An Equilibrium Constitutive Model of Anisotropic Cartilage Damage to Elucidate Mechanisms of Damage Initiation and Progression.

Traumatic injuries and gradual wear-and-tear 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, time-dependent effects, such as viscoelasticity and poroelasticity, were neglected, and thus all results represent the equilibrium response after all time-dependent effects have dissipated. The resulting CDAC model was implemented in two different finite-element 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.

A poroelastic finite element model of the bone-cartilage unit to determine the effects of changes in permeability with osteoarthritis.

The changes experienced in synovial joints with osteoarthritis involve coupled chemical, biological, and mechanical processes. The aim of this study was to investigate the consequences of increasing permeability in articular cartilage (AC), calcified cartilage (CC), subchondral cortical bone (SCB), and subchondral trabecular bone (STB) as observed with osteoarthritis. Two poroelastic finite element models were developed using a depth-dependent anisotropic model of AC with strain-dependent permeability and poroelastic models of calcified tissues (CC, SCB, and STB). The first model simulated a bone-cartilage unit (BCU) in uniaxial unconfined compression, while the second model simulated spherical indentation of the AC surface. Results indicate that the permeability of AC is the primary determinant of the BCU's poromechanical response while the permeability of calcified tissues exerts no appreciable effect on the force-indentation response of the BCU. In spherical indentation simulations with osteoarthritic permeability properties, fluid velocities were larger in magnitude and distributed over a smaller area compared to normal tissues. In vivo, this phenomenon would likely lead to chondrocyte death, tissue remodeling, alterations in joint lubrication, and the progression of osteoarthritis. For osteoarthritic and normal tissue permeability values, fluid flow was predicted to occur across the osteochondral interface. These results help elucidate the consequences of increases in the permeability of the BCU that occur with osteoarthritis. Furthermore, this study may guide future treatments to counteract osteoarthritis.

An evolutionary model of osteoarthritis including articular cartilage damage, and bone remodeling in a computational study.

With osteoarthritis, a complex set of progressive chemical, biological, and mechanical changes occur in both cartilage and bone. The aim of this study is to develop a high-fidelity computational model of the complete bone-cartilage unit to study the evolution of osterarthritis-induced articular cartilage (AC) damage and remodeling of subchondral cortical bone (SCB) and subchondral trabecular bone (STB). A finite element model of spherical indentation was developed with a depth-dependent anisotropic model of degenerating articular cartilage, a calcified cartilage (CC) zone, and SCB and STB remodeling regions. Calcified tissue (CC, SCB, and STB) and AC material regions were integrated to form an evolutionary bone-cartilage unit model. Results indicate that with indentation loading, articular cartilage damage occurs at the articular surface. Furthermore, bone remodeling was predicted to occur with a net stiffening of the subchondral bone plate. Changes in indentation force were minimal (<2%) between initial and final peak indentation loading. However, additional degradation and wear of AC and/or alterations in loading may have more pronounced effects on the mechanical response of the bone-cartilage unit. Bone remodeling and articular cartilage damage predictions are consistent with experimental observations that cartilage damage begins at the articular surface and subchondral bone experiences a thickening (i.e., stiffening) response with osteoarthritis. Our results provide insight into the early-term initiation behavior of osteoarthritis; the potential consequences of evolutions in AC, SCB, and STB with disease progression; and may guide future experimental and computational studies to elucidate mechanisms of osteoarthritis progression.