血管内皮生长因子基因转染促进股骨头坏死修复

目的　探索治疗股骨头及其它骨缺血性坏死新方法。方法　将血管内皮生长因子真核表达质粒pCD hVEGF1652 0 0 μg与胶原混合植入坏死的兔股骨头内 ,术后 2、4周用免疫组化SABC方法检测血管内皮生长因子 (VEGF)表达情况 ,组织形态学分析术后 2、4周修复区血管生成情况及术后 6、8周股骨头新骨形成情况。结果　术后 2周免疫组化证实基因转染组股骨头内有VEGF表达 ,组织形态学检测发现术后 2、4周转染基因的股骨头内血管生长快于对照组 ,术后 4、8周转染基因股骨头新骨形成多于对照组 ,差异均有显著性(P <0 0 1)。结论　利用VEGF基因转染刺激坏死骨组织内血管再生 ,可促进坏死骨修复 ,为临床治疗骨缺血性坏死提供了新的研究方向     

富血小板血浆复合物对腱-骨愈合界面力学性能影响的组织学研究

目的通过对健康成年新西兰大白兔行生物力学拉伸试验后标本的腱骨界面、移植物及其断裂层面进行组织学及组织化学观察,评价富血小板血浆(platelet rich plasma,PRP)复合异体脱蛋白骨(deproteined bone,DPB)对前交叉韧带(anterior cruciate ligament,ACL)重建后腱骨愈合的影响。方法 36只成年新西兰大白兔,随机分为3组,每组12只:富血小板血浆复合异体脱蛋白骨组(PRP+DPB组),异体脱蛋白骨组(DPB组),空白对照组。建立双侧自体单股半腱肌肌腱重建ACL模型,前2组骨隧道内分别植入PRP凝胶与DPB复合物、DPB,空白对照组行单纯ACL重建。术后4、8、12、24周取材行生物力学测试(单一轴向的拉伸试验)后,采用HE、Alcian blue、Masson染色及VEGF免疫组织化学观察各组腱骨愈合、移植物及其断裂层面组织学特点,分析各自的力学薄弱点。结果行拉伸试验后,术后4、8周各组标本肌腱移植物均从股骨隧道内断裂拉出,但PRP+DPB组术后8周时标本肌腱断裂处靠近股骨隧道内口,DPB组及空白对照组断裂部位位于隧道中段。术后12周时PRP+DPB组6个标本中有5个肌腱断裂部位在关节腔内部分,另2组仍从隧道内断裂拉出。术后24周时各组标本均在关节腔内部分断裂。组织学观察:术后4周时PRP+DPB组HE染色见断裂层面在腱骨结合部,可见少许疏松的纤维组织,Alcian blue染色未见细胞异染,Masson染色见肌腱断端纤维排列紊乱,VEGF免疫组化染色见较多阳性细胞表达;DPB组及空白对照组断裂层面在腱骨界面,断端见瘢痕组织。术后8周时PRP+DPB组HE染色见断裂层面在隧道内口处腱骨结合部,可见较致密的纤维结缔组织,Alcian blue染色未见细胞异染,Masson染色见肌腱断端纤维排列较前规则,VEGF免疫组化染色仍有较多阳性细胞表达,但较之前少;DPB组及空白对照组在靠近隧道中段处腱骨界面断裂,断端见疏松纤维组织。术后12周时PRP+DPB组肌腱断端见胶原纤维排列较前有序,梭形细胞散在分布,Alcian blue染色见断端有少量细胞异染,VEGF免疫组化阳性细胞数量少;DPB组及空白对照组在靠近隧道内口处腱骨界面断裂,断端见较致密的纤维组织,肌腱断端纤维排列紊乱,Alcian blue染色未见异染。术后24周时各组断端纤维排列整齐,PRP+DPB组可见椭圆形细胞,Alcian blue染色呈异染,较另2组明显,VEGF免疫组化3组均难以检出。术后4、8、12周,PRP+DPB组VEGF表达与DPB组、空白对照组有显著性差异(P<0.05),即表达增强;DPB组与空白对照组各时间点VEGF表达差异无统计学意义(P>0.05);术后24周3组标本的VEGF表达差异无统计学意义(P>0.05)。结论 ACL重建术后早期(8周以内)的薄弱点在腱骨界面,晚期在于移植肌腱。PRP可以提高腱骨间骨向肌腱内长入,从而增加腱骨愈合后的抗拉伸力。     

