Changes in bone mineral density in a rabbit model of steroid-induced osteonecrosis of the femoral head

doi:10.3969/j.issn.2095-4344.2017.28.015

Abstract

Abstract:

BACKGROUND: The rabbit model of osteonecrosis of the femoral head (ONFH) has been successfully established by glucocorticoid combined with lipopolysaccharide.
OBJECTIVE: To observe the dynamic changes of bone mass in the early steroid-induced ONFH.
METHODS: Twenty-four adult New Zealand white rabbits were randomly divided into experimental and control groups (n=12 per group). Rabbits in the experimental group were injected with lipopolysaccharide and glucocorticoid to establish the model of ONFH, while those in the control group given the same volume of normal saline. The changes in the femoral head structure, morphology and distribution of the trabecular bone at 5, 10, 15 and 20 days after modeling were observed through multi-slice spiral CT, micro-CT and hematoxylin-eosin staining; the bone mineral density and rate of empty lacunae were detected.
RESULTS AND CONCLUSION: The imaging examinations showed that the rabbit femoral head was intact and smooth in both groups; on days 15 and 20, in the experimental group, the cortical bone became thinner, the trabecular bone became sparse and discontinuous, and the bone mineral density, tissue mineral density and bone volume/total volume were significantly lower than those in the control group (P < 0.01). The histological observation indicated that there were more empty lacunae and adipocytes, as well as less osteocytes and hematopoietic cells in the experimental group; the rate of empty lacunae in the experimental group was significantly higher than that in the control group on days 15 and 20 (P < 0.01). These findings suggest that in the early stage of ONFH, necrotic osteocytes increase in number, accompanied by trabecular micro-fractures, which leads to a decrease in bone mineral density, eventually resulting in bone remodeling disturbance.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Femur Head Necrosis, Lipopolysaccharides, Bone Density, Tissue Engineering

CLC Number:

R318

Yu Jun-lun, Tang Xi, Huang Yu, Yang Lu-xi, Wu Shao-ping. Changes in bone mineral density in a rabbit model of steroid-induced osteonecrosis of the femoral head[J]. Chinese Journal of Tissue Engineering Research, 2017, 21(28): 4518-4522.

Figures/Tables 1

2.1 实验动物数量分析实验选用新西兰大白兔24只，分为2组。实验组第1周死亡2只，其余存活至实验结束，后续补充实验组2只兔数据；对照组全部存活，无明显变化。 2.2 螺旋CT观察骨质的变化为了观察激素性股骨头坏死兔骨质形态及密度的变化，在建模后第5，10，15，20天进行双髋关节螺旋CT扫描。观察发现，实验组与对照组股骨头形态完整，关节面光滑，骨皮质厚度相当。与对照组相比，第15，20天实验组股骨头骨质密度欠均匀，骨松质密度减低，以第20天明显。以上结果表明，实验组股骨头形态保持完整，未发生骨质塌陷、囊变或硬化，但是骨内结构已发生改变，主要表现为股骨头骨松质形态与密度的改变。 2.3 Micro-CT观察骨质的变化为进一步观察激素性股骨头坏死兔骨内部结构的变化，在建模后第5，10，15，20 天进行Micro-CT扫描。观察发现，实验组第15，20天股骨头骨皮质变薄，骨小梁分布稀疏，间距增宽，不连续，可见断裂(图2)。结果表明，股骨头内骨小梁发生微细骨折。为进一步定量分析股骨头骨量变化，通过Micro-CT测定股骨头骨矿物质密度，组织矿物质密度，骨体积分数值。结果显示，随着观察时间延长，实验组骨矿物质密度、组织矿物质密度、骨体积分数值呈逐渐下降趋势，在第15，20天骨矿物质密度、组织矿物质密度、骨体积分数值均显著低于对照组(P < 0.01)(图3)。以上结果表明，实验组股骨头内骨量不断下降，骨质强度减低，可能与骨小梁发生微细骨折密切有关。 2.4 苏木精-伊红染色观察骨病理学变化以上都是从影像学的角度观察激素性股骨头坏死的骨质变化，接下来从组织病理学的角度进一步观察股骨头发生骨坏死的情况。在建模后第5，10，15，20 天取股骨头行病理切片、苏木精-伊红染色。观察发现，实验组股骨头内骨小梁分布稀疏、变细，形态不完整，部分断裂，随观察时间延长，空骨陷窝和脂肪细胞逐渐增多，骨细胞和造血细胞逐渐减少(图4)。两组比较，实验组第15，20天空骨陷窝百分率显著高于对照组(P < 0.01)(表1)。以上结果表明，实验组股骨头内骨髓细胞与骨细胞坏死增加，骨小梁发生微细骨折，造成骨重塑障碍。推理可能原因是骨内微循环发生紊乱，引起破骨与成骨细胞作用不平衡，骨细胞坏死增多，破骨细胞作用进一步增强，骨质吸收增加，骨量不断丢失，伴随骨小梁发生微细骨折，骨质强度减低，最终引起骨重塑障碍。 2.5 统计学分析结果实验组与对照组采用t检验，第15，20天，实验组骨矿物质密度、组织矿物质密度、骨体积分数值均显著低于对照组(P < 0.01)；实验组空骨陷窝百分率显著高于对照组(P < 0.01)。"

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