中华创伤骨科杂志
中華創傷骨科雜誌
중화창상골과잡지
CHINESE JOURNAL OF ORTHOPAEDIC TRAUMA
2008年
5期
440-445
,共6页
黄正%冯伟%傅文彧%肖德常%周琦%王晋申
黃正%馮偉%傅文彧%肖德常%週琦%王晉申
황정%풍위%부문욱%초덕상%주기%왕진신
骨折%不愈合%血管生成%血管内皮生长因子
骨摺%不愈閤%血管生成%血管內皮生長因子
골절%불유합%혈관생성%혈관내피생장인자
Fracture,nonunion%Angiogenesis%Vascular endothelial growth factor (VEGF)
目的 研究扩髓治疗骨折不愈合过程中血管生成和血管内皮细胞生长因子(VEGF)表达的时间和空间特点以及相互联系.探讨扩髓并更换粗直径髓内钉治疗骨折不愈合的生物学机理,为临床运用扩髓治疗长骨骨折延迟愈合及不愈合提供理论依据. 方法 3个月龄雄性SD大鼠200只.对大鼠一侧股骨干骨折用不稳定固定方法制备肥大性骨折不愈合模型,随机选取40只作为模型鉴定,剩下160只随机分为试验组扩髓治疗和对照组不扩髓治疗,每组80只进行随机配对研究.术后第1、3、5、7、14、21、28、42天取材.用血管性血友病因子(VWF)标记血管,免疫组化方法检测骨折处VWF和VEGF的表达,来研究骨折处血管生成的时空特点以及与VEGF表达的关系. 结果 实验组的骨折愈合率显著高于对照组.时空分布上,在早期(1~7 d),实验组血管生成主要在骨外膜和软骨痂中.对照组主要在骨内膜;中期(7~14 d)实验组血管随着肉芽组织长入骨折间隙,对照组近骨内膜处血管增加,但是骨折间隙没有血管;后期(14~42 d)实验组骨内膜处出现血管,骨折间隙血管大量增加,对照组血管仍然局限在肉芽组织和骨内膜处,骨折间隙没有血管.实验组血管总数始终高于对照组.VEGF出现的时间和空间顺序与血管生成顺序一致,实验组VEGF表达普遍高于对照组. 结论 在骨折不愈合的治疗中,扩髓可使骨外膜和骨痂血供代偿性增加以及刺激VEGF表达增加,血管总数要高于不扩髓组.VEGF表达时间和分布与血管的生成关系密切,提示治疗骨折不愈合中,VEGF可能起着至关重要的作用,决定着血管形成的时间、部位与数量.
目的 研究擴髓治療骨摺不愈閤過程中血管生成和血管內皮細胞生長因子(VEGF)錶達的時間和空間特點以及相互聯繫.探討擴髓併更換粗直徑髓內釘治療骨摺不愈閤的生物學機理,為臨床運用擴髓治療長骨骨摺延遲愈閤及不愈閤提供理論依據. 方法 3箇月齡雄性SD大鼠200隻.對大鼠一側股骨榦骨摺用不穩定固定方法製備肥大性骨摺不愈閤模型,隨機選取40隻作為模型鑒定,剩下160隻隨機分為試驗組擴髓治療和對照組不擴髓治療,每組80隻進行隨機配對研究.術後第1、3、5、7、14、21、28、42天取材.用血管性血友病因子(VWF)標記血管,免疫組化方法檢測骨摺處VWF和VEGF的錶達,來研究骨摺處血管生成的時空特點以及與VEGF錶達的關繫. 結果 實驗組的骨摺愈閤率顯著高于對照組.時空分佈上,在早期(1~7 d),實驗組血管生成主要在骨外膜和軟骨痂中.對照組主要在骨內膜;中期(7~14 d)實驗組血管隨著肉芽組織長入骨摺間隙,對照組近骨內膜處血管增加,但是骨摺間隙沒有血管;後期(14~42 d)實驗組骨內膜處齣現血管,骨摺間隙血管大量增加,對照組血管仍然跼限在肉芽組織和骨內膜處,骨摺間隙沒有血管.實驗組血管總數始終高于對照組.VEGF齣現的時間和空間順序與血管生成順序一緻,實驗組VEGF錶達普遍高于對照組. 結論 在骨摺不愈閤的治療中,擴髓可使骨外膜和骨痂血供代償性增加以及刺激VEGF錶達增加,血管總數要高于不擴髓組.VEGF錶達時間和分佈與血管的生成關繫密切,提示治療骨摺不愈閤中,VEGF可能起著至關重要的作用,決定著血管形成的時間、部位與數量.
