Post-traumatic osteoarthritis is a musculoskeletal disorder where inflammatory processes and abnormal joint loading predispose articular cartilage to degradation after a mechanical injury. Since inflamed and injured cartilage cannot be reversed back to healthy state, prevention of osteoarthritis progression is advisable, a prestigious goal where computational models could serve as tools. The current literature is short of computational models combining both biochemical and biomechanical aspects of osteoarthritis. Thus, here we implemented inflammation of living cartilage tissue followed by biochemical perturbations of tissue homeostasis and shear strain-induced biomechanical degradation in novel cell-to-tissue-level finite element models. The models presented in this paper and enriched by our experimental findings/previous literature provide profound new mechanobiological insights and predictions about cartilage degradation in injured and inflamed tissue under physiologically relevant mechanical loading. We suggest that mechanobiological computational models could be applied as in silico analysis tools that provide clinicians information of the personalized progression of post-traumatic osteoarthritis and decision-making guidance for treatment of the disease. This dataset includes experimental data on cartilage degeneration obtained with digital densitometry (optical density near and away from chondral lesions), results from finite element models (loss of fixed charge density due to inflammation and biomechanical degradation), and the files needed to run the computational models.

2020