Similarities and Discrepancies in Subchondral Bone Structure in Two Differently Induced Canine Models of Osteoarthritis
Similarities and Discrepancies in Subchondral Bone Structure in Two Differently Induced Canine Models of Osteoarthritis
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DOI：
10.1002/jbmr.39
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发表时间：
2010-07-01
影响因子：
6.2
通讯作者：
Mastbergen, Simon C.
中科院分区：
文献类型：
--
作者：
Intema, Femke;Sniekers, Yvonne H.;Mastbergen, Simon C.
在骨关节炎（OA）中，软骨退化伴随着软骨下骨的变化。OA中骨改变的发病机制和生理学尚不清楚。比较不同方法诱导的实验性OA模型软骨下骨结构和软骨损伤的变化。实验性OA通过前交叉韧带横断（ACLT）或软骨创伤（Groove模型）双侧诱导;双侧假手术作为对照。随时间推移测量赖氨酰吡啶啉（LP，骨吸收）和II型胶原蛋白（CTX-II，软骨分解）的C-端肽。术后20周，通过显微计算机断层扫描（mu CT）分析胫骨的软骨下皮质板和松质骨，并对软骨退变进行组织学和生物化学分析。在两种模型中，软骨退化和皮质软骨下板变薄。在两种模型中，CTX-II水平均随时间升高。仅在ACLT模型中观察到软骨下骨小梁变化，而在Groove模型中未观察到。相应地，在ACLT模型中LP水平随时间升高，而在Groove模型中则没有。有趣的是，ACLT模型中的骨小梁变化扩展到干骺端区域。在两种模型中均存在早期板厚度降低，以及软骨损伤，这表明板变薄是OA过程固有的现象，与OA的原因/诱导无关。另一方面，软骨下骨和干骺端骨中的小梁变化不是OA发展的常见途径的一部分，并且可能在不稳定和负荷较小的ACLT关节中通过生物力学诱导。(C)2010年美国骨与矿物质研究学会。
In osteoarthritis (OA), cartilage degradation is accompanied by subchondral bone changes. The pathogenesis and physiology of bone changes in OA are still unclear. The changes in subchondral bone architecture and cartilage damage were compared in differently induced experimental models of OA. Experimental OA was induced bilaterally by anterior cruciate ligament transection (ACLT) or by cartilage trauma (Groove model); bilateral sham surgery served as control. Lysylpyridinoline (LP, bone resorption) and C-telopeptide of type II collagen (CTX-II, cartilage breakdown) were measured over time. At 20 weeks after surgery, the subchondral cortical plate and trabecular bone of the tibia were analyzed by micro computed tomography (mu CT) and cartilage degeneration was analyzed histologically and biochemically. In both models, cartilage degeneration and cortical subchondral plate thinning were present. CTX-II levels were elevated over time in both models. Subchondral trabecular bone changes were observed only in the ACLT model, not in the Groove model. Correspondingly, LP levels were elevated over time in the ACLT model and not in the Groove model. Interestingly, the trabecular bone changes in the ACLT model were extended to the metaphyseal area. The early decrease in plate thickness, present in both models, as was cartilage damage, suggests that plate thinning is a phenomenon that is intrinsic to the process of OA independent of the cause/induction of OA. On the other hand, trabecular changes in subchondral and metaphyseal bone are not part of a common pathway of OA development and may be induced biomechanically in the destabilized and less loaded ACLT joint. (C) 2010 American Society for Bone and Mineral Research.