목적 연구확수치료골절불유합과정중혈관생성화혈관내피세포생장인자(VEGF)표체적시간화공간특점이급상호련계.탐토확수병경환조직경수내정치료골절불유합적생물학궤리,위림상운용확수치료장골골절연지유합급불유합제공이론의거. 방법 3개월령웅성SD대서200지.대대서일측고골간골절용불은정고정방법제비비대성골절불유합모형,수궤선취40지작위모형감정,잉하160지수궤분위시험조확수치료화대조조불확수치료,매조80지진행수궤배대연구.술후제1、3、5、7、14、21、28、42천취재.용혈관성혈우병인자(VWF)표기혈관,면역조화방법검측골절처VWF화VEGF적표체,래연구골절처혈관생성적시공특점이급여VEGF표체적관계. 결과 실험조적골절유합솔현저고우대조조.시공분포상,재조기(1~7 d),실험조혈관생성주요재골외막화연골가중.대조조주요재골내막;중기(7~14 d)실험조혈관수착육아조직장입골절간극,대조조근골내막처혈관증가,단시골절간극몰유혈관;후기(14~42 d)실험조골내막처출현혈관,골절간극혈관대량증가,대조조혈관잉연국한재육아조직화골내막처,골절간극몰유혈관.실험조혈관총수시종고우대조조.VEGF출현적시간화공간순서여혈관생성순서일치,실험조VEGF표체보편고우대조조. 결론 재골절불유합적치료중,확수가사골외막화골가혈공대상성증가이급자격VEGF표체증가,혈관총수요고우불확수조.VEGF표체시간화분포여혈관적생성관계밀절,제시치료골절불유합중,VEGF가능기착지관중요적작용,결정착혈관형성적시간、부위여수량.
Objective To investigate the space-time characteristics of angiogenesis and of the vascular endothelial growth factor (VEGF) expression in the treatment of fracture nonunion by reamed and unreamed intramedullary nailings. Methods Models of fracture nonunion were set up using 200 3-month-old male SD rats which were randomized into 2 groups. In the experiment group (80 rats) reamed intramedullary nailing was applied and in the control group (80 rats) unreamed intramedullary nailing was used. Samples were obtained at the site of fracture at 1st, 3rd, 5th, 7th, 14th, 21st, 28th and 42nd days after operation. The remaining 40 rats were used for appraisal of the models of fracture nonunion. We counted vessels through Von Willebrand Factor (VWF) expression. VWF and VEGF were detected with immunohistochemistry. Results In the treatment of fracture nonunion, the curative rate was higher for the experiment group than for the control group. In the experiment group: from 1st to 7th day, vessels were detected in periosteum and bony callus; from 7th to 14th day, vessels grew into bone fracture gap along with granulation tissue; from 14th to 42nd day, vessels were detected in endosteum. In the control group: from 1st to 7th day,vessels were detected in endosteum; from 7th to 14th day, vessels appeared in granulation tissue but did not grow into bone fracture gap; from 14th to 42nd day, vessels still remained in endosteum and granulation tissue. Vessel counts and VEGF expression in the experiment group were higher than in the control group.Conclusions Since VEGF seems to determine the space-time characteristics of angiogenesis and the amount of vessels, it plays an important role in treatment of nonunion. It maybe an important mechanism by which reamed intramedullary nailing can facilitate healing of fracture nonunion.