骨髓基质干细胞移植治疗兔股骨头缺血性坏死的实验研究

[目的]探讨骨髓基质干细胞移植对股骨头缺血性坏死的治疗作用和修复机理，为临床应用提供依据。[方法]24只新西兰大白兔随机分为两组，A组为髓芯减压组，B组为干细胞移植组。采用液氮冷冻法造模。A组钻孔后植入空白明胶海绵，B组钻孔后植入复合有骨髓基质干细胞的明胶海绵。术后每组分别于2、4、6、8周各处死3只动物，做X线及组织学检查。[结果]（1）X线结果：2周时A、B组钻孔区均呈低密度，4周时A组钻孔边缘密度增加，B组整个钻孔区密度增加，8周时A组钻孔区均呈低密度，边缘形成硬化线，B组钻孔区形成骨小梁结构。（2）组织学结果：2周时A组钻孔区出现少许炎症细胞，边缘出现较多成骨细胞并有骨组织形成，至8周时，钻孔区内形成骨髓组织，只在边缘形成骨小梁结构。2周时B组钻孔区有大量的成骨细胞，边缘有较多骨组织形成，4周时钻孔区内充满新生骨小梁结构，8周时钻孔区内骨小梁成熟，小梁有骨髓组织填充。[结论]骨髓基质干细胞对兔股骨头缺血性坏死有良好的修复作用。     

bFGF基因转染促进股骨头坏死修复的实验研究

目的 :为临床治疗股骨头及其它骨缺血性坏死探索新方法。方法 :将碱性成纤维细胞生长因子 (bFGF)真核表达质粒pCD rbFGF与胶原混合植入坏死的兔股骨头内 ,术后RT PCR及免疫组化方法检测bFGF表达情况 ,组织切片及组织形态学分析股骨头内血管生长及新骨形成情况。结果 :术后 2周RT PCR及免疫组化证实转染bFGF基因的股骨头内有bFGF表达。术后 2周股骨头内血管生长与对照组相比 ,术后 8周股骨头内新骨形成与对照组相比 ,差异均有非常显著意义 (P <0 .0 1)。结论 :利用bFGF基因转染可刺激股骨头坏死内血管再生和新骨形成 ,为临床治疗骨缺血性坏死提供了新的研究方向     

脱蛋白骨复合牛骨形态发生蛋白（BMP）对前交叉韧带重建术后骨隧道扩大的影响

目的探讨兔异体脱蛋白松质骨（deproteined bone,DPB）复合骨形态发生蛋白（bone morphogenetic protein,BMP）对前交叉韧带重建术后骨隧道扩大的影响。方法取96只成年新西兰大白兔用自体半腱肌腱进行膝关节前交叉韧带重建,共分4组,DPB＋BMP组在股骨隧道内植入DPB-BMP复合体,DPB组和BMP组分别在股骨隧道内植入DPB、BMP,空白对照组的股骨隧道内不植入任何材料。于术后4、8、12、16周时分别处死各组中的6只动物,切取标本,测量股骨隧道的宽度,计算隧道扩大率。结果术后4周时,DPB＋BMP组、DPB组、BMP组及空白对照组的骨隧道扩大率分别为（23.52±0.43）%、（34.83±0.52）%、（51.57±0.76）%、（56.90±0.81）%,术后8周为（22.21±0.34）%、（35.35±0.46）%、（60.97±0.63）%、（67.18±0.70）%,术后12周为（21.94±0.37）%、（33.01±0.41）%、（50.56±0.54）%、（54.61±0.55）%,术后16周为（20.96±0.35）%、（32.11±0.50）%、（49.29±0.66）%、（53.31±0.59）%,各时点骨隧道扩大率DPB＋BMP组〈DPB组〈BMP组〈空白对照组，差异均有显著性（P〈0．05）。结论脱蛋白骨复合BMP能减轻前交叉韧带重建术后的骨隧道扩大程度。     

