An Equilibrium Constitutive Model of Anisotropic Cartilage Damage to Elucidate Mechanisms of Damage Initiation and ProgressionSource: Journal of Biomechanical Engineering:;2015:;volume( 137 ):;issue: 008::page 81010DOI: 10.1115/1.4030744Publisher: The American Society of Mechanical Engineers (ASME)
Abstract: Traumatic injuries and gradual wearandtear of articular cartilage (AC) that can lead to osteoarthritis (OA) have been hypothesized to result from tissue damage to AC. In this study, a previous equilibrium constitutive model of AC was extended to a constitutive damage articular cartilage (CDAC) model. In particular, anisotropic collagen (COL) fibril damage and isotropic glycosaminoglycan (GAG) damage were considered in a 3D formulation. In the CDAC model, timedependent effects, such as viscoelasticity and poroelasticity, were neglected, and thus all results represent the equilibrium response after all timedependent effects have dissipated. The resulting CDAC model was implemented in two different finiteelement models. The first simulated uniaxial tensile loading to failure, while the second simulated spherical indentation with a rigid indenter displaced into a bilayer AC sample. Uniaxial tension to failure simulations were performed for three COL fibril Lagrangian failure strain (i.e., the maximum elastic COL fibril strain) values of 15%, 30%, and 45%, while spherical indentation simulations were performed with a COL fibril Lagrangian failure strain of 15%. GAG damage parameters were held constant for all simulations. Our results indicated that the equilibrium postyield tensile response of AC and the macroscopic tissue failure strain are highly dependent on COL fibril Lagrangian failure strain. The uniaxial tensile response consisted of an initial nonlinear ramp region due to the recruitment of intact fibrils followed by a rapid decrease in tissue stress at initial COL fibril failure, as a result of COL fibril damage which continued until ultimate tissue failure. In the spherical indentation simulation, damage to both the COL fibril and GAG constituents was located only in the superficial zone (SZ) and near the articular surface with tissue thickening following unloading. Spherical indentation simulation results are in agreement with published experimental observations. Our results indicate that the proposed CDAC model is capable of simulating both initial small magnitude damage as well as complete failure of AC tissue. The results of this study may help to elucidate the mechanisms of AC tissue damage, which initiate and propagate OA.
|
Collections
Show full item record
contributor author | Stender, Michael E. | |
contributor author | Regueiro, Richard A. | |
contributor author | Klisch, Stephen M. | |
contributor author | Ferguson, Virginia L. | |
date accessioned | 2017-05-09T01:15:20Z | |
date available | 2017-05-09T01:15:20Z | |
date issued | 2015 | |
identifier issn | 0148-0731 | |
identifier other | bio_137_08_081010.pdf | |
identifier uri | http://yetl.yabesh.ir/yetl/handle/yetl/157165 | |
description abstract | Traumatic injuries and gradual wearandtear of articular cartilage (AC) that can lead to osteoarthritis (OA) have been hypothesized to result from tissue damage to AC. In this study, a previous equilibrium constitutive model of AC was extended to a constitutive damage articular cartilage (CDAC) model. In particular, anisotropic collagen (COL) fibril damage and isotropic glycosaminoglycan (GAG) damage were considered in a 3D formulation. In the CDAC model, timedependent effects, such as viscoelasticity and poroelasticity, were neglected, and thus all results represent the equilibrium response after all timedependent effects have dissipated. The resulting CDAC model was implemented in two different finiteelement models. The first simulated uniaxial tensile loading to failure, while the second simulated spherical indentation with a rigid indenter displaced into a bilayer AC sample. Uniaxial tension to failure simulations were performed for three COL fibril Lagrangian failure strain (i.e., the maximum elastic COL fibril strain) values of 15%, 30%, and 45%, while spherical indentation simulations were performed with a COL fibril Lagrangian failure strain of 15%. GAG damage parameters were held constant for all simulations. Our results indicated that the equilibrium postyield tensile response of AC and the macroscopic tissue failure strain are highly dependent on COL fibril Lagrangian failure strain. The uniaxial tensile response consisted of an initial nonlinear ramp region due to the recruitment of intact fibrils followed by a rapid decrease in tissue stress at initial COL fibril failure, as a result of COL fibril damage which continued until ultimate tissue failure. In the spherical indentation simulation, damage to both the COL fibril and GAG constituents was located only in the superficial zone (SZ) and near the articular surface with tissue thickening following unloading. Spherical indentation simulation results are in agreement with published experimental observations. Our results indicate that the proposed CDAC model is capable of simulating both initial small magnitude damage as well as complete failure of AC tissue. The results of this study may help to elucidate the mechanisms of AC tissue damage, which initiate and propagate OA. | |
publisher | The American Society of Mechanical Engineers (ASME) | |
title | An Equilibrium Constitutive Model of Anisotropic Cartilage Damage to Elucidate Mechanisms of Damage Initiation and Progression | |
type | Journal Paper | |
journal volume | 137 | |
journal issue | 8 | |
journal title | Journal of Biomechanical Engineering | |
identifier doi | 10.1115/1.4030744 | |
journal fristpage | 81010 | |
journal lastpage | 81010 | |
identifier eissn | 1528-8951 | |
tree | Journal of Biomechanical Engineering:;2015:;volume( 137 ):;issue: 008 | |
contenttype | Fulltext |