Effect of muscle weakness and joint inflammation on the onset and progression of osteoarthritis in the rabbit knee

Medicine &Amp; Science in Sports &Amp; Exercise

Bryant

Modenese

et al. 2016

Section: Discussionmentioning

confidence: 99%

Tibiofemoral Contact Forces in the Anterior Cruciate Ligament–Reconstructed Knee

Medicine &Amp; Science in Sports &Amp; Exercise

Bryant

Modenese

et al. 2016

“…Increased external knee adduction moment (KAM), which is related to increased MTFF [7], has been associated with fast progression of medial knee OA [8], development of chronic knee pain [9], progression of articular tissue pathologies [10], and poor outcomes after high tibial osteotomy surgery [2, 11]. Conversely, muscle atrophy, known to reduce maximum muscle force production [12], is also associated with tissue-induced damage in animal knee OA [13, 14] and fast progression to knee OA [15]. These results implicate impaired muscle action in the pathogenesis of knee OA—although it is not yet known how it may affect MTFF.…”

Section: Introductionmentioning

confidence: 99%

Biofeedback for Gait Retraining Based on Real-Time Estimation of Tibiofemoral Joint Contact Forces

Pizzolato

Reggiani

IEEE Trans. Neural Syst. Rehabil. Eng.

et al. 2017

102

Biofeedback assisted rehabilitation and intervention technologies have the potential to modify clinically relevant biomechanics. Gait retraining has been used to reduce the knee adduction moment, a surrogate of medial tibiofemoral joint loading often used in knee osteoarthritis research. In this study we present an electromyogram-driven neuromusculoskeletal model of the lower-limb to estimate, in real-time, the tibiofemoral joint loads. The model included 34 musculotendon units spanning the hip, knee, and ankle joints. Full-body inverse kinematics, inverse dynamics, and musculotendon kinematics were solved in real-time from motion capture and force plate data to estimate the knee medial tibiofemoral contact force (MTFF). We analyzed 5 healthy subjects while they were walking on an instrumented treadmill with visual biofeedback of their MTFF. Each subject was asked to modify their gait in order to vary the magnitude of their MTFF. All subjects were able to increase their MTFF, whereas only 3 subjects could decrease it, and only after receiving verbal suggestions about possible gait modification strategies. Results indicate the important role of knee muscle activation patterns in modulating the MTFF. While this study focused on the knee, the technology can be extended to examine the musculoskeletal tissue loads at different sites of the human body.

“…However, other studies have noted that indirect measures of lower than normal magnitude loading to the joint, particularly following ligament transection 7,8 , are also associated with joint degeneration. Moreover, in the extreme cases of spinal cord injury 78,79 , surgical amputation 58 , denervation 19 , or load deprivation appear to be important factors driving articular tissue degeneration. Together, these studies have set the foundation of our modern understanding, whereby it is both over-and/or under-loading of the articular tissues are pathways to joint degeneration.…”

Section: Introductionmentioning

confidence: 99%

Osteoarthritis year in review 2016: mechanics

Osteoarthritis and Cartilage

Lloyd

2017

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.