富血小板血浆复合物促进兔前交叉韧带重建后腱骨愈合的组织学研究

目的探讨富血小板血浆(PRP)复合小牛脱蛋白松质骨(DPB)对兔前交叉韧带(ACL)重建术后腱骨愈合的影响。 方法取36只成年新西兰大白兔,随机分为3组：PRP+ DPB组,PRP组,空白对照组,每组12只。建立右侧膝关节ACL完全断裂模型,行白体半腱肌重建ACL。于PRP+ DPB组和PRP组骨隧道内分别植入PRP凝胶结合DPB和PRP凝胶,空白对照组骨隧道内单纯植入肌腱。术后6、12、18周行大体观察、组织学、免疫组化评价腱骨愈合情况。 结果大体观察术后各个时间点,与其他2组比较,PRP+ DPB组移植肌腱与骨隧道壁纤维组织连接更为致密。HE染色显示PRP+DPB组在各时间点腱骨界面的胶原纤维连接及纤维组织分级结果均优于其他2组。PRP+ DPB组、PRP组及空白对照组标本术后6周时TGF-β1表达量平均分别为119.5±9.3、93.0±7.3、73.3±5.4,12周时平均分别为76.8±5.7、48.0±6.7、26.8±4.7;术后6周时VEGF的表达量平均分别为117.5±8.4、90.5±8.2、69.8±5.8,12周时平均分别为76.6±5.7、48.0±6.7、26.8±4.7,以上指标3组之间两两比较差异均有统计学意义(P＜0.05),PRP+DPB组优于其他2组。术后18周时3组标本TGF-β1及VEGF的表达量差异均无统计学意义(P＞0.05)。 结论在兔膝关节ACL重建模型中,PRP复合DPB能促进术后的腱骨愈合。     

自体半腱肌复合骨形态发生蛋白和同种异体骨重建前交叉韧带后腱-骨愈合的生物力学研究

目的研究骨形态发生蛋白(BMP)复合同种异体骨(DPB)对自体半腱肌肌腱重建前交叉韧带后腱-骨愈合的影响。方法取64只成年新西兰大白兔,分成4组,建立左侧膝前交叉韧带(ACL)完全断裂模型。重建ACL时,于股骨隧道内分别植入BMP结合DPB、BMP、DPB。结果术后3、6、12及24周BMP结合DPB腱-骨愈合及移植物抗拉强度大于其他各治疗组,P<0.05。结论缓释载体DPB能延长BMP作用时间,提高移植物生物力学特性,拮抗骨吸收因子的负面效应,促进腱-骨愈合。     

hVEGF165及hBMP-7共表达重组腺相关病毒载体对兔激素性股骨头坏死的修复作用研究

目的探讨hVEGF165及hBMP-7双基因共表达重组腺相关病毒载体对兔激素性股骨头坏死的修复作用。方法应用细菌脂多糖联合甲基强地松龙制备兔激素性股骨头坏死模型。30只经MRI筛选造模成功动物随机分为模型组、髓芯减压组和病毒治疗组。病毒治疗组动物于髓芯减压术后将rAAV-hVEGF165-IRES-hBMP-7病毒载体注入减压区内。选取病毒注射后12周时间点分别行核素骨扫描,股骨头大体观察、HE染色、VEGF和BMP免疫组化染色检测。结果 MRI检测、大体观察以及HE染色发现早期股骨头坏死动物模型建立成功,且病毒治疗组较髓芯减压组及模型组相比股骨头坏死表现明显减轻,VEGF及BMP表达增强,髓腔组织代谢旺盛,组间差别有统计学意义（P〈0.05）。结论重组腺相关病毒载体rAAV-hVEGF165-IRES-hBMP-7通过增加髓腔组织的血运、增强股骨头区骨组织质量提高激素性股骨头坏死区骨修复能力。     

