|
| 兔骨质疏松与骨坏死模型骨组织病理变化的比较研究 |
| Comparative study of pathological changes of bone tissues between the rabbit osteoporosis and osteonecrosis model |
| |
| DOI：10. 3969/j. issn. 1006-7108. 2012. 12. 003 |
| 中文关键词: 骨质疏松 骨坏死 病理 相关性 |
| 英文关键词:Osteoporosis Osteonecrosis Pathology Relationship |
| 基金项目:珠海市卫生局和贵州省科技厅基金资助（珠卫[2007 ]271-2008083 ;黔科合J字[2007 ]2227。 |
|
| 摘要点击次数: 829 |
| 全文下载次数: 996 |
| 中文摘要: |
| 目的 建立骨质疏松和骨坏死的大白兔模型，比较骨质疏松与骨坏死病理学变化的异同点。
方法 取32只3月龄雌性新西兰大白兔，随机分成4组即A组（肌注激素组，8只。）B组（去势组，8 只。）C组（去势+肌注激素组，8只。）D组（空白对照组：假手术+肌注生理盐水组，8只。）B、C两组动物取下腹部正中切口，完整切除双侧卵巢，A、D两组除未行卵巢结扎切除外，其余步骤同B、C两 组。分别在给药后5周、10周后处死4只，取双侧股骨头，行HE染色、油红O染色及扫描电镜检测。结果 造模后5周，A、B、C三组空骨陷窝阳性率（%）较D组明显增高（15.20 ±1.09、14. 13 ±1. 05、18.53 ±0. 67 vs 10.40 ±0.97,P <0.05）。A、B、C三组骨小梁可见不同程度的稀疏，部分断裂。造模 后10周，A、B、C三组空骨陷窝阳性率较D组明显增高（22.43 ±0.78、21. 20 ± 1. 19、26. 78 ± 1.21 vs 11. 13 ±0. 87,P <0. 05）。A、B、C三组股骨头成不同程度的骨髓腔内脂肪细胞增生，骨小梁稀疏变细，结构紊乱、断裂，空骨陷窝增多。D组股骨头骨小梁致密，骨陷窝内骨细胞形态正常，分布均匀，骨髓腔内脂肪细胞形态正常，含量适中。结论 骨质疏松病变主要是骨小梁的超微结构退化；骨坏死 的发生由脂肪细胞的增生、骨细胞脂肪变性起主导作用。这对进一步讨论骨坏死与骨质疏松的发病相关性及调控机制具有重要的理论和实践意义。 |
| 英文摘要: |
| Objective To establish the models of osteoporosis and osteonecrosis with white rabbits， and to compare the similarity and difference of pathological changes between the osteoporosis and osteonecrosis model Methods Thirty-two female New Zealand white rabbits ( 3 months old) were randomly divided in to 4 groups: Group A ( intramuscular hormone group，n = 8)， Group B ( ovariectomized group，n = 8)， Group C (ovariectomized + intramuscular hormone group， n =8)， and Group D ( blank control group ： sham operation + intramuscular saline ， n =8). Rabbits in Group B and C were ovariectomized bilaterally via the hypogastrium median incision. Rabbits in Group A and D received the same surgery except ovariectomy. Four rabbits in each group were killed on 5 and 10 weeks after drug administration，respectively. The bilateral femoral heads of the 4 rabbits were collected and underwent HE staining， oil red O staining， and electron microscope scanning. Results At the 5Th week after modeling，the positive rate of empty bone lacunas in Group A，B，and C was significantly higher than that in Group D ( 15. 20 ±1. 09， 14. 13 ±1. 05，
18. 53 ± 0. 67 vs 10. 40 ±0. 97，P <0. 05). The trabeculae in Group A，B，and C showed different degrees of porotic， and some trabeculae fractured. At the 10th week after modeling，the positive rate of empty bone lacunas in Group A，B，and C was significantly higher than that in Group D ( 22. 43 ±0. 78，21. 20 ±1. 19，
26. 78 土 1. 21 vs 11. 13 ±0. 87,P<0. 05 ). Different extent of adipocytes hyperplasia existed in the femoral head marrow cavity in Group A, B，and C. The trabeculae were porotic， thin，disorganized，and fractured. The empty bone lacunas increased. Yet the trabeculae were compact. Bone cells in the bone lacunas were eumorphism and distributed homogeneously. The adipocytes in the bone marrow cavity were eumorphism and moderate in Group D. Conclusion The pathological changes of osteoporosis are mainly caused by the degradation of trabeculae ultrastructure. The hyperplasia of adipocytes and the fatty degeneration of osteocyte play a leading role in the course of osteonecrosis. It is important in theory and practice to investigate the pathogenesis and regulation of osteonecrosis and osteoporosis. |
| 查看全文 查看/发表评论 下载PDF阅读器 |
| 关闭 |