Mechanical load and primary guinea pig osteoarthrosis.
Mechanical load and primary guinea pig osteoarthrosis.
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DOI：
10.3109/17453679808999046
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发表时间：
1998-08
期刊：
影响因子：
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通讯作者：
L. Wei;E. de Bri;A. Lundberg;O. Svensson
中科院分区：
文献类型：
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作者：
L. Wei;E. de Bri;A. Lundberg;O. Svensson
哈特利豚鼠自发发展膝关节骨关节病。可重复的过程中，首先出现在中央内侧髁，然后进行周边和横向的变化，使该动物的干预研究的合适模型。将9月龄雄性动物随机分为4组：即刻处死组、股骨中段30 °外翻截骨组、假手术组和膝下截肢组。3个月后，胫骨近端逐步切片，并通过光学显微镜进行体视学检查。从内侧髁到外侧髁的局部负荷重新分配（截骨术）使内侧软骨纤维化减少22%，外侧增加27%。内侧髁的软骨下骨厚度减少了36%。相比之下，一般负荷重新分配（截肢）并不影响纤颤的进展，尽管明显的骨萎缩。然而，软骨厚度没有变化;钙化软骨厚度保持显著恒定，并且在外侧总是较高。因此，潮标推进似乎不是早期豚鼠骨关节病的重要机制。因此，当手术干预豚鼠骨关节病的自然病程时，在早期阶段，骨的变化比软骨的变化更明显，这进一步表明机械载荷和刚度梯度是重要的发病机制。
Hartley guinea pigs spontaneously develop knee osteoarthrosis. The reproducible course, the changes first appearing at the central medial condyle and then progressing peripherally and laterally, makes this animal a suitable model for intervention studies. We studied the effect of load, and randomized 9-month-old male animals into 4 groups: immediate killing, mid-femoral 30 degrees-valgus osteotomy, sham operation or below-knee amputation. After 3 months, the proximal tibia was step-sectioned and examined stereologically by light microscopy. Local load-redistribution from the medial to the lateral condyle (osteotomy) reduced cartilage fibrillation by 22% medially and increased it 27% laterally. Subchondral bone thickness decreased by 36% in the medial condyle. In contrast, general load-redistribution (amputation) did not affect the progress of fibrillation, despite pronounced bone atrophy. Cartilage thickness, however, did not change; calcified cartilage thickness remained remarkably constant, and it was always higher on the lateral side. Therefore tide-mark advancement does not appear to be an important mechanism in early guinea pig osteoarthrosis. Thus, when the natural course of guinea pig osteoarthrosis is interfered with surgically, in the early phase, changes in bone are more conspicuous than those in cartilage, which further indicates that mechanical load and stiffness gradients are important pathogenetic mechanisms.