小鼠慢性根尖周炎中RANKL的表达  

Expression of RANKL in chronic periapical periodontitis in mice

作　　者：仉红 叶丹丹[1] 董明[1] 牛卫东[1] Zhang Hong;Ye Dandan;Dong Ming;Niu Weidong(Department of Endodontics,School of Stomatology,Dalian Medical University,Dalian 116041,Liaoning Province,China)

机构地区：[1]大连医科大学口腔医学院牙体牙髓教研室,辽宁省大连市116041

出　　处：《中国组织工程研究》2019年第3期391-395,共5页Chinese Journal of Tissue Engineering Research

基　　金：国家自然科学基金(81171538);项目负责人:仉红~~

摘　　要：背景:慢性根尖周炎根尖区发生不同程度的骨吸收及炎性肉芽组织,研究表明RANK-RANKL-骨保护素信号通路被认为是调节骨吸收的关键通路。目的:检测RANKL在小鼠根尖周炎中的表达及作用。方法:C57BL/6J小鼠分为正常对照组和实验组,实验组将双侧下颌第一磨牙直接开髓,暴露于口腔环境中,建立小鼠根尖周炎模型,分别在建模后1,2,3,4周收集下颌骨组织,苏木精-伊红染色观察根尖周组织的变化,免疫组织化学染色检测各时间点RANKL的表达情况。结果与结论:①苏木精-伊红染色显示,成功建立了小鼠慢性根尖周炎动物模型。正常对照组小鼠下颌第1磨牙根尖区仅有少数炎性细胞,牙周组织完整;术后1-4周,实验组根尖周组织炎性细胞不断增多,浸润范围逐渐变大,牙槽骨破坏逐渐增多;②免疫组织化学染色显示,实验组各时间点RANKL的表达量较正常对照组明显升高(P <0.05),术后1,2周RANKL的表达量明显增加(P <0.05),术后3周表达量持续增加,4周时表达量降低(P<0.05);③结果表明,实验成功建立小鼠慢性根尖周炎模型,RANKL在小鼠慢性根尖周炎中的表达量较高且具有明显趋势,可能对小鼠慢性根尖周炎的进展及骨破坏起促进作用。BACKGROUND:Different degrees of bone resorption and granulation tissues appear in the apical region of chronic periapical periodontitis.RANK-RANKL-osteoprotegerin signaling pathway has been shown to be the key pathway for regulating bone resorption.OBJECTIVE:To detect the expression and role of RANKL in mouse apical periodontitis.METHODS:C57BL/6J mice were allocated into experimental and control groups.In the experimental group,were used to open the mandibular first molars exposed to the oral environment were open to create the model of periapical periodontitis.The mandibular tissue was collected at 1,2,3 and 4 weeks after modeling,and the periapical tissue changes were observed by hematoxylin-eosin staining.The expression level of RANKL at each time point was detected by immunohistochemical staining.RESULTS AND CONCLUSION:Hematoxylin-eosin staining results showed that the mouse model of chronic periapical periodontitis was successfully established.In the control group,only a few inflammatory cells were found in the apical area of mandibular first molars,and the periodontal tissue was intact.The extent of inflammatory infiltration was gradually increased from 1 week to 4 weeks after modeling,and the alveolar bone destruction gradually increased.The results of immunohistochemistry showed that the expression level of RANKL in the experimental group was significantly higher than that in the control group,the level increased significantly from 1 week to 2 weeks after modeling,continued to increase at 3 weeks,and reduced at 4 weeks(all P<0.05).To conclude,the model of chronic periapical periodontitis is successfully established in mice.The expression level of RANKL in mouse chronic apical periodontitis is high and shows a clear trend,which may promote the progress of chronic apical periodontitis and bone destruction.

关 键 词：慢性根尖周炎 RANKL 骨破坏 破骨细胞 免疫组织化学染色 组织构建 牙 根尖周炎 RANK配体 破骨细胞 组织工程 

分 类 号：R446[医药卫生—诊断学]