Objective:To observe the clinical effect of minimally invasive treatment on lumbar disc herniation aided by Mast-Quadrant system so as to provide theoretical basis for clinical use.Methods:Retrospective analysis was taken in 50 patients including 35 males and 15 females with lumbar disc herniation which received the treatment of minimally invasive surgery aided by Mast-Quadrant system in our hospital from January 2010 to December 2014.Patients aged 19 to 59 and the average age of them was 31.1 years.All cases were L4-L5 and L5-S1 segment lumbar disc herniation including 42 cases with single-level lumbar disc herniation and 8 cases with double-level.The surgical efficacy was evaluated after follow up visit and the evaluation criteria included length of incision,duration of operation,amount of bleeding,hospital stays,postoperative recovery time,Japanese Orthopaedic Association (JOA) score and Macnab criteria.Results:The average incision length was 2.5 cm (2-3 cm),with an average bleeding amount of 100 ml (50-150 ml).The average operative time was 51 minutes (30-90 min),with a mean hospital stay of 10 days (7-17 days).The average postoperative recovery time was 1.2 months (1-3 mon).All cases were then followed up for 3-12 months (average 8 months).JOA scores of operation,1 month after operation and last follow-up were 10.32±2.12,20.65±2.62 and 26.55±3.74,repectively.Macnab criteria used to determine clinical outcome revealed that excellent results in 43 patients and good results in 7 cases.Conclusion:Minimally invasive surgery aided by Mast-Quadrant system may be a kind of safe and effective treatment of lumbar disc herniation with fine surgical outcomes,small incisions,less bleeding and better exposure of operative field.

目的:构建趋化因子CXCL12的重组腺病毒表达载体,观察其对间充质干细胞(MSC)中成骨特异性转录因子Runx2表达的影响.方法:将目的基因CXCL12全长cDNA模板进行PCR扩增、酶切后与pHBAd-MCMV-GFP载体结合,获得pHBAd-MCMV-CXCL12-GFP重组载体;将重组载体和包装质粒共转染HEK293细胞进行包装、扩增;利用所携带的绿色荧光蛋白基因测定病毒滴度,观察基因转染效率,QPCR和Western印迹检测CXCL12重组腺病毒转染后MSC中CXCL12和Runx2的表达.结果:酶切、PCR及测序结果证实CXCL12重组腺病毒载体构建成功,转染MSC后CXCL12和Runx2的表达明显升高,AMD3100可以降低CXCL12基因转染后MSC中Runx2的表达.结论:趋化因子CXCL12和MSC表面的CXCR4结合对MSC中成骨特异性转录因子Runx2的表达具有促进作用.

目的:探讨经皮侧路椎间孔镜下椎间盘髓核摘除术(percutaneous transforaminal endoscopic discectomy,PTED)与后路椎板开窗髓核摘除术(fenestration decompression,FD)治疗腰椎间盘突出症(lumbar disc herniation,LDH)的临床疗效.方法:回顾性分析2014年1月至2015年6月,在我院治疗确诊为单节段腰椎间盘突出症的患者80例,其中经皮椎间孔镜治疗(PTED组)37例,椎间开窗髓核摘除术(FD组)43例,记录两组患者术中透视次数、切口长度、手术时间、术中出血量、术后卧床及住院时间,治疗前后视觉模拟评分(visual analogue scale,VAS)和Oswestry功能障碍指数(Oswestry disability index,ODI)进行随访,评估两种手术方式治疗效果.结果:PTED组在手术切口长度(7.91±0.69 mm VS 64.09± 9.90 mm)、术中出血量(9.77± 2.36 mL VS 64.16± 16.95 mL)、术后卧床时间(6.31± 2.31 hVS 81.55± 77.93 h)及住院时间(3.79± 1.14d VS 8.65± 2.27-d)的比较上优于FD组,差异性均有统计学意义;FD组较PTED组在手术时间更短(58.23±9.98 min VS 88.00±10.82 min)、术中透视次数更少(2.74± 0.90次VS 16.54±3.10次),差异性均有统计学意义.两组VAS、ODI评分术后与术前比较,均有明显地改善,差异性有统计学意义(t=1.06,P=0.00).末次随访Macnab标准疗效评分,PTED组优良率为83.78-％,FD组优良率为79.06-％,两组比较差异无统计学意义(xⅫ.874P=0.918).结论:PTED和FD两种手术方式均能有效治疗单节段腰椎间盘突出症;PTED手术方式具有手术切口小、术中出血量少、术后卧床及住院时间短、术后并发症少及恢复快等优点.FD具有X射线辐射小,手术时间更短,学习曲线短、更易掌握等优点.

目的:观察Runt相关转录因子2(Runx2)基因过表达对骨髓间充质干细胞(MSCs)体外迁移能力的影响.方法:分离培养兔MSCs,用已构建的携带Runx2基因的腺病毒载体Ad-Runx2、单纯腺病毒及AMD3100处理MSCs;应用Transwell小室检测MSCs体外迁移能力的变化,QPCR检测基质细胞衍生因子(SDF-1)和趋化因子受体(CXCR4)mRNA的表达,ELISA检测各组细胞培养液上清中SDF-1的含量,Western印迹检测CXCR4蛋白表达水平.结果:Ad-Runx2转染MSCs组细胞迁移数明显增多(P＜0.01),AMD3100处理MSCs后细胞迁移数明显降低(P＜0.01);QPCR、ELISA、Western印迹结果显示Ad-Runx2转染能促进MSCs中SDF-1及CXCR4的表达(P＜0.01).结论:Runx2基因过表达能促进MSCs的体外迁移,这与其激活SDF-1/CXCR4信号轴相关.

目的:应用Micro-CT评价Runx2基因修饰的骨髓间充质干细胞(MSC)静脉移植促进兔坏死股骨头修复效果.方法:24只大耳白兔经缺血性股骨头坏死造模4周后随机分为4组,A组静脉移植1×107个Runx2基因修饰的MSC,B组静脉移植1×107个Runx2 siRNA修饰的MSC,C组单纯植入1×107个MSC,D组静脉植入等量生理盐水,细胞移植后2、4、6、8周取出股骨头标本行Micro-CT检测,评价股骨头坏死修复情况.结果:2周后各组动物股骨头关节面模糊,骨密度降低,骨小梁数量及厚度均下降,骨小梁结构紊乱,但组间差异不明显;4、6周后,A、B、C组动物股骨头内骨密度和骨小梁结构未明显变化,但可见修复反应,而D组动物股骨头内骨小梁结构破坏进一步加剧;8周后,D组动物股骨头关节面塌陷,骨小梁严重缺失形成较大空洞,A、B、C组股骨头可见明显修复反应,关节面完整度、关节面下骨密度、骨小梁体积及数量、骨小梁连续性表现为A＞C＞B＞D组.结论:MSC静脉移植可有效治疗股骨头坏死,且过表达Runx2基因修饰后能有效提升MSC移植后的治疗效果.

Bone metabolism in the human body is a complicate process, which is a dynamic balance that consists of osteoclastic resorption of the old bone and osteoblastic formation of the new bone.Runx2 is the key regulator of bone formation by regulating the differentiation of osteoblasts and osteoclasts.It promotes bone formation and inhibits bone resorption by regulating the expression of specific extracellular matrix protein genes in osteoblasts and the cell cycle of osteoblasts.This paper reviews the effect of Runx2 in bone metabolism.