血管内皮细胞生长因子165及骨形态发生蛋白2促进兔骨缺损部位再血管化的研究

目的为大段骨缺损修复过程的血管再生探索一条可行的途径。方法成年大耳白兔30只,随机分为五组。右前肢为实验肢体,缺损长度约15 mm。第1～4组都采用胶原膜引导,结合纳米羟基磷灰石／聚酰胺骨水泥,不同的是在第1组中,复合血管内皮生长因子165(VEGF165)及骨形态发生蛋白2(BMP2)质粒;第2组复合VEGF165质粒;第3组复合BMP2质粒;第4组不复合任何质粒;第5组仅制作动物模型而不做任何处理,作为空白对照组。结果术后2周,核素断层摄影(ECT)结果显示第1组骨缺损修复后的局部血流量高于第2、3、4组(P<0．05);术后4周,X线片示第1组骨缺损处的骨痂明显增多;SEM显示在正常骨与工程骨交界处可见新生的骨小梁结构以及成骨细胞的附着;ECT结果照示第1组骨缺损的局部血流量高于第2、3、4组(P<0．01);第2组骨缺损的局部血流量高于第3、4组(P<0．01);术后8周,SEM显示第1组工程骨表面成骨细胞的附着多于其它各组, ECT结果显示与术后4周相同。结论在骨缺损的局部,联合应用表达VEGF165和BMP2质粒可以促进骨缺损局部的血液供应;附着质粒DNA的纳米羟基磷灰石／聚酰胺及引导性胶原膜在大段骨缺损局部的联合应用有助于新骨的形成。     

Osteoinductive activity of demineralized bone matrix and deprotenized bone derived from human avascular necrotic femoral head

Objective: To observe the osteoinductive activity of demineralized bone matrix (DBM) and deprotenized bone (DPB) made from human avascular necrotic femoral head. Methods: The femoral head was cut into pieces with the size of 3 mm×3mm×5 mm, which were made into DBM and DPB. These two kinds of biomaterials were cocultured with human bone mesenchymal stem cells (hBMSCs). Monolayer cells without biomaterials were cultured as control. Proliferative activity of hBMSCs was evaluated on days 1, 3, 5, 7 and 14. The concentration of alkaline phosphatase (ALP), osteocalcin (OC), and Ca2+ were detected on days 1, 7, 14 and 21. Results: Cells cultured in DBM showed higher proliferative activity than did in DPB and monolayer cells (F= 39.773, P<0.01). DBM and DPB also had osteoinductive activity. The concentrations of ALP (F=93.162, P<0.01), OC (F=236.852, P<0.01),Ca2+(F=80.711, P<0.01) of DBM group were significantly higher than that of DPB and control groups. Conclusions: In vitro, DBM and DPB made from avascular necrotic femoral head have osteoinductive activity when cocultured with hBMSCs, and the former is stronger than the latter.     

带蒂大转子骨瓣修复股骨头生物力学研究

目的探讨带血管蒂大转子骨瓣转移治疗股骨头缺血性坏死的生物力学特点。方法比格犬22只,8—12个月龄,雌、雄各11例,体重7—10kg;分为3组,A组2只（4髋）作为正常对照组,B组右侧股骨头坏死组（20髋）,C组左侧带血管蒂大转子骨瓣修复组（20髋）。分别于术后3、6、10、12、18、24周行CT扫描,24周后行生物力学测试和股骨头三维有限元分析。结果24周后影像学检查发现C组大转子骨瓣与周围骨组织有很好的相融性,C组再造的股骨头抗压强度与A组正常接近,而与坏死股骨头统计学有明显的差异（P〈0．05）,三维有限元分析修复的股骨头最大应变和应力接近正常,而与坏死有显著的差别。结论带血管蒂大转子骨瓣修复股骨头能恢复其生物力学     

Upregulation of VEGF in Subchondral Bone of Necrotic Femoral Heads in Rabbits with Use of Extracorporeal Shock Waves

