Mechanical loading of in situ chondrocytes in lapine retropatellar cartilage after anterior cruciate ligament transection
Mechanical loading of in situ chondrocytes in lapine retropatellar cartilage after anterior cruciate ligament transection
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DOI：
10.1098/rsif.2009.0458
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发表时间：
2010-06-06
影响因子：
3.9
通讯作者：
Herzog, Walter
中科院分区：
文献类型：
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作者：
Han, Sang-Kuy;Seerattan, Ruth;Herzog, Walter
这项研究的目的是(I)量化完全完整的关节软骨附着在其自然骨上的软骨细胞力学，以及(Ii)比较健康和早期骨关节炎(OA)组织中细胞的软骨细胞力学。我们假设，在给定关节表面压力的情况下，健康组织中的细胞比早期骨关节炎组织中的细胞变形更少，这是因为早期骨关节炎组织中基质完整性的丧失以及与之相关的被认为保护软骨细胞的结构完整性的丧失。通过使用定制设计的共焦压痕系统测量软骨细胞对完全完整的软骨的受控加载的变形反应来量化软骨细胞的动力学。兔膝关节前交叉韧带(ACL)切断后9周即可发生早期骨性关节炎。实验对象为早期骨性关节炎兔膝关节(4个关节，48个细胞)、健侧对照膝关节(4个关节，48个细胞)和正常对照膝关节(4个关节，48个细胞)。前交叉韧带切断9周后，实验关节的关节软骨厚度显著增加，并通过组织学分级评估其向骨性关节炎的进展。实验关节浅层局部基质应变(38+/-4%)大于对侧(27+/-5%)和正常关节(28+/-4%)(p=0.04)。在压痕加载过程中，所有实验组的软骨细胞在轴向和深度方向的变形都是相似的。然而，实验软骨细胞(12+/-1%)比对侧(6+/-1%)和正常对照软骨细胞(6+/-1%；p，0.001)的细胞宽度增加得更多。平均而言，随着压痕负荷的增加，早期骨性关节炎软骨细胞体积增加(8+/-3%，p=0.001)，而两个对照组的软骨细胞体积减少(对侧为28+/-2%，p=0.002，正常对照组为28+/-1%，p=0.004)。从这些结果我们得出结论，我们关于早期骨性关节炎组织中细胞变形的假说仅部分得到支持：具体地说，早期骨性关节炎软骨细胞力学的变化是方向特定的，尽管平均轴向基质变形显著增加，但原发轴向变形仍然不受影响。令人惊讶的是，在早期骨关节炎中，软骨细胞在特定的横向方向上的变形增加，这一点到目前为止还很少受到关注，但可能对早期骨关节炎的软骨细胞信号传导至关重要。
The aims of this study were (i) to quantify chondrocyte mechanics in fully intact articular cartilage attached to its native bone and (ii) to compare the chondrocyte mechanics for cells in healthy and early osteoarthritis (OA) tissue. We hypothesized that cells in the healthy tissue would deform less for given articular surface pressures than cells in the early OA tissue because of a loss of matrix integrity in early OA and the associated loss of structural integrity that is thought to protect chondrocytes. Chondrocyte dynamics were quantified by measuring the deformation response of the cells to controlled loading of fully intact cartilage using a custom-designed confocal indentation system. Early OA was achieved nine weeks following transection of the anterior cruciate ligament (ACL) in rabbit knees. Experiments were performed on the retropatellar cartilage of early OA rabbit knees (four joints and 48 cells), the corresponding intact contralateral control knees (four joints and 48 cells) and knees from normal control rabbits (four joints and 48 cells). Nine weeks following ACL transection, articular cartilage of the experimental joints showed substantial increases in thickness, and progression towards OA as assessed using histological grading. Local matrix strains in the superficial zone were greater for the experimental (38 +/- 4%) compared with the contralateral (27 +/- 5%) and normal (28 +/- 4%) joints (p = 0.04). Chondrocyte deformations in the axial and depth directions were similar during indentation loading for all experimental groups. However, cell width increased more for the experimental cartilage chondrocytes (12 +/- 1%) than the contralateral (6 +/- 1%) and normal control chondrocytes (6 +/- 1%; p, 0.001). On average, chondrocyte volume increased with indentation loading in the early OA cartilage (8 +/- 3%, p = 0.001), while it decreased for the two control groups (28 +/- 2%, p = 0.002 for contralateral and 28 +/- 1%, p = 0.004 for normal controls). We conclude from these results that our hypothesis of cell deformations in the early OA tissue was only partially supported: specifically, changes in chondrocyte mechanics in early OA were direction-specific with the primary axial deformations remaining unaffected despite vastly increased average axial matrix deformations. Surprisingly, chondrocyte deformations increased in early OA in specific transverse directions which have received little attention to date but might be crucial to chondrocyte signalling in early OA.