Knee osteoarthritis is multifactorial. The signature pathologic feature is hyaline articular cartilage loss, however it is increasingly recognised that OA is a disease of the whole joint, with bone remodelling and attrition occurring relatively early in the disease process. Fibrocartilage degeneration including the meniscus is integral to disease and changes in the load-distributing function of this fibrocartilage may induce injury to adjacent hyaline cartilage. Chondro-osteophytes (protrusions of new cartilage which subsequently ossify) form both at the joint margin and centrally in areas where cartilage has eroded. The synovium often develops lining cell hyperplasia and in some cases becomes infiltrated with subsynovial inflammatory cells. Activated synovium secretes excess synovial fluid, leading to capsular swelling which in turn inhibits complete activation of muscles leading to weakness and atrophy. Inflammation triggers changes in the peripheral nervous system with nociceptive signals from the joint and surrounding tissues.
It has been argued that knee OA is almost always caused by increased physical forces causing damage to the joint, often aberrant loading (Felson, 2009). It has not been possible to conduct ethical research to demonstrate causal agents. Causation has to be inferred where there has been a consistently found and temporally appropriate relationship between a risk factor and later onset of disease (Felson, 2013).
In the young patient, the pathogenesis of knee OA is predominantly related to an unfavourable biomechanical environment at the joint, resulting in mechanical demand that exceeds the ability of a joint to repair and maintain itself. Chondrocytes are responsible for both synthesis and degradation of the cartilaginous matrix, and cytokines with anabolic and catabolic effects appear to have important roles. Osteoarthritis results from failure of chondrocytes to maintain the homeostasis. There appears to be an age-related reduction in the number of chondrocytes and they become less responsive to growth factors. High levels of shear stress appear to play a significant part in creating and sustaining this imbalance when a combination of oxidative and metabolic stress leads to chemically induced damage. A a period of rest may be protective against some types of chemically induced damage, and biological interventions can decrease mechanical stress-induced chondrocyte damage (Heijink et al., 2012).
FELSON, D. T. 2009. Developments in the clinical understanding of osteoarthritis. Arthritis Res Ther, 11, 203.
FELSON, D. T. 2013. Osteoarthritis as a disease of mechanics. Osteoarthritis Cartilage, 21, 10-5.
HEIJINK, A., GOMOLL, A. H., MADRY, H., DROBNIC, M., FILARDO, G., ESPREGUEIRA-MENDES, J. & VAN DIJK, C. N. 2012. Biomechanical considerations in the pathogenesis of osteoarthritis of the knee. Knee Surg Sports Traumatol Arthrosc, 20, 423-35.