The progressive degeneration of articular cartilage is an underlying problem in the pathogenesis of osteoarthritis(OA) as well as in rheumatoid arthritis (RA) and other inflammation arthritides. It leads to a loss of joint function, frequently accompanied by debilitating pain. In idiopathic OA this is a degenerative process that may cover a period of 20–30 years, culminating in clinical presentation and a need for joint replacement as the only effective means of managing this condition. There are as yet no recognisable disease modifying treatments for OA; only symptomatic treatment (pain relief) is possible. The physical and economic burden of OA is enormous, affecting up to 15% of the total population (>50% of the aging population over 60 years of age). We face an enormous challenge in the management of this condition. Yet with recent progress in reaching an improved understanding of the pathobiology of this condition there is a realisation that there are recognisable targets for treatment. With the advent and promise of new methodologies to detect early disease and predict its progression, there are new opportunities for its future management. In this paper we review what we know about the pathobiology of OA and how it can be investigated, focusing on the chondrocyte and the collagen fibrils that it produces which form the endoskeletal backbone of the extensive extracellularmatrix.
This overview of some of the work of this and other laboratories has sought to capture some of the recent developments in our understanding and management of the pathobiology of OA. New therapeutic targets have been identified. In vivo assessment of disease activity and progression is now a more realistic opportunity than a couple of years ago. The immediate future should herald some major advances in creating and assessing the first disease modifying treatments for OA.