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Vascular deprivation-induced necrosis of the femoral head of the rat. An experimental model of avascular osteonecrosis in the skeletally immature individual or Legg-Perthes disease

机译:血管剥夺引起的大鼠股骨头坏死。骨骼未成熟个体或Legg-Perthes疾病的无血管性骨坏死的实验模型

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摘要

The blood supply of rats' femoral heads was severed by cutting the ligamentum teres and stripping the periostium. Histologically, necrosis of the marrow was apparent on the 2nd postoperative day, necrosis of the bone on the 5th postoperative day and fibrous ingrowth on the 7th postoperative day. During the following 5 weeks, progressive resorption of the intertrabecular necrotic debris and necrotic bony trabeculae and subchondral bone plate and, concurrently, appositional and intramembranous new bone formation resulted in remodeling of the femoral heads. In 2 of 7 femoral heads, replacement of the necrotic bone by viable bone was complete at the 42-day postoperative interval. Also, the articular cartilage of the deformed and flattened femoral heads was undergoing degenerative changes. Reduplicating the pathogenically inferred clinical settings of blood supply deprivation, it is proposed that this model, in a small laboratory animal, satisfies the requirements sought for preclinical studies of treatment modalities of avascular osteonecrosis in man.
机译:通过切开韧带和剥离骨膜,切断了大鼠股骨头的血液供应。组织学上,术后第二天出现骨髓坏死,术后第五天出现骨坏死,术后第七天出现纤维长入。在接下来的5周内,小梁间坏死碎片和坏死性骨小梁和软骨下骨板的逐渐吸收,以及并发和膜内新骨的形成导致股骨头重塑。在7个股骨头中,有2个在术后42天的间隔内完成了用活骨替代坏死骨。而且,变形和扁平的股骨头的关节软骨正在发生退行性变化。重复了病原学推断的供血不足的临床背景,建议该模型在小型实验动物中满足对人类无血管性骨坏死的治疗方式进行临床前研究的要求。

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