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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Diminished bone formation during diabetic fracture healing is related to the premature resorption of cartilage associated with increased osteoclast activity.
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Diminished bone formation during diabetic fracture healing is related to the premature resorption of cartilage associated with increased osteoclast activity.

机译：糖尿病性骨折愈合过程中骨形成的减少与破骨细胞活性增加相关的软骨的过早吸收有关。

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Histological and molecular analysis of fracture healing in normal and diabetic animals showed significantly enhanced removal of cartilage in diabetic animals. Increased cartilage turnover was associated with elevated osteoclast numbers, a higher expression of genes that promote osteoclastogenesis, and diminished primary bone formation. INTRODUCTION: Diminished bone formation, an increased incidence of nonunions, and delayed fracture healing have been observed in animal models and in patients with diabetes. Fracture healing is characterized by the formation of a stabilizing callus in which cartilage is formed and then resorbed and replaced by bone. To gain insight into how diabetes affects fracture healing, studies were carried out focusing on the impact of diabetes on the transition from cartilage to bone. MATERIALS AND METHODS: A low-dose treatment protocol of streptozotocin in CD-1 mice was used to induce a type 1 diabetic condition. After mice were hyperglycemic for 3 weeks, controlled closed simpletransverse fractures of the tibia were induced and fixed by intramedullary pins. Histomorphometric analysis of the tibias obtained 12, 16, and 22 days after fracture was performed across the fracture callus at 0.5 mm proximal and distal increments using computer-assisted image analysis. Another group of 16-day samples were examined by microCT. RNA was isolated from a separate set of animals, and the expression of genes that reflect the formation and removal of cartilage and bone was measured by real-time PCR. RESULTS: Molecular analysis of collagen types II and X mRNA expression showed that cartilage formation was the same during the initial period of callus formation. Histomorphometric analysis of day 12 fracture calluses showed that callus size and cartilage area were also similar in normoglycemic and diabetic mice. In contrast, on day 16, callus size, cartilage tissue, and new bone area were 2.0-, 4.4-, and 1.5-fold larger, respectively, in the normoglycemic compared with the diabetic group (p < 0.05). Analysis of microCT images indicated that the bone volume in the normoglycemic animals was 38% larger than in diabetic animals. There were 78% more osteoclasts in the diabetic group compared with the normoglycemic group (p < 0.05) on day 16, consistent with the reduction in cartilage. Real-time PCR showed significantly elevated levels of mRNA expression for TNF-alpha, macrophage-colony stimulating factor, RANKL, and vascular endothelial growth factor-A in the diabetic group. Similarly, the mRNA encoding ADAMTS 4 and 5, major aggrecanases that degrade cartilage, was also elevated in diabetic animals. CONCLUSIONS: These results suggest that impaired fracture healing in diabetes is characterized by increased rates of cartilage resorption. This premature loss of cartilage leads to a reduction in callus size and contributes to decreased bone formation and mechanical strength frequently reported in diabetic fracture healing.
机译：正常动物和糖尿病动物骨折愈合的组织学和分子分析表明，糖尿病动物软骨的去除明显增强。软骨周转的增加与破骨细胞数量的增加，促进破骨细胞形成的基因的表达增加以及初级骨形成减少有关。简介：在动物模型和糖尿病患者中，观察到骨形成减少，骨不连增加和骨折愈合延迟。骨折愈合的特征是形成稳定的愈伤组织，在该愈伤组织中形成软骨，然后再被骨头吸收和替代。为了深入了解糖尿病如何影响骨折愈合，进行了一些研究，重点是糖尿病对软骨到骨骼过渡的影响。材料与方法：用低剂量的CD-1小鼠链脲佐菌素治疗方案诱发1型糖尿病。小鼠高血糖3周后，通过髓内钉诱导并固定胫骨的闭合性闭合性横断骨折。使用计算机辅助图像分析方法，以0.5 mm的近端和远端增量跨骨折骨us对骨折后12、16和22天获得的胫骨进行组织形态计量学分析。另一组16天的样品通过microCT检查。从另一套动物中分离出RNA，并通过实时PCR测量反映软骨和骨骼形成和去除的基因表达。结果：对II型和X型胶原蛋白表达的分子分析表明，在愈伤组织形成的初期，软骨形成是相同的。对第12天骨折call的组织形态计量学分析显示，在正常血糖和糖尿病小鼠中，愈伤组织的大小和软骨面积也相似。相反，在第16天，正常血糖患者的愈伤组织大小，软骨组织和新骨面积分别比糖尿病组大2.0倍，4.4倍和1.5倍（p <0.05）。 microCT图像分析表明，正常血糖动物的骨体积比糖尿病动物大38％。第16天，与正常血糖组相比，糖尿病组的破骨细胞增加了78％（p <0.05），与软骨减少一致。实时PCR显示糖尿病组中TNF-α，巨噬细胞集落刺激因子，RANKL和血管内皮生长因子-A的mRNA表达水平显着升高。同样，在糖尿病动物中，编码ADAMTS 4和5的主要软骨聚集蛋白聚糖酶的mRNA降解，软骨的降解也升高。结论：这些结果表明糖尿病的骨折愈合受损的特征在于软骨吸收率增加。软骨的这种过早丧失导致愈伤组织的大小减小，并且导致糖尿病性骨折愈合中经常报道的骨形成和机械强度降低。

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