Joint contact mechanics in the early stages of osteoarthritis.
Joint degeneration in the early stages of osteoarthritis (OA) may be reflected in changes in structural and material properties in articular cartilage. The aim of the present study was to simulate numerically the contact area and stress distribution in normal and "diseased" cartilage layers for dynamic loading. The initial stages of osteoarthritis were simulated based on an experimental model: the anterior cruciate ligament-transected cat knee. In this model, cartilage layers become thicker, softer, and more permeable than the corresponding healthy cartilage layers within weeks of intervention. In our numerical simulations, the diseased cartilage was modelled by changing the thickness, permeability, shear modulus, and Poisson's ratio of the cartilage in accordance with observations in this experimental model of osteoarthritis. The theoretical model of normal and diseased articular cartilage was based on a biphasic representation of cartilage, and the joint was assumed to be axi-symmetric. It was found that, for a given loading condition, the contact areas increase and peak stresses decrease in the diseased compared to the normal joint. According to our simulations, areas of normal joint contact become unloaded and areas of little or no contact become overloaded in the early stages of osteoarthritis compared to the situation in normal joints. Based on these results, we speculate that OA may be initiated following ACL transection because of an overloading of specific regions of the joint, either because of the altered contact mechanics or the disrupted joint stability, despite a general decrease in the contact pressure.
Wu
J Z
JZ
Human Performance Laboratory, Faculty of Kinesiology, Department of Mechanical Engineering, Faculty of Engineering, The University of Calgary, 2500 University Drive N.W., Calgary, Canada.
Herzog
W
W
Epstein
M
M
D000818:Animals; D001696:Biomechanical Phenomena; D002358:Cartilage, Articular / Q000503:physiopathology; D002415:Cats; D006801:Humans; D007596:Joints / Q000503:physiopathology*; D008954:Models, Biological; D010003:Osteoarthritis / Q000209:etiology / Q000503:physiopathology*