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.