仔猪模型股骨骨骺缺血性坏死后扁平和明显碎裂的发展

H. Kim, Phi-Huynh Su
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引用次数: 122

摘要

背景:未成熟股骨头缺血性坏死后的修复反应以及导致股骨头畸形和碎裂的生物学过程尚未明确定义。采用仔猪模型研究股骨头畸形和缺血性坏死后碎裂发生前和发生过程中的影像学和组织病理学变化。方法:以25头公仔猪为研究对象。将不可吸收的绷带紧紧缠绕在股颈周围,以阻断股骨干骨骺的血液供应。小鼠在缺血诱导后3天至8周处死。对整个股骨头和股骨头切片进行x线片拍摄,x线片的表现与标本的组织病理学变化相吻合。结果:缺血诱导后4周出现轻度股骨头扁平,8周出现严重的股骨头扁平和碎裂。血管重建术后观察到的主要修复反应是破骨细胞骨吸收。在扁平化发展之前,在股骨头中央区域观察到大面积破骨细胞骨吸收。许多破骨细胞沿血运重建前沿存在,我们认为这是坏死小梁骨主动吸收的原因。作为成人缺血性坏死修复反应的标志,在骨吸收区未观察到相应的新骨形成。取而代之的是,被吸收骨的区域被纤维血管组织所取代,这种组织可以持续8周。观察到相应的新骨形成,但仅限于小区域,其中血运重建后没有破骨细胞骨吸收,并且仍然存在坏死的小梁骨。骨吸收区和新骨形成区同时存在,导致股骨头在x线片上呈现碎片状。结论:在仔猪缺血性坏死模型中观察到的主要修复反应是破骨细胞骨吸收。早期骨丢失,缺乏新骨形成,以及骨吸收区纤维血管组织的持续存在损害了股骨头的结构完整性,并随着时间的推移导致股骨头逐渐变平。这种修复反应不同于从成年缺血性坏死患者股骨头中取出的股骨头和在成年缺血性坏死兔模型中观察到的股骨头。临床意义:仔猪缺血性坏死模型可能有助于研究未成熟股骨头缺血性坏死后导致股骨头畸形的生物学过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Development of Flattening and Apparent Fragmentation Following Ischemic Necrosis of the Capital Femoral Epiphysis in a Piglet Model
Background: The repair response that follows ischemic necrosis of the immature femoral head and the biological processes that are responsible for the development of femoral head deformity and fragmentation have not been clearly defined. A piglet model was used to study the radiographic and histopathologic changes that occur prior to and during the development of femoral head deformity and fragmentation following ischemic necrosis.Methods: Twenty-five male piglets were studied. A nonabsorbable ligature was placed tightly around the femoral neck to disrupt the blood supply to the capital femoral epiphysis. The animals were killed three days to eight weeks following the induction of ischemia. Radiographs of whole and sectioned femoral heads were made, and the radiographic findings were correlated with the histopathologic changes observed in the specimens.Results: Mild femoral head flattening was observed by four weeks after the induction of ischemia, and severe flattening and fragmentation were observed by eight weeks. The predominant repair response observed following revascularization was osteoclastic bone resorption. Prior to the development of flattening, a large area of osteoclastic bone resorption was observed in the central region of the femoral head. Many osteoclasts were present along the revascularization front, which we believe were responsible for active resorption of the necrotic trabecular bone. Appositional new-bone formation, the hallmark of the repair response in adult ischemic necrosis, was not observed in the area of bone resorption. Instead, the areas of resorbed bone were replaced with a fibrovascular tissue that persisted for up to eight weeks. Appositional new-bone formation was observed, but it was limited to small areas in which revascularization was not followed by osteoclastic bone resorption and in which necrotic trabecular bone was still present. The simultaneous presence of the areas of bone resorption and new-bone formation contributed to the fragmented radiographic appearance of the femoral head.Conclusions: The predominant repair response observed in the piglet model of ischemic necrosis was osteoclastic bone resorption. The early bone loss, the lack of new-bone formation, and the persistence of fibrovascular tissue in the areas of bone resorption compromised the structural integrity of the femoral head and produced progressive femoral head flattening over time. The repair response was different from that observed in femoral heads removed from adult patients with ischemic necrosis and from that observed in the adult rabbit model of ischemic necrosis.Clinical Relevance: The piglet model of ischemic necrosis may be useful for the investigation of the biological processes that lead to the development of femoral head deformity following ischemic necrosis of the immature femoral head.
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