Extracorporeal shock wave treatment appears to be effective in patients with avascular necrosis of the femoral head. However, the pathway of biological events whereby this is accomplished has not been fully elucidated. The purpose of this study was to investigate the effect of extracorporeal shock waves on vascular endothelial growth factor (VEGF) expression in necrotic femoral heads of rabbits. VEGF expression was assessed by immunohistochemistry, quantitative real-time PCR, and Western blot analysis. The degree of angiogenesis was also assessed, as determined by the microvessel density (MVD), the assessment of which was based on CD31-expressing vessels. Bilateral avascular necrosis of femoral heads was induced with methylprednisolone and lipopolysaccharide in 30 New Zealand rabbits. The left limb (the study side) received shock wave therapy to the femoral head. The right limb (the control side) received no shock wave therapy. Biopsies of the femoral heads were performed at 1, 2, 4, 8, and 12 weeks. Western blot analysis and real-time PCR showed that shock wave therapy significantly increased VEGF protein and mRNA expression, respectively, in the subchondral bone of the treated necrotic femoral heads. Compared with the contralateral control without shock wave treatment, the VEGF mRNA expression levels increased to a peak at 2 weeks after the shock wave treatment and remained high for 8 weeks, then declined at 12 weeks, whereas the VEGF protein expression levels increased to a peak at 4 weeks after the shock wave treatment and remained high for 12 weeks. The immunostaining of VEGF was weak in the control group, and the immunoreactivity level in the shock-wave-treated group increased at 4 weeks and persisted for 12 weeks. The most intensive VEGF immunoreactivity was observed in the proliferative zone above the necrotic zone. At 4, 8, and 12 weeks after the shock wave treatment, MVD in subchondral bone from treated femoral heads was significantly higher than that in subchondral bone from untreated femoral heads. These data clearly show that extracorporeal shock waves can significantly upregulate the expression of VEGF. The upregulation of VEGF may play a role in inducing the ingrowth of neovascularization and in improving the blood supply to the femoral head.     

Therapeutic effect of osteogenically induced adipose derived stem cells on vascular deprivation-induced osteonecrosis of the femoral head in rabbits

Objective: To explore the therapeutic effect of osteogenically induced adipose-derived stem cells (ADSCs) on vascular deprivation-induced osteonecrosis of the femoral head (ONFH) in rabbit model. Methods: Vascular deprivation-induced ONFH was established by intramuscular injection of methylprednisolone, and vascular occlusion of the capital femoral epiphysis by electrocoagulation in adult New Zealand white rabbits. Eight weeks after the establishment of vascular deprivation-induced ONFH, animals were randomly divided into three equal groups. In Group A (control), no therapy was given. In Group B, core decompression was performed by drilling a hole (1.2 mm in diameter) from the outer cortex 2.5 cm distal to the proximal end of the greater trochanter. In Group C, 1 ×107 osteogenically induced ADSCs were resuspended in 0.5 ml PBS, and then injected directly into the femoral head. Femoral head specimens were obtained at postoperative 8 weeks. The bone formation and three-dimensional microstructure of the femoral head was evaluated by micro-computed tomography scans (μ-CT). Immunohistochemical analysis was performed to detect the expression of osteocalcin. Angiogenesis and repair of the femoral head were observed histologically. Results: In trabecular bone at the proximal femur region, the trabecular volume was higher in Group C (130.70 mm3± 4.33 mm3) than that in Groups A (101.07 mm3±7.76 mm3) and B (107.89 mm3±8.68 mm3, P＜0.01). Bone volume was significantly increased in Group C (40.09 mm3±6.35 mm3) than in Groups A (29.65 mm3±4.61 mm3) and B (31.80 mm3± 4.01 mm3, P＜0.01). The trabecular number was higher in Groups C (1.58±0.25) than other two groups (1.15±0.18, 1.16± 0.21, P＜0.01). Bone mineral density showed statistically significant difference between Groups C and A or B (375.38± 23.06) mg HA/ccm, vs (313.73 ±19.30) mg HA/ccm and (316.09± 16.45) mg HA/ccm, P<0.01). Histological examination indicated that there was more new bone formation in Group C than in other groups. Conclusion: Treatment with autologous osteogenically induced ADSCs transplantation results in an enhanced osteogenesis and microstructure of the vascular deprivation-induced osteonecrosis in rabbits.     

