Early post-traumatic osteoarthritis-like changes in human articular cartilage following rupture of the anterior cruciate ligament
Early post-traumatic osteoarthritis-like changes in human articular cartilage following rupture of the anterior cruciate ligament
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DOI：
10.1016/j.joca.2005.08.005
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发表时间：
2006-02-01
影响因子：
7
通讯作者：
Poole, AR
中科院分区：
文献类型：
--
作者：
Nelson, F;Billinghurst, RC;Poole, AR
目的：前交叉韧带（ACL）损伤常导致创伤后骨关节炎（OA）。在这项研究中，我们确定特发性OA的早期退行性改变是否在前交叉韧带损伤后的关节软骨中引起。方法：手术切除一小块股骨关节软骨样本，作为前交叉韧带重建的一部分，共50例前交叉韧带损伤患者。其中28例在受伤后不到1年的时间内接受了手术。对照软骨在尸检时取自21人的同一部位。检查所有软骨的分子变化。用免疫分析法测定ⅱ型胶原的含量、胶原酶裂解率和变性率。用比色法测定了糖胺聚糖（GAG）的总含量，其中糖胺聚糖主要为聚集蛋白。数据以单位DNA （GAG和胶原含量）表示，或以总胶原蛋白的百分比表示。其他来自同一部位的软骨（8个作为对照，12个损伤后不到1年，8个损伤后超过1年）被冷冻切片并进行组织学检查，以确定Mankin分级软骨退变。结果：组织学分析显示，对照组显示蛋白多糖染色，在一些ACL破裂患者中蛋白多糖染色减少。有时在前交叉韧带破裂1年后观察到关节面退行性变。尽管破裂后的曼金分级随时间增加，但变化不显著。然而，免疫分析显示，1年内GAG含量增加，1年后保持不变，但不再显著。在研究期间未观察到总II型胶原蛋白含量的变化。然而，在acl破裂后不到1年和超过1年的时间里，II型胶原变性和劈裂明显增加。三组总II型胶原含量与GAG含量均有直接相关性，在1年以上显著性最弱。1年后，观察到总II型胶原含量与胶原裂解和变性之间呈负相关。结论：这些观察结果表明，由前交叉韧带损伤引起的关节不稳定迅速导致退行性改变，这是关节置换术中特发性OA和前交叉韧带手术后实验性OA的特征。这些变化可能导致前交叉韧带损伤后常见的创伤后骨关节炎的发生。这些观察结果支持并扩展了其他关于人类和动物关节软骨和滑膜液的研究得出的结论，这些研究表明，实验性OA在acl损伤后会迅速发生II型胶原的损伤，并且最初会出现蛋白多糖含量增加的特征。本研究为前交叉韧带损伤后骨性关节炎的退行性变化特征的快速发展提供了直接证据。(c) 2005年国际骨关节炎研究学会。Elsevier Ltd.出版。版权所有。
Objective: Injury to the anterior cruciate ligament (ACL) frequently leads to post-traumatic osteoarthritis (OA). In this study we determined whether early degenerative changes characteristic of idiopathic OA are induced in articular cartilage following ACL injury.Methods: A small sample of femoral articular cartilage was removed at surgery, as part of ACL reconstruction, from a total of 50 patients with ACL injuries. Of these, 28 underwent surgery less than 1 year post-injury. Control cartilages were obtained from the same site from 21 persons at autopsy. All cartilages were examined for molecular changes. The content of type II collagen, its cleavage by collagenases and its denaturation were determined by immunoassay. The total content of glycosaminoglycan (GAG), which is principally aggrecan, was measured colorimetrically. Data were expressed per unit DNA (GAG and collagen content) or as a percentage of total collagen cleaved or denatured. Other cartilages from the same site (8 controls, 12 less than 1 year and 8 more than 1 year post-injury) were frozen sectioned and examined histologically to determine by Mankin grading cartilage degeneration.Results: Histological analyses revealed that control subjects exhibited staining for proteoglycan, which was reduced in some patients following ACL rupture. Degeneration of the articular surface was sometimes observed 1 year after ACL rupture. Although the Mankin grade increased with time after rupture these changes were not significant. Immunoassays, however, revealed an increase in GAG content within 1 year which was maintained after 1 year although no longer significant. No changes in total type II collagen content were observed during the period of study. However, there were significant increases in the denaturation and cleavage of type II collagen less than and more than 1 year post-ACL rupture. Total type II collagen content was directly correlated with GAG content in all three groups, with the significance being weakest at more than 1 year. After 1 year an inverse correlation was observed between total type II collagen content and collagen cleavage as well as denaturation.Conclusions: These observations reveal that joint instability resulting from ACL injury rapidly results in degenerative changes characteristic of those seen in idiopathic OA at arthroplasty and in experimental OA following ACL surgery. These changes may contribute to the development of post-traumatic OA that is commonly observed following ACL injury. The observations support and extend conclusions from other studies on human and animal articular cartilage and synovial fluids post-ACL injury that have revealed a rapid onset of damage to type II collagen and an initial increase in proteoglycan content characteristic of experimental OA post-ACL injury. This study provides direct evidence for the rapid development of degenerative changes characteristic of OA following ACL injury. (c) 2005 OsteoArthritis Research Society International. Published by Elsevier Ltd. All rights reserved.