中文摘要：

目的利用改良的小鼠颅骨缺损模型，活体动态观察颅骨缺损后骨形成过程，并对Wnt信号相关基因进行检测，为颅骨再生修复机制及促进修复措施研究提供新的数据。方法用直径2mm的金刚石钻头于小鼠右侧颅顶骨建立颅骨缺损模型，术后2周和4周通过Micro-CT及组织病理切片来观察缺损部位新生骨生长情况，测量其面积大小，定量分析缺损部位的骨形成能力。同时提取缺损后不同时间点缺损周围骨组织RNA，定量PCR检测成骨分化相关基因Cbfal、OP和OC，以及Wnt通路基因Wnt3a、B—catenin及下游转录因子cyclinD1、Tcfl的表达。结果术后2周Micro—CT扫描示缺损愈合百分比为（20．1±6．0）％；术后4周缺损进一步愈合，缺损愈合百分比为（30．1±5．0）％。定量PCR结果显示Cbfal和OP在缺损后2周表达较高，而OC则在缺损后4周达到高峰。Wnt3a、B-catenin、cyclinD1和Tcfl的mRNA表达水平在缺损后2周和4周均较缺损前明显升高。结论成功改良制作了小鼠颅骨缺损模型，并通过活体Micro-CT和组织病理染色对颅骨缺损后的修复过程进行了动态观察，进一步发现Wnt信号通路的激活可能参与颅骨缺损后骨形成过程。

英文摘要：

Objective To explore the regeneration and repair of calvaria defect through observing bone formation dynamically and detecting Wnt signal-related genes in a calvarial defect mouse model. Methods Calvarial defect of 2-mm diameter was made in mouse right parietal bone using a diamond-coated trephine bit. In 2 and 4 weeks after operation, micro-CT scanning combined with histopathological staining were utilized to observe calvarial bone formation. New bone areas were measured to quantitatively evaluate calvarial bone regeneration ability. Total RNA of the defect site was extracted at different time points before and after injury and then real-time PCR was employed to evaluate the mRNA temporal expression patterns of wnt3a, β-catenin, cyclin D1, Tcfl and osteoblast differentiation molecular markers Cbfal, OP, and OC during bone formation. Results Two weeks after operation, bone healing percentages measured by micro-CT scanning were （20.1 ± 6.0） %. Four weeks after operation, further healing occurred, with bone healing percentages reaching （30.1 ± 5.0） %. The mRNA expression levels of Cbfal and OP were most up-regulated in 2 weeks after injury, while that of OC was most increased in 4 weeks after injury. Wnt3a, β-catenin, cyclin D1 and Tcfl expression levels were up-regulated after calvarial damage. Conclusion The calvarial defect mouse model is improved. Micro- CT scanning and histopathological staining are good tools to quantitatively evaluate calvarial bone formation ability. Wnt signaling pathway participates in the bone formation process after calvarial damage.