Customized,degradable, functionally graded scaffold for potential treatment of early stage osteonecrosis of the femoral head

Osteonecrosis of the femoral head (ONFH) is a debilitating disease that results in progressive collapse of the femoral head and subsequent degenerative arthritis. Few treatments provide both sufficient mechanical support and biological cues for regeneration of bone and vascularity when the femoral head is still round and therefore salvageable. We designed and 3D printed a functionally graded scaffold (FGS) made of polycaprolactone (PCL) and β‐tricalcium phosphate (β‐TCP) with spatially controlled porosity, degradation, and mechanical strength properties to reconstruct necrotic bone tissue in the femoral head. The FGS was designed to have low porosity segments (15% in proximal and distal segments) and a high porosity segment (60% in middle segment) according to the desired mechanical and osteoconductive properties at each specific site after implantation into the femoral head. The FGS was inserted into a bone tunnel drilled in rabbit femoral neck and head, and at 8 weeks after implantation, the tissue formation as well as scaffold degradation was analyzed. Micro‐CT analysis demonstrated that the FGS‐filled group had a significantly higher bone ingrowth ratio compared to the empty‐tunnel group, and the difference was higher at the distal low porosity segments. The in vivo degradation rate of the scaffold was higher in the proximal and distal segments than in the middle segment. Histological analysis of both non‐decalcified and calcified samples clearly indicated new bone ingrowth and bone marrow‐containing bone formation across the FGS. A 3D printed PCL‐β‐TCP FGS appears to be a promising customized resorbable load‐bearing implant for treatment of early stage ONFH. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1002–1011, 2018.

     

Vascular endothelial growth factor gene-activated matrix (VEGF165-GAM) enhances osteogenesis and angiogenesis in large segmental bone defects.

Healing of fractures is dependent on vascularization of bone, which is in turn promoted by VEGF. It was shown that 0.1 and 1 mg of pVEGF165-GAM led to a significant increase in vascularization and bone regeneration in defects that would otherwise have led to atrophic nonunions. INTRODUCTION: One reason for lack of bone healing in nonunions is the absence of vascularization. In skeletogenesis, which is tightly linked to angiogenesis, vascular endothelial growth factor (VEGF) promotes the vascularization of the growth plate and transformation of cartilage to bone. We postulate that a gene-activated matrix (GAM), created with a plasmid coding for human VEGF165, coated on a collagen sponge could efficiently accelerate bone healing in large segmental defects. MATERIALS AND METHODS: Sixty New Zealand white rabbits received a 15-mm critical size defect on one radius, which was filled with either 0.1 or 1 mg plasmid-DNA as GAM. Radiographs were obtained every 3 weeks. After 6 or 12 weeks, animals were killed. New bone was measured by microCT scans. Vascularity was measured using anti-CD31 staining of endothelial cells in 18 regions of interest per implant. RESULTS: Scaffold and control plasmid showed no defect healing, whereas most of the animals in the VEGF groups showed partial or total bone regeneration. Significantly more bone was found in the VEGF groups, with no significant differences between the 0.1- and 1-mg groups. Immunohistochemical staining of endothelial cells revealed that the VEGF groups showed two to three times the number of vessels and a significantly larger endothelial area after 6 weeks. Twelve weeks after surgery, the amount of vascularization decreased, whereas more new bone was detectable. CONCLUSIONS: The rabbit critical size defect was appropriate in size to produce atrophic nonunions. We showed that angiogenesis and osteogenesis can be promoted by a VEGF165-GAM that is an appropriate tool to induce bone healing in atrophic nonunions.     

血管束植入组织工程骨修复兔股骨缺损对血管内皮生长因子表达的影响

目的 探讨血管束植入组织工程骨修复兔股骨缺损对局部血管内皮生长因了(VEGF)表达的影响.方法 将兔自体骨髓基质下细胞经诱导后与β-磷酸三钙材料复合,植入制备的兔股骨缺损处,其中实验组在材料侧槽中植入股骨的动静脉血管束,对照组则单纯植入组织工稗骨,分别于术后2、4、8、12周通过形态学检测新生骨量,免疫组织化学方法检测新生骨中VEGF的表达量.结果 随着时间进展,各组成骨量逐渐增加,差异有统计学意义(P<0.05),并且从第4周开始实验组成骨量高于对照组,差异有统计学意义(P<0.05);符时问点实验组新生骨中VEGF的表达最均高于对照组,差异有统汁学意义(P<0.05),且4周时达到最人值.结论 血管束植入组织工程骨可明显增加新生骨中VEGF的表达并能促进骨缺损的修复.     

