Mechanical behaviour of in-situ chondrocytes subjected to different loading rates: a finite element study

被引:33
|
作者
Moo, E. K. [1 ]
Herzog, W. [2 ,3 ]
Han, S. K. [2 ]
Abu Osman, N. A. [1 ]
Pingguan-Murphy, B. [1 ]
Federico, S. [3 ]
机构
[1] Univ Malaya, Fac Engn, Dept Biomed Engn, Kuala Lumpur, Malaysia
[2] Univ Calgary, Fac Kinesiol, Human Performance Lab, Calgary, AB, Canada
[3] Univ Calgary, Schulich Sch Engn, Dept Mech & Mfg Engn, Calgary, AB, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Finite element modelling; Impact loading; Chondrocyte mechanics; Cell membrane damage; Osteoarthritis; Cartilage mechano-biology; ARTICULAR-CARTILAGE EXPLANTS; PRESSURE INDUCES APOPTOSIS; PERICELLULAR MICROENVIRONMENT; VISCOELASTIC PROPERTIES; THEORETICAL-ANALYSIS; MEMBRANE DISRUPTION; STRAIN-RATE; WATER-LOSS; MATRIX; MODEL;
D O I
10.1007/s10237-011-0367-2
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Experimental findings indicate that in-situ chondrocytes die readily following impact loading, but remain essentially unaffected at low (non-impact) strain rates. This study was aimed at identifying possible causes for cell death in impact loading by quantifying chondrocyte mechanics when cartilage was subjected to a 5% nominal tissue strain at different strain rates. Multi-scale modelling techniques were used to simulate cartilage tissue and the corresponding chondrocytes residing in the tissue. Chondrocytes were modelled by accounting for the cell membrane, pericellular matrix and pericellular capsule. The results suggest that cell deformations, cell fluid pressures and fluid flow velocity through cells are highest at the highest (impact) strain rate, but they do not reach damaging levels. Tangential strain rates of the cell membrane were highest at the highest strain rate and were observed primarily in superficial tissue cells. Since cell death following impact loading occurs primarily in superficial zone cells, we speculate that cell death in impact loading is caused by the high tangential strain rates in the membrane of superficial zone cells causing membrane rupture and loss of cell content and integrity.
引用
收藏
页码:983 / 993
页数:11
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