A Framework for the in Vivo Pathomechanics of Osteoarthritis at the Knee

Abstract

The in vivo pathomechanics of osteoarthritis (OA) at the knee is described in a framework that is based on an analysis of studies describing assays of biomarkers, cartilage morphology, and human function (gait analysis). The framework is divided into an Initiation Phase and a Progression Phase. The Initiation Phase is associated with kinematic changes that shift load bearing to infrequently loaded regions of the cartilage that cannot accommodate the loads. The Progression Phase is defined following cartilage breakdown. During the Progression Phase, the disease progresses more rapidly with increased load. While this framework was developed from an analysis of in vivo pathomechanics, it also explains how the convergence of biological, morphological, and neuromuscular changes to the musculoskeletal system during aging or during menopause lead to the increased rate of idiopathic OA with aging. Understanding the in vivo response of articular cartilage to its physical environment requires an integrated view of the problem that considers functional, anatomical, and biological interactions. The integrated in vivo framework presented here will be helpful for the interpretation of laboratory experiments as well as for the development of new methods for the evaluation of OA at the knee.

Kinematic adaptations to a variable stiffness shoe: Mechanisms for reducing joint loading

“…The motion of the knee was determined by relating the motion of the marker clusters to the anatomical coordinate systems. Details of the axes orientations of the femoral and tibial anatomic coordinate systems have been described previously (Andracchi 2003, 2005, Dyrby and Andriacchi 2004, Scanlan et al, 2010. The pelvic and foot coordinate systems and corresponding hip and ankle joint complex coordinate systems followed the ISB recommendations (Wu et al, 2002).…”

“…One important marker and target for non-invasive intervention is the first peak of the external knee adduction moment in walking (Miyazaki et al, 2002). It is a surrogate marker of the relative load on the medial compartment (Schipplein and Andriacchi, 1991) and has been correlated with OA radiographic severity, rate of disease progression and severity of disease symptoms (Andriacchi et al, 2004;Andriacchi et al, 2009;Andriacchi and Mundermann, 2006;Astephen et al, 2007;Baliunas et al, 2002;Sharma et al, 1998).…”

Gait Mechanics Influence Healthy Cartilage Morphology and Osteoarthritis of the Knee

“…A s noted above, it has been suggested that knee cartilage adapts to the cyclic loading that is specific to walking 1,3 . An examination of the regional variation of healthy cartilage thickness indicates that the thickest cartilage is in the loadbearing areas of the tibiofemoral articulation, which are in contact during the stance phase of walking, when the knee is near full extension.…”

“…The importance of walking in the context of cartilage homeostasis suggests that the knee cartilage becomes conditioned 2 to both the load and the number of load cycles associated with walking. Thus, an activity like walking, the most common activity of daily living as well as one that produces a large cyclically reproducible pattern of loading, should be an important consideration in the analysis of the maintenance of the structure, organization, and biology of healthy knee cartilage 3 . Likewise, the mechanics of walking can influence the initial breakdown of cartilage 4 if the normal patterns of loading are changed due to injury or other conditions that would alter the normal balance between loading and the biological maintenance of healthy cartilage [5][6][7] .…”

Resistance exercise recovers the structure of cartilage and synovial membrane of the ankle joint of rats after sciatic compression

“…According to Whiting and Zernicke 2 , prolonged physical exercise in animals can produce hypertrophy of the chondrocytes and an increase in their number. The articular kinematics may promote the reduction or increase in the number of chondrocytes 38 , with a consequent alteration in the composition and organization of the cartilage matrix 39 . Thus, both the decrease in weight bearing caused by the nervous injury and the increase generated by the exercise, mechanically change the cartilage, resulting in changes in the density of chondrocytes.…”