Establishment of a rat model of alcohol-induced avascular necrosis of the femoral head

doi:10.3969/j.issn.2095-4344.2016.27.004

Abstract

Abstract:

BACKGROUND: The relationship between long-term heavy drinking and alcohol-induced necrosis of the femoral head has long been clear, but the pathogenesis of alcohol-induced necrosis of the femoral head is currently not fully understood.
OBJECTIVE: To establish a rat model of alcohol-induced avascular necrosis of femoral head and to study its pathogenesis.
METHODS: Eighty Wistar rats were randomly divided into experimental and control groups (40 rats per group). Rats in the experimental group were intragastrically administered strong wine 10 mL/kg, once a day, for 6 consecutive days. Rats in the control group were given physiological saline 10 mL/kg, once a day, for 6 consecutive days. Bilateral femoral heads were randomly collected from six rats every month for histomorphological observation.
RESULTS AND CONCLUSION: (1) Osteonecrosis: in the experimental group, at 3 months, trabecular bone became thin, arranged disorderly, and the number of empty lacuna began to increase. At 6 months, typical osteonecrosis appeared, and vacant lacunaes increased significantly. In the control group, trabecular bone was complete and neatly arranged. Osteocytes were visible in bone lacuna, and normal morphology of cells was seen. (2) Injury of blood vessels: in the experimental group, at 3 months, micro-intimal hyperplasia was observed. Elastic fibers of partial vascular endothelium were reduced. Elastic fiber and middle-layer smooth muscle breakage and proliferation were found. At 6 months, above manifestations were more remarkable. In the control group, arteriole film was not thickened, and vessel wall was normal. (3) Formation of microthrombus, in the experimental group, the number of microthrombus was increased at 3 months, and became significant at 6 months. In the control group, the number of microthrombus was not altered. (4) Results indicated that chronic alcohol intake can lead to microvascular endothelial injury in the rat femoral head. Abnormal blood microcirculation was detected in local region, and resulted in avascular necrosis of the femoral head. The degree of necrosis was associated with alcohol intake.

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

Key words: Femur Head Necrosis, Models, Animal, Tissue Engineering

CLC Number:

R318

Yang Yun, Fan Hai-yan, Huang Jian, Ma Zhong-ping, Zhang Zhi-feng. Establishment of a rat model of alcohol-induced avascular necrosis of the femoral head[J]. Chinese Journal of Tissue Engineering Research, 2016, 20(27): 3977-3983.

Figures/Tables 2

2.1 实验动物一般状况实验过程中，实验组大鼠随灌胃量的增加，毛发枯黄渐无光泽且易脱落，皮下脂肪菲薄，反应迟钝，易流涎，活动少，进食不好，体质量增长缓慢，甚至后期有下降趋势，个别大鼠出现消化道出血；对照组大鼠毛发光滑顺泽，进食良好，皮下脂肪丰富，体质量逐渐增加。80只大鼠中6只因灌胃技术、对乙醇不耐受及腹胀气等原因死亡，未给予补足。 2.2 两组股骨头大体观察结果实验组大鼠股骨头外观改变明显，1个月时未见明显异常，2-4个月时可见股骨头软骨颜色晦暗，失去原有的润泽，五六月时在原有病变基础上还可见股骨头表面软骨破坏，与软骨下骨结合松散，甚至脱落，骨质疏脆，未见股骨头明显变形塌陷及髋臼磨损改变；对照组1-6个月股骨头外观均未见明显改变，骨质坚硬，软骨表面光滑富有光泽，与其下骨组织结合紧密，见图1。 2.3 苏木精-伊红染色观察骨坏死情况实验组3个月时光镜下即可见骨小梁变细，排列紊乱，空骨陷窝数开始增加，6个月时出现典型的骨坏死，坏死主要集中于股骨头软骨下区域，骨小梁稀疏、纤细，结构紊乱，髓内造血细胞明显减少，空缺骨陷窝明显增加，见图2；对照组骨小梁完整，排列整齐，致密饱满，骨陷窝中骨细胞清晰可见，细胞形态正常，见图3。各组空骨陷窝率见表1。 2.4 Verhoeff氏染色观察血管损伤情况实验组一两个月可见血管内皮下弹力纤维较对照组略减少，弹力纤维排列不规则，三四个月弹力纤维部分中断，排列紊乱，五六个月可见血管内皮下弹力纤维排列紊乱更加明显，中层平滑肌断裂增生；对照组微动脉膜未见增厚，血管壁正常，见图4；各组血管损伤阳性率见表2。 2.5 微血栓染色情况连续50个高倍镜视野(×400)观察微血栓数量(个)。实验组制模后3个月开始出现微血栓数量明显增加，6个月时变化更加显著；对照组各时间点微血栓数量无明显变化，见图5。两组血栓数见表3。"

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