DO SUBCHONDRAL BONE CHANGES EXACERBATE OR PRECEDE ARTICULAR-CARTILAGEDESTRUCTION IN OSTEOARTHRITIS OF THE ELDERLY

Research into the aetiology of osteoarthritis has for several decades been concentrated on the destruction of the articular cartilage, the i nitiating events being believed to be changes in the proteoglycans and subsequently in the supporting collagenous framework, whereafter the disease is irreversible. Recent evidence has supported an old contenti on that the underlying bone may be involved, namely, increased technet ium scintigraphy correlated with increased severity of the osteoarthri tis as demonstrated by joint narrowing, and a demonstration of increas ed metabolism of cancellous bone collagen compared to age-matched cont rols. These studies have not been able to answer the question of the p rimary initiating event: does increased bone metabolism initiate carti lage destruction or vice versa? However. recent detailed studies on an imal models, particularly the macaque, have demonstrated that in this case thickening of the subchondral bone precedes fibrillation of the c artilage, which is possibly due to increased resistance of the bone to compression. Further, MRI studies on the guinea pig suggest that the initial site of activity is at the ligament bone insertion site, prior to endochondral bone sclerosis. We propose that the biomechanics of t he joint are perturbed by the loss of tension from the ligament follow ing trauma, leading to remodelling of the subchondral bone. Certainly in humans damage to the cruciate ligament often results in osteoarthri tis. It may be that subclinical damage also ultimately results in oste oarthritis. Although the results from animal models will need to be tr eated with caution, the concept that bone ligament changes precede art icular cartilage destruction should lead to a redirection of research, and perhaps therapy, for this important and cruelly disabling disease .