全部存活至造模后第8周，未发生异位骨化模型组共有18只实验兔存活至造模后第8N，有14只发生异位骨化。异位骨化组异位骨组织中的OPG表达水平明显高于对照组（P〈0.05），异位骨化组异位骨组织中的OPG／RANKL比值明显高于对照组（P〈0.05）。结论OPG／RANKLI比值在异位骨化中增加，可能参与异位骨化的发病发展。

Objective To investigate the expression of OPG and RANKL in the the model of post-traumatic heterotopic ossification and the regulative effects of the OPG/RANKL system on the pathogenesis of formation of heterotopic ossification after trauma. Methods A total of 30 healthy adult male New Zealand laboratorial rabbits were randomly divided into a modeling group （n=20） and a control group （n=10） . Heterotopic ossification was induced in the modeling group. New Zealand laboratorial rabbits in the control group were not established model of heterotopic ossification. All animals were sacrificed at the end of 8 weeks. Ectopic bone specimens from New Zealand laboratorial rabbits in the modeling group and normal tissue from New Zealand laboratorial rabbits in the control group was harvested and stained immunohistochemically to detect OPG and RANKL expression. Results None of the 10 New Zealand white rabbits in the control group showed heterotopic ossification. A total of 18 New Zealand laboratorial rabbits in the modeling group survived after eight weeks and 14 showed heterotopic ossification. The level of OPG expression in ectopic bone specimens was significantly higher in the modeling group than in the control group （ P〈0.05 ） .The OPG and RANKL expression ratio in ectopic bone specimens was also significantly higher in the modeling group than in the control group （ P〈0.05 ） . Conelusion OPG/RANKL system may play a regulative role in the development ofheterotopic ossification. The increased OPG to RANKL ratio may be related to the formation ofheterotopic ossification.