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机构地区:[1]南方医科大学珠江医院内分泌科,广东省广州市510282 [2]南方医科大学外科学教研室,广东省广州市510282
出 处:《中国组织工程研究与临床康复》2010年第9期1521-1524,共4页Journal of Clinical Rehabilitative Tissue Engineering Research
摘 要:背景:骨质疏松症中骨微结构的破坏是导致骨强度下降、骨脆性增加以及骨折发生率增加的重要原因。目的:通过扫描电镜观察糖皮质激素作用下大鼠股骨远端松质骨超微结构的改变。方法:3.5月龄SPF级雌性SD大鼠32只,随机分为2组,糖皮质激素组皮下注射甲泼尼龙3.5mg/(kg·d)诱导糖皮质激素性骨质疏松,对照组皮下注射等量生理盐水。分别于干预4,9周后取大鼠股骨远端沿冠状面切开,蒸馏水冲洗骨髓腔,乙醇梯度脱水,表面喷金后利用扫描电镜观察大鼠股骨远端松质骨超微结构的改变。结果与结论:与对照组相比,糖皮质激素组大鼠骨小梁数目减少,且骨小梁变细、变脆、连接中断,立体网状结构破坏,同时骨吸收面积增加,骨胶原排列紊乱,骨微损伤增加,且糖皮质激素干预4周组较干预9周组能更好地保持骨微结构。提示糖皮质激素可导致大鼠松质骨的骨量减少、骨三维网状结构破坏、骨吸收活动增强,从而导致骨脆性增加,骨生物力学性能下降。BACKGROUND:Bone ultrastructural destruction is an important cause for bone strength decrease,bone friability and bone fracture incidence increase in osteoporosis.OBJECTIVE:To observe the ultrastructural changes of distal femur cancellous bone in glucocorticoid(GC)-treated rats by scanning electron microscopy(SEM).METHODS:A total of 32 female Sprague-Dawley rats,aged 3.5 months old,were respectively treated with methylprednisolone 3.5 mg/kg per day by subcutaneous injection to induce osteoporosis and normal saline.At 4 and 9 weeks,the distal femurs were coronary sectioned and rinsed with distilled water,dehydrated in graded ethanol,coated with gold,and observed by SEM.RESULTS AND CONCLUSION:Compared to the control,the number of bone trabeculae in the GC group was significantly decreased,and the bone trabeculae became thin,fragile,discontinuous;network structures of bone trabeculae were destroyed,and bone resorption surface increased,with disorderly arranged collagenous fibers and increased micro-damage.Rats treated with GC for 4 weeks maintained better bone ultrastructure compared with rats treated with GC for 9 weeks.Results show that GC can induce bone mass lost,destroy network structures of bone trabeculae,accelerate bone resorption in rat cancellous bone,and accordingly lead to increased bone brittleness and decreased bone functional of biodynamics.
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