Individual contributions to tibiofemoral compartment loads in healthy and osteoarthritic gait

© 2016 Dr. Prasanna SritharanIncreased cyclic compressive loading in the medial compartment of the knee is associated with the progression of knee osteoarthritis (OA). However as medial knee OA is accompanied by a range of neuromuscular, morphological and structural changes throughout the lower limb, a clear consensus of the etiology of the disease is yet to emerge. Of particular recent interest are the roles of non-knee-spanning muscles and the lower-limb kinematic chain in the pathomechanics of knee OA. Joint loads during gait occur due to contributions from all muscles, gravity and inertia. As such the aim of this work was to utilise experimental gait data in conjunction with musculoskeletal modelling to undertake a novel and detailed examination of these individual constituent factors influencing loading in the osteoarthritic knee. Specifically, the objective was to decompose the time-histories of loads in the medial and lateral tibiofemoral compartments of osteoarthritic knees into contributions by individual muscles, gravity and inertia, and to explain the results in light of the known neuro-musculoskeletal changes associated with OA. A novel computational method for decomposing the tibiofemoral compartment loads into contributions by muscles, gravity and inertia was developed and integrated into an advanced musculoskeletal modelling pipeline. Experimental gait data from varus mal-aligned unilateral medial knee OA patients and healthy controls were input into the musculoskeletal modelling pipeline and used to quantify the contributions to the forces and cumulative loads in the medial and lateral compartments of the tibiofemoral-joint, and also to surrogate measures of medial compartment loading. The findings have revealed substantive differences in the composition of joint loads between healthy and osteoarthritic knees, and have explained some of the underlying mechanisms by which elevated knee-joint loads arise in OA patients. Importantly, the findings establish the substantial role played by non-knee-spanning muscles in modulating knee-joint loads. Furthermore, this thesis has also quantified and explained some of the potential limitations associated with surrogate measure of joint loads. The improved understanding of the pathomechanics of medial knee OA brought about by this thesis may be potentially valuable in the design of non-pharmacologic interventions to mitigate medial knee OA progression, and may facilitate the development of more robust surrogate measures of knee-joint loads to improve clinical assessment of OA patients