CAJ | 학술논문

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10 mL/(kg·d)静脉注射,连续7 d.氟美松组肌肉注射氟美松10 mL/(kg·d),连续7 d.马血清组静脉注射马血清10 mL/kg,间隔3周,重复注射同量的马血清一次并连续7 d肌肉注射氟美松10 mL/(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.
배경:장기대량응용당피질격소가유발고골두배사,기발병궤제상수심입연구.목적:통과토고골두배사모형,응용광、전경관찰,종형태학각도탐토기발병궤제.설계:수궤대조관찰.단위:유방의학원형태학실험실,병이학교연실,외과학실험실.재료:실험우2002-03/2003-03재유방의학원형태실험중심완성,성년신서란백토40지,수궤분위생리염수대조(10지)、불미송조(10지)、마혈청3조(20지).방법:생리염수대조조용생리염수10 mL/(kg·d)정맥주사,련속7 d.불미송조기육주사불미송10 mL/(kg·d),련속7 d.마혈청조정맥주사마혈청10 mL/kg,간격3주,중복주사동량적마혈청일차병련속7 d기육주사불미송10 mL/(kg·d).분별재제5주、제10주취실험동물적고골두적연골하구,용광경、전경관찰조직학급초미결구변화.주요관찰지표:①각조동물적조직형태학관찰.②초미결구변화.결과:소유적실험동물균존활병납입실험결과분석.①조직형태학관찰:생리염수대조조고골두연골하골세포배렬규칙,골세포체적소,정편타원형,포체위우골함와내,골수강내혈관분포균균.불미송,마혈청량조고골병변특정상사:골수강내조혈조직현저감소,지방조직명현증다;재고골간후단급연골하구발현골소량위축,골세포핵고축,공골함와수증다.②초미결구변화:생리염수대조조정상골세포정편타원형,위우골함와내.세포핵위우세포일단,핵막완정,세포질내선립체봉부.불미송,마혈청량조전경발현골세포내유지적,골수강모세혈관협착,혈관내피세포수손.결론:신상선당피질격소가유발토고골두배사,격소인기지방재골수강내퇴적,골수강내압승고이도치고골두결혈,유발골세포배사.
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 7consecutive 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 injection 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 10weeks 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 Ultrastructural 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 haracteristics 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 with ered, 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.