骨质疏松对膜内成骨和软骨内成骨两种骨修复方式的影响

发布时间：2019-04-08 16:42

【摘要】：骨质疏松症是以骨量减少、骨微结构破坏导致的骨脆性增加、骨折危险性增加为特征的全身性疾病[1]。骨折的发生是骨质疏松症最为危险的并发症,是骨质疏松在临床和公共卫生领域如此重要的唯一原因[1]。临床研究表明骨质疏松病人骨折愈合时间明显延长,有极高的致残率和致死率,带来极大的社会负担。因此研究骨质疏松如何影响骨修复过程,并依此研究相应的治疗方案有重要的社会意义。本实验通过观测骨质疏松小鼠骨损伤后的软骨内成骨和膜内成骨两种骨修复情况,研究骨质疏松影响骨修复的方式。方法1、采用去势手术和皮下注射糖皮质激素的方法构建小鼠骨质疏松模型,采用显微CT扫描确定骨质疏松模型构建成功。2、构建骨质疏松小鼠和正常小鼠膜内化骨骨修复模型,于术后第7、10、14、21天取材,第7、10天时间点小鼠处死前2小时腹腔注射Brdu。利用HE染色、免疫组织化学染色、TRAP染色观测膜内化骨骨修复过程的变化。3、构建骨质疏松小鼠和正常小鼠软骨内化骨骨修复模型,于术后第7、10、14、21天取材,并利用HE染色、免疫组织化学染色、甲苯胺蓝染色观测软骨内成骨骨修复过程的变化。结果显微CT数据表明,在皮下注射甲强龙3.5mg/kg持续8周,及双侧卵巢去势8周后骨质疏松模型成功建立。2、与对照组相比,骨质疏松模型小鼠膜内成骨骨修复过程明显延缓。3、与对照组相比,骨质疏松模型小鼠软骨内成骨骨修复过程明显延缓。结论骨质疏松后干细胞向成骨细胞增殖分化过程受损,从而影响骨修复的膜内成骨骨修复过程;影响软骨细胞成熟肥大分化过程,以及骨化中心出现的时间影响软骨内成骨骨修复过程。尽管糖皮质激素和雌激素缺乏引起糖皮质激素的机制不同,但是均以相似的方式延缓了骨折愈合中膜内成骨骨修复过程和软骨内成骨骨修复过程。
[Abstract]:Osteoporosis is a systemic disease characterized by a decrease in bone mass, an increase in bone fragility caused by bone microstructure destruction and an increase in the risk of fracture [1]. Fracture is the most dangerous complication of osteoporosis and the only reason that osteoporosis is so important in clinic and public health [1]. Clinical studies have shown that the fracture healing time of osteoporosis patients is significantly prolonged, with a very high rate of disability and mortality, resulting in a great social burden. Therefore, it is of great social significance to study how osteoporosis affects the process of bone repair. In this study, the effects of osteoporosis on bone repair were studied by observing two types of bone repair: endochondral osteogenesis and intramembranous osteogenesis after bone injury in osteoporosis mice. Methods 1. The osteoporosis model of mice was established by castration and subcutaneous injection of glucocorticoid, and the osteoporosis model was successfully constructed by scanning microscope CT. The bone repair models of osteoporosis mice and normal mice were established. Brdu. was injected intraperitoneally at 7, 10, 14, 21 days after operation, and the mice were killed at 7 and 10 days after operation by intraperitoneal injection of Brdu.. HE staining, immunohistochemical staining, and TRAP staining were used to observe the changes of bone repair process in membranous internalized bone. 3. A model of cartilage osseous repair in osteoporosis mice and normal mice was established. On the 7th, 10th, 14th, 21st day after operation, the bone repair models were obtained and stained by HE. Immunohistochemical staining and toluidine blue staining were used to observe the changes of osteogenesis in cartilage. Results MicroCT data showed that the osteoporosis model was successfully established after subcutaneous injection of methylprednisolone 3.5mg/kg for 8 weeks and bilateral ovariectomy for 8 weeks, compared with the control group. The process of osteogenesis was obviously delayed in osteoporosis model mice. (3) compared with the control group, the process of osteogenesis in the cartilage of osteoporosis model mice was significantly delayed. Conclusion the process of proliferation and differentiation of stem cells into osteoblasts is damaged after osteoporosis, which affects the process of osteogenesis in bone repair. It affects the mature hypertrophy and differentiation of chondrocytes, and the time of ossification center affects the process of osteogenesis and bone repair. Although the mechanism of glucocorticoid and estrogen deficiency is different, both of them delay the process of osteogenesis and osteogenesis in fracture healing in a similar way.
【学位授予单位】：第四军医大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R687.3

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