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关节软骨细胞在急性半月板切除诱导的软骨退变发病机制中的被动作用

Passive role of articular chondrocytes in the pathogenesis of acute meniscectomy-induced cartilage degeneration.

作者信息

Bendele A M, Bean J S, Hulman J F

机构信息

Lilly Research Laboratories, Eli Lilly and Co., Indianapolis, IN.

出版信息

Vet Pathol. 1991 May;28(3):207-15. doi: 10.1177/030098589102800304.

DOI:10.1177/030098589102800304
PMID:1858253
Abstract

The importance of viable articular chondrocytes and enzymes or factors from surgically traumatized synovium in the pathogenesis of acute meniscectomy-induced cartilage degeneration was examined in guinea pigs (nine groups of five animals each). Iodoacetate injected intra-articularly was used to kill articular chondrocytes of guinea pigs prior to meniscectomy to determine if they were active participants in the acute lesion induction. Lesions of similar severity to those occurring in animals with viable chondrocytes at the time of surgery were observed, suggesting that the chondrocytes were not actively involved in the pathogenesis in this group. In an additional group of guinea pigs in which chondrocytes were killed by iodoacetate, the medial collateral ligament was transected to determine if acute degenerative changes could be induced in acellular cartilage exposed to a surgical manipulation that does not by itself induce lesions but does expose cartilage to enzymes/factors from traumatized synovium. Transecting the medial collateral ligament and entering the joint space without induction of instability via meniscectomy did not result in histologic evidence of cartilage damage. This suggests that synovial trauma and mild inflammation were insufficient to induce matrix degeneration in the absence of abnormal load bearing. In further support of this, guinea pigs subjected to unilateral sciatic neurectomy at the time of meniscectomy were protected against development of acute cartilage degeneration. Results of this study suggest that articular cartilage devoid of viable chondrocytes at the time of meniscectomy responds acutely in much the same way as intact cartilage subjected to this procedure.

摘要

在豚鼠(共9组,每组5只动物)中研究了存活的关节软骨细胞以及手术创伤滑膜中的酶或因子在急性半月板切除诱导的软骨退变发病机制中的重要性。在半月板切除术前,通过关节内注射碘乙酸来杀死豚鼠的关节软骨细胞,以确定它们是否是急性损伤诱导的积极参与者。观察到的损伤严重程度与手术时具有存活软骨细胞的动物所发生的损伤相似,这表明软骨细胞在该组发病机制中未积极参与。在另一组通过碘乙酸杀死软骨细胞的豚鼠中,切断内侧副韧带,以确定在暴露于一种本身不会诱导损伤但会使软骨暴露于创伤滑膜的酶/因子的手术操作的无细胞软骨中是否能诱导急性退变改变。切断内侧副韧带并在不通过半月板切除术诱导不稳定的情况下进入关节腔,未产生软骨损伤的组织学证据。这表明在没有异常负重的情况下,滑膜创伤和轻度炎症不足以诱导基质退变。进一步支持这一点的是,在半月板切除时接受单侧坐骨神经切除术的豚鼠可防止急性软骨退变的发生。本研究结果表明,半月板切除时缺乏存活软骨细胞的关节软骨的急性反应与接受该手术的完整软骨大致相同。

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