血管束植入组织工程骨修复兔股骨缺损对血管内皮生长因子表达的影响

目的 探讨血管束植入组织工程骨修复兔股骨缺损对局部血管内皮生长因了(VEGF)表达的影响.方法 将兔自体骨髓基质下细胞经诱导后与β-磷酸三钙材料复合,植入制备的兔股骨缺损处,其中实验组在材料侧槽中植入股骨的动静脉血管束,对照组则单纯植入组织工稗骨,分别于术后2、4、8、12周通过形态学检测新生骨量,免疫组织化学方法检测新生骨中VEGF的表达量.结果 随着时间进展,各组成骨量逐渐增加,差异有统计学意义(P<0.05),并且从第4周开始实验组成骨量高于对照组,差异有统计学意义(P<0.05);符时问点实验组新生骨中VEGF的表达最均高于对照组,差异有统汁学意义(P<0.05),且4周时达到最人值.结论 血管束植入组织工程骨可明显增加新生骨中VEGF的表达并能促进骨缺损的修复.     

血管束植入组织工程骨修复兔股骨缺损对血管内皮生长因子表达的影响

目的 探讨血管束植入组织工程骨修复兔股骨缺损对局部血管内皮生长因了(VEGF)表达的影响.方法 将兔自体骨髓基质下细胞经诱导后与β-磷酸三钙材料复合,植入制备的兔股骨缺损处,其中实验组在材料侧槽中植入股骨的动静脉血管束,对照组则单纯植入组织工稗骨,分别于术后2、4、8、12周通过形态学检测新生骨量,免疫组织化学方法检测新生骨中VEGF的表达量.结果 随着时间进展,各组成骨量逐渐增加,差异有统计学意义(P<0.05),并且从第4周开始实验组成骨量高于对照组,差异有统计学意义(P<0.05);符时问点实验组新生骨中VEGF的表达最均高于对照组,差异有统汁学意义(P<0.05),且4周时达到最人值.结论 血管束植入组织工程骨可明显增加新生骨中VEGF的表达并能促进骨缺损的修复.     

血管束植入组织工程骨修复兔股骨缺损对血管内皮生长因子表达的影响

目的 探讨血管束植入组织工程骨修复兔股骨缺损对局部血管内皮生长因了(VEGF)表达的影响.方法 将兔自体骨髓基质下细胞经诱导后与β-磷酸三钙材料复合,植入制备的兔股骨缺损处,其中实验组在材料侧槽中植入股骨的动静脉血管束,对照组则单纯植入组织工稗骨,分别于术后2、4、8、12周通过形态学检测新生骨量,免疫组织化学方法检测新生骨中VEGF的表达量.结果 随着时间进展,各组成骨量逐渐增加,差异有统计学意义(P<0.05),并且从第4周开始实验组成骨量高于对照组,差异有统计学意义(P<0.05);符时问点实验组新生骨中VEGF的表达最均高于对照组,差异有统汁学意义(P<0.05),且4周时达到最人值.结论 血管束植入组织工程骨可明显增加新生骨中VEGF的表达并能促进骨缺损的修复.     

血管束植入组织工程骨修复兔股骨缺损对血管内皮生长因子表达的影响

目的 探讨血管束植入组织工程骨修复兔股骨缺损对局部血管内皮生长因了(VEGF)表达的影响.方法 将兔自体骨髓基质下细胞经诱导后与β-磷酸三钙材料复合,植入制备的兔股骨缺损处,其中实验组在材料侧槽中植入股骨的动静脉血管束,对照组则单纯植入组织工稗骨,分别于术后2、4、8、12周通过形态学检测新生骨量,免疫组织化学方法检测新生骨中VEGF的表达量.结果 随着时间进展,各组成骨量逐渐增加,差异有统计学意义(P<0.05),并且从第4周开始实验组成骨量高于对照组,差异有统计学意义(P<0.05);符时问点实验组新生骨中VEGF的表达最均高于对照组,差异有统汁学意义(P<0.05),且4周时达到最人值.结论 血管束植入组织工程骨可明显增加新生骨中VEGF的表达并能促进骨缺损的修复.