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骨软骨病自发性及实验性病变中软骨的缺血性坏死

Ischemic necrosis of cartilage in spontaneous and experimental lesions of osteochondrosis.

作者信息

Carlson C S, Meuten D J, Richardson D C

机构信息

Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh.

出版信息

J Orthop Res. 1991 May;9(3):317-29. doi: 10.1002/jor.1100090303.

DOI:10.1002/jor.1100090303
PMID:2010836
Abstract

This study was designed to examine the association of spontaneous lesions of osteochondrosis with vascular supply to epiphyseal cartilage, and to determine whether similar lesions could be experimentally reproduced by selective interruption of cartilage canal blood supply. The vascular supply to the articular-epiphyseal cartilage complex of the distal end of the femur was studied in 27 microfil- or barium-injected and cleared specimens and 24 serially sectioned microangiographic specimens from 27 clinically normal female swine (3.6 to 71.0 kg). Blood vessels supplying the articular-epiphyseal cartilage complex were consistently restricted to the epiphyseal region and the number of vessels decreased as the pigs increased in weight (p less than 0.001). Spontaneous lesions of osteochondrosis (i.e., cartilage necrosis) were initially seen in the first areas of epiphyseal cartilage to become avascular and were associated with necrotic blood vessels. The number and size of foci of necrotic cartilage increased as the pigs increased in weight (p less than 0.001). Blood supply to epiphyseal cartilage from cartilage canal vessels was surgically interrupted in a highly vascular area of the medial femoral condyle in eight additional 23-kg female swine. This procedure resulted in necrosis of blood vessels within cartilage canals followed by necrosis of surrounding cartilage, lesions that appeared to be identical to early spontaneous lesions of osteochondrosis. These results suggest that the viability of epiphyseal cartilage in the articular-epiphyseal cartilage complex is highly dependent on an adequate blood supply from cartilage canal vessels, and strongly implicates a defect in blood supply in the pathogenesis of osteochondrosis.

摘要

本研究旨在探讨骨软骨病的自发性病变与骨骺软骨血管供应之间的关联,并确定通过选择性阻断软骨管血液供应是否能在实验中重现类似病变。对27只临床正常的雌性猪(体重3.6至71.0千克)的27个注射微丝或钡剂并经清除处理的标本以及24个连续切片的微血管造影标本进行了研究,观察股骨远端关节-骨骺软骨复合体的血管供应情况。供应关节-骨骺软骨复合体的血管始终局限于骨骺区域,且血管数量随猪体重增加而减少(p<0.001)。骨软骨病的自发性病变(即软骨坏死)最初出现在骨骺软骨最早变为无血管的区域,并与坏死血管相关。坏死软骨灶的数量和大小随猪体重增加而增加(p<0.001)。在另外8只体重23千克的雌性猪的股骨内侧髁高度血管化区域,通过手术阻断软骨管血管对骨骺软骨的血液供应。该操作导致软骨管内血管坏死,随后周围软骨坏死,这些病变似乎与骨软骨病早期的自发性病变相同。这些结果表明,关节-骨骺软骨复合体中骨骺软骨的存活高度依赖于软骨管血管的充足血液供应,并强烈提示血液供应缺陷在骨软骨病发病机制中起作用。

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