激素诱发兔股骨头坏死的组织学及超微结构变化(英文)

Histological and ultrastructural changes in steroid-induced necrosis of the femoral head in adult rabbits

背景:长期大量应用糖皮质激素可诱发股骨头坏死,其发病机制尚需深入研究。目的:通过兔股骨头坏死模型,应用光、电镜观察,从形态学角度探讨其发病机制。设计:随机对照观察。单位:潍坊医学院形态学实验室,病理学教研室,外科学实验室。材料:实验于2002-03/2003-03在潍坊医学院形态实验中心完成,成年新西兰白兔40只,随机分为生理盐水对照(10只)、氟美松组(10只)、马血清3组(20只)。方法:生理盐水对照组用生理盐水10mL/(kg·d)静脉注射,连续7d。氟美松组肌肉注射氟美松10mL/(kg·d),连续7d。马血清组静脉注射马血清10mL/kg,间隔3周,重复注射同量的马血清一次并连续7d肌肉注射氟美松10mL/(kg·d)。分别在第5周、第10周取实验动物的股骨头的软骨下区,用光镜、电镜观察组织学及超微结构变化。主要观察指标:①各组动物的组织形态学观察。②超微结构变化。结果:所有的实验动物均存活并纳入实验结果分析。①组织形态学观察:生理盐水对照组股骨头软骨下骨细胞排列规则,骨细胞体积小,呈扁椭圆形,胞体位于骨陷窝内,骨髓腔内血管分布均匀。氟美松,马血清两组股骨病变特征相似:骨髓腔内造血组织显著减少,脂肪组织明显增多;在股骨干骺端及软骨下区发现骨小梁萎缩,骨细胞核固缩,空骨陷窝数增多。②超微结构变化:生理盐水对照组正常骨细胞呈扁椭圆形,位于骨陷窝内。细胞核位于细胞一端,核膜完整,细胞质内线粒体丰富。氟美松,马血清两组电镜发现骨细胞内有脂滴,骨髓腔毛细血管狭窄,血管内皮细胞受损。结论:肾上腺糖皮质激素可诱发兔股骨头坏死,激素引起脂肪在骨髓腔内堆积,骨髓腔内压升高而导致股骨头缺血,诱发骨细胞坏死。

BACKGROUND： Femoral head necrosis can be induced in adult rabbits when a large dose of steroid has been used for a long time. However, the pathogenesis of steroid-induced femoral head necrosis needs further study. OBJECTIVE： To probe into the mechanism of the disease by light microscope and transmission microscope from morphological perspective based on the model of femoral head necrosis in rabbits. DESIGN： A randomized controlled observation. SETTING： Laboratory of Morphology; Teaching and Research Division of Pathology; Laboratory of Surgery, Weifang Medical College. MATERIALS： The experiment was carried out at the Experimental Center of Morphology, Weifang Medical College, between March 2002 and March 2003. Totally 40 adult New Zealand white rabbits were randomly divided into control group （n=10）, dexamethasone group （n=10） and horse serum group （n=20）. METHODS： Control group was given intravenous injection of normal saline of 10 mL/（kg.d） for 7 consecutive days. Dexamethasone group was given intramuscular injection of dexamethasone of 10 mL/（kg·d）for 7 consecutive days. Horse serum group was given intravenous administration of horse serum of 10 mL/kg; 3 weeks later the same volume of horse serum was injected once again, followed intramuscular ;njection of dexamethasone of 10 mL/（kg·d）for 7 consecutive days. Inferior sections of cartilage of the femoral head necrosis in the experimental animals were obtained 5 and 10 weeks later, and then histological and ultrastructural changes were observed under the light microscope and transmission microscope. MAIN OUTCOME MEASURES： ① Histo-morphological observation of the animals in each group. ② Uhrastructural changes. RESULTS： All the experimental animals survived and entered the result analysis. ① Histo-morphological observation： The cells of inferior sections of cartilage of the femoral head necrosis of the experimental animals in control group were arranged regularly and had a small volume of elliptical bone cells. The cell body was located at bone lacuna, blood vessel arranged well in the medullary cavity of bone. Lesion characteristics of femoral head in dexamethasone group and horse serum group were similar： Hematopoietic adipose in the medullary cavity of bone was significantly decreased while fat adipose obviously increased; bone trabecula of metaphysis and the inferior sections of cartilage of femoral head were found withered, and so was the bone nucleus. The number of lacuna of bone was increased. ② Ultrastructural changes： Normal bone cells in control group were elliptical, located at bone lacuna. Nucleus was at one end of the cell with complete karyotheca and many mitochondria in the cytoplasm. In dexamethasone group and horse serum group there were lipid droplets in the osteocytes, narrowed blood capillary in the medullary cavity of bone and injured vascular endothelial cells. CONCLUSION： Corticotropin can induce necrosis of femoral head; the hormone causes accumulated fat adipose in the medullary cavity of bone. The increased internal pressure in the medullary cavity leads to ischemia of femoral head, thus inducing the necrosis of osteocytes.