Osteoarthritis (OA) is one of the leading causes of disability in the nation. With an increase in the middle age and elderly population, arthritis-related disability is expected to dramatically increase in the coming years. The mechanically initiated progression of the disease may stem from alterations in joint kinetics, kinematics and muscular control. The purpose of this work was to examine multiple facets of human gait that may contribute to altered joint loading and in turn, the progression of arthritis. This was addressed through four studies. In order to discern how persons with knee OA can decrease contribution of the knee to support during walking, the first study analyzed the contribution from ipsilateral joints to the total support moment. The results suggested that adaptive strategies are related to self-selected walking speed and involve a reduction of the knee contribution to support moment with a subsequent increase in ankle and hip contribution. The second study aimed to determine how differences in walking patterns affect a multitude of gait variables that have been previously associated with abnormal or detrimental joint loading. We attempted to differentiate between the adaptive gait strategies associated with alterations in walking speed and strategies that were an inherent part of the disease progression. The results from this study suggest that the selection of a slower self-selected walking speed reduces joint loading and appears to be a beneficial gait strategy, however certain potentially detrimental gait alterations exist regardless of freely chosen walking speed. The third study evaluated the effect of neuromuscular control on joint loading. Higher antagonistic muscle activity results in higher intersegmental forces. Analysis of muscular contribution to abnormal joint loading provides information beyond alterations in joint kinematics and kinetics. It was found that subjects with knee OA utilize higher co-contraction and potentially higher muscle forces during walking. The final study evaluated the potential end effect of alterations in muscular control on the dynamic joint stiffness in the knee during walking. Subjects with severe OA had higher levels of dynamic joint stiffness during walking than persons with less severe OA or persons without radiographic evidence of the disease. From these studies we have drawn two overall conclusions:​ 1) persons with knee OA exploit slower freely chosen walking speeds to reduce joint loading and 2) certain variables associated with detrimental effects on joint integrity cannot be reduced through the reduction of walking speed. This work should be used as the basis for future longitudinal studies which will help determine the effect of altered loading on joint progression and lead to rehabilitative strategies to reduce the progression of the disease.