Volume 7 Issue 1, January 2011

Digital ulcers in patients with systemic sclerosis (SSc) can cause considerable disability; however, clinical trials addressing the treatment and prevention of digital ulcers in SSc are rare. A study has evaluated the potential benefit of the endothelin receptor antagonist bosentan in the treatment of SSc-related digital ulcers.

The effect of biological therapies on cancer risk in JIA is controversial owing to confounding factors such as the use of concomitant immunosuppressants. A study has shed new light on this association, but questions still remain on the effect of the disease itself and biological therapies on cancer risk.

Autologous bone grafts are the 'gold standard' repair strategy for large defects of bone, but a growing body of evidence suggests that synthetic biomaterials designed to have osteoinductive properties could provide an alternative approach.

The 1987 ACR classification criteria for rheumatoid arthritis were criticized for their lack of sensitivity in early disease. To overcome this limitation, new criteria have now been developed. The question is how will these criteria be implemented in clinical and basic research, and in daily clinical practice?

Current therapeutic strategies for osteoarthritis (OA) are mostly palliative; modifying the structural progression of OA has, therefore, become a focus of drug development. This Review discusses the challenges involved in the discovery and development of disease-modifying OA drugs, and describes specific agents that have shown promise in phase II and III trials.

Severe osteoarthritis (OA) is the main cause of an increasing need for joint replacements and is, therefore, a large burden on both patients and the health-care sector. This Review discusses the genetic contribution to hip and knee OA and the authors suggest that identifying individuals at a high risk of OA with a combination of genetic markers might aid preventive and disease-management strategies.

The etiology and pathogenesis of osteoarthritis (OA) are poorly understood, although proinflammatory cytokines are known to be critically implicated in the disease. In this Review, the authors discuss the current knowledge regarding the role of proinflammatory cytokines, particularly interleukin (IL) 1β, tumor necrosis factor and IL 6 in the pathophysiology of OA, and give an overview of efforts to develop adequate and specific anticytokine therapies.

Osteoarthritis (OA) is a disease of the whole joint, at the centre of which lies the interface between cartilage and bone. Altered transfer of mechanical stress across this boundary is thought to result from, and to exacerbate, OA, but molecular crosstalk was presumed to be minimal. Accumulating data challenge this assumption, and this Review explores the biology and pathology of the bone–cartilage functional unit.

The factors that trigger osteoarthritis (OA) have been difficult to identify, as the earliest molecular changes substantially precede clinical presentation of symptoms. Nevertheless, we are beginning to piece together the processes that occur in articular cartilage, and new tools promise to expedite completion of the puzzle. This Review outlines some of the events in early stages of OA development, focusing on the changes that occur in cartilage both before and after substantial loss of the tissue occurs.

Research into the effects of lower-extremity muscle weakness on osteoarthritis onset and progression has increased over the past decade, owing to its potential for modification using exercise training interventions. Similarly, afferent sensory dysfunction has also been suggested as an important yet modifiable risk factor for OA progression. In this Review, the authors provide an overview of these risk factors, and discuss the effectiveness of preventive or therapeutic neuromuscular and exercise training interventions.

The mechanical effect of excess weight is commonly thought to be the direct cause of osteoarthritis. In this Perspectives article, the author questions whether the evidence actually supports this prevalent view, and instead proposes that the increase in adipose tissue associated with obesity might drive the development of widespread osteoarthritis.

This Focus issue on osteoarthritis includes a series of specially commissioned Reviews from leading researchers in the field looking at disease pathogenesis in terms of cytokines, subchondral bone, cartilage matrix, and muscle strength and proprioception, with the hope of clarifying what the key processes are; in addition, Reviews focusing on the prospects for disease-modifying therapies for osteoarthritis, and on the genetic epidemiology of this disease are included.