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首页> 外文期刊>Journal of orthopaedic research >Axial shortening during distraction osteogenesis leads to enhanced bone formation in a rabbit model through the HIF-1alpha/vascular endothelial growth factor system.
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Axial shortening during distraction osteogenesis leads to enhanced bone formation in a rabbit model through the HIF-1alpha/vascular endothelial growth factor system.

机译：分心成骨过程中的轴向缩短导致兔模型通过HIF-1alpha /血管内皮生长因子系统增强骨形成。

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摘要

Axial micromotion of bone fragments enhances callus formation during fracture repair or limb lengthening. To examine this, we used an axial-shortening model of the tibial callus in rabbits and performed histological analyses. After 10-mm lengthening of the left tibia with an external fixator, we shortened the callus by 2 mm. Radiographs and quantitative evaluation of corrected bone mineral density showed a significant increase in mineralization in the shortened callus (57.3 vs. 36.2%, p = 0.001). Histologically, greater osteoblast proliferation and more vigorous trabecular bone formation were noted in the shortened calluses than in the controls. Around the front of membranous bone formation in the shortened callus, there was a significant decrease in mean percentage area of vascular lumens (1.8 vs. 4.5%, p = 0.009), which seemed attributable to compressive force, and a significantly increased production of vascular endothelial growth factor (VEGF; 422.5 vs. 142.7 pg/mg protein, p = 0.007) and its receptors. There were also increased numbers of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts and proliferating cell nuclear antigen (PCNA)-positive cells. A marked increase of hypoxia inducible factor-1alpha (HIF-1alpha) expression in osteoblasts was also observed in this area. Thus, enhancement of membranous bone formation by static compression or axial dynamization may be at least partly attributable to HIF-1alpha-mediated VEGF induction following the local hypoxia caused by collapse of vascular lumens.
机译：骨碎片的轴向微动会增强骨折修复或肢体延长期间的骨call形成。为了检查这一点，我们使用了兔胫骨骨call的轴向缩短模型并进行了组织学分析。用外部固定器将左胫骨延长10毫米后，我们将骨us缩短了2毫米。射线照片和校正骨矿物质密度的定量评估显示，缩短的愈伤组织中矿化作用显着增加（57.3比36.2％，p = 0.001）。组织学上，与对照相比，缩短的愈伤组织中观察到更大的成骨细胞增殖和更强健的小梁骨形成。在缩短的愈伤组织中，膜状骨形成的前部周围，血管腔的平均面积百分比显着下降（1.8对4.5％，p = 0.009），这似乎是由于压缩力所致，并且血管生成显着增加内皮生长因子（VEGF; 422.5 vs. 142.7 pg / mg蛋白，p = 0.007）及其受体。抗酒石酸酸性磷酸酶（TRAP）阳性的破骨细胞和增殖细胞核抗原（PCNA）阳性的细胞数量也增加。在该区域还观察到成骨细胞中缺氧诱导因子-1α（HIF-1alpha）表达的明显增加。因此，通过静态压缩或轴向动力化来增强膜性骨形成可能至少部分归因于由血管腔塌陷引起的局部缺氧后的HIF-1α介导的VEGF诱导。

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