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Biomechanics of cartilage articulation: effects of lubrication and degeneration on shear deformation.软骨关节的生物力学:润滑和退变对剪切变形的影响。
Arthritis Rheum. 2008 Jul;58(7):2065-74. doi: 10.1002/art.23548.
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Experimental measurement and quantification of frictional contact between biological surfaces experiencing large deformation and slip.经历大变形和滑动的生物表面之间摩擦接触的实验测量与量化
J Biomech. 2008;41(6):1333-40. doi: 10.1016/j.jbiomech.2008.01.006. Epub 2008 Mar 10.
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Indentation probing of human articular cartilage: Effect on chondrocyte viability.人体关节软骨的压痕探测:对软骨细胞活力的影响。
Osteoarthritis Cartilage. 2007 Jan;15(1):9-18. doi: 10.1016/j.joca.2006.06.007. Epub 2006 Jul 25.
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Effect of the size and location of osteochondral defects in degenerative arthritis. A finite element simulation.退行性关节炎中骨软骨缺损的大小和位置的影响。有限元模拟。
Comput Biol Med. 2007 Mar;37(3):376-87. doi: 10.1016/j.compbiomed.2006.04.004. Epub 2006 Jun 21.
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Indentation testing of human articular cartilage: effects of probe tip geometry and indentation depth on intra-tissue strain.人体关节软骨的压痕测试:探针尖端几何形状和压痕深度对组织内应变的影响
J Biomech. 2006;39(6):1039-47. doi: 10.1016/j.jbiomech.2005.02.018. Epub 2005 Apr 22.
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Causes of mechanically induced collagen damage in articular cartilage.关节软骨中机械诱导的胶原蛋白损伤的原因。
J Orthop Res. 2006 Feb;24(2):220-8. doi: 10.1002/jor.20027.
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Depth-dependent biomechanical and biochemical properties of fetal, newborn, and tissue-engineered articular cartilage.胎儿、新生儿及组织工程化关节软骨的深度依赖性生物力学和生化特性
J Biomech. 2007;40(1):182-90. doi: 10.1016/j.jbiomech.2005.11.002. Epub 2006 Jan 4.
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Factors affecting progression of knee cartilage defects in normal subjects over 2 years.影响正常受试者膝关节软骨缺损两年进展的因素。
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The clinical correlates of articular cartilage defects in symptomatic knee osteoarthritis: a prospective study.有症状的膝关节骨关节炎中关节软骨缺损的临床相关性:一项前瞻性研究。
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10
Association of cartilage defects with loss of knee cartilage in healthy, middle-age adults: a prospective study.健康中年成年人软骨缺损与膝关节软骨缺失的相关性:一项前瞻性研究。
Arthritis Rheum. 2005 Jul;52(7):2033-9. doi: 10.1002/art.21148.

局灶性关节缺损对软骨接触力学的影响。

The effects of focal articular defects on cartilage contact mechanics.

作者信息

Gratz Kenneth R, Wong Benjamin L, Bae Won C, Sah Robert L

机构信息

Department of Bioengineering, University of California-San Diego, 9500 Gilman Drive, Mail Code 0412, La Jolla, California 92093-0412, USA.

出版信息

J Orthop Res. 2009 May;27(5):584-92. doi: 10.1002/jor.20762.

DOI:10.1002/jor.20762
PMID:18979528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2862585/
Abstract

Focal damage to articular cartilage is common in arthroscopy patients, and may contribute to progressive tissue degeneration by altering the local mechanical environment. The effects of a focal defect, which may be oriented at various orientations relative to the subchondral bone, on the dynamics of cartilage contact and deformation are unclear. The objective of this study was to elucidate the effect of experimental full thickness focal defects, oriented at 80 degrees or 100 degrees relative to the subchondral bone, on intratissue strain and surface sliding of opposing cartilage surfaces during compression and stress relaxation. Pairs of intact bovine osteochondral blocks were compressed uniaxially by 20%, and allowed to stress relax. Tissue deformation was recorded by video microscopy. A full-thickness defect (with either 80 degrees or 100 degrees edges) was created in one block from each pair. Blocks were allowed to reswell and retested. Defect edges were then recut with the opposite orientation, allowed to reswell, and retested again. Stained nuclei were tracked by digital image correlation and used to quantify cartilage strains and surface sliding. The results indicated that loading of intact samples caused axial strain magnitudes that decreased with depth and relatively little sliding. With loading of samples containing defects, strain magnitudes were elevated in cartilage adjacent to, and opposing, defects. For samples with edge orientations of 100 degrees, sliding magnitudes were increased over surfaces adjacent to defects. These local mechanical changes due to full-thickness articular cartilage defects may contribute to altered chondrocyte metabolism, tissue damage, or accelerated wear.

摘要

关节软骨的局灶性损伤在关节镜检查患者中很常见,并且可能通过改变局部力学环境导致组织进行性退变。局灶性缺损相对于软骨下骨可能有不同的取向,其对软骨接触和变形动力学的影响尚不清楚。本研究的目的是阐明相对于软骨下骨呈80度或100度取向的实验性全层局灶性缺损在压缩和应力松弛过程中对相对软骨表面的组织内应变和表面滑动的影响。将成对的完整牛骨软骨块单轴压缩20%,并使其应力松弛。通过视频显微镜记录组织变形。从每对中选取一个块体制造一个全层缺损(边缘呈80度或100度)。让块体再膨胀并重新测试。然后以相反的取向重新切割缺损边缘,使其再膨胀,并再次进行测试。通过数字图像相关技术追踪染色的细胞核,并用于量化软骨应变和表面滑动。结果表明,完整样本加载时引起的轴向应变大小随深度降低且滑动相对较小。含有缺损的样本加载时,缺损相邻及相对处的软骨应变大小升高。对于边缘取向为100度的样本,缺损相邻表面的滑动大小增加。全层关节软骨缺损引起的这些局部力学变化可能导致软骨细胞代谢改变、组织损伤或加速磨损。