Osteoarthritis year in review 2016: mechanics

Inappropriate biomechanics, namely wear-and-tear, has been long believed to be a main cause of osteoarthritis (OA). However, this view is now being re-evaluated, especially when examined alongside mechanobiology and new biomechanical studies. These are multiscale experimental and computational studies focussing on cell- and tissue-level mechanobiology through to organ- and whole-body-level biomechanics, which focuses on the biomechanical and biochemical environment of the joint tissues. This review examined papers from April 2015 to April 2016, with a focus on multiscale experimental and computational biomechanical studies of OA. Assessing the onset or progression of OA at organ- and whole-body-levels, gait analysis, medical imaging and neuromusculoskeletal modelling revealed the extent to which tissue damage changes the view of inappropriate biomechanics. Traditional gait analyses studies reported that conservative treatments can alter joint biomechanics, thereby improving pain and function experienced by those with OA. Results of animal models of OA were consistent with these human studies, showing interactions among bone, cartilage and meniscus biomechanics and the onset and/or progression OA. Going down size scales, experimental and computational studies probed the nanosize biomechanics of molecules, cells and extracellular matrix, and demonstrated how the interactions between biomechanics and morphology affect cartilage dynamic poroelastic behaviour and pathways to OA. Finally, integration of multiscale experimental data and computational models were proposed to predict cartilage extracellular matrix remodelling and the development of OA. Summarising, experimental and computational methods provided a nuanced biomechanical understanding of the sub-cellular, cellular, tissue, organ and whole-body mechanisms involved in OA.