Volume 6 Issue 2, February 2010

Several lines of evidence both from experimental models and from clinical studies reveal that TNF-like ligand 1A (TL1A) and its interaction with death receptor 3 (DR3) is critically involved in the pathogenesis of rheumatoid arthritis and other autoimmune diseases.

Since the introduction of new biologic agents and intensive treatment strategies that aim to tightly control disease activity, clinical remission has become a realistic target in patients with rheumatoid arthritis. Once patients are in continuous remission, however, is it realistic to consider withdrawing DMARD therapy?

Minimizing the potential adverse effects of clinical investigators' financial conflicts of interest involves, in part, determining how much of an investigator's 'business' should be disclosed to participants in research studies. What should be disclosed and why? How will we know if disclosure matters?

Interactions between HLA and PTPN22 genotypes and smoking have been implicated in overall susceptibility to rheumatoid arthritis as well as the incidence of particular disease phenotypes in case–control and case-only studies. As recent epidemiological evidence shows, deciphering these interactions demands consideration of the analytical approach used.

To date, understanding of the molecular mechanisms of bone metabolism has centered on three tumor necrosis factor family members—RANK, its ligand RANKL and its decoy receptor osteoprotegrin. This view should now be modified, however, to incorporate the role of interferon regulatory factor-8.

Any form of treatment for patients with ankylosing spondylitis (AS) is defined as being disease-modifying on the basis of its ability to decrease inflammation, improve function and inhibit the progression of structural damage. This Review outlines clinical outcomes that are relevant to the concept of disease modification, looks at what is known about the disease-modifying properties of currently available agents and considers the challenges involved in developing future therapies for AS.

The clinical importance of glucocorticoid-induced osteoporosis has gained increasing recognition over recent years, but its management generally remains suboptimal. The currently recommended pharmacologic therapies and the development of clinical guidelines for the management of patients with this condition are discussed in this article.

Invariant natural killer T cells have been implicated in a number of autoimmune diseases. In this Review, the authors highlight recent advances in our understanding of distinct subsets of these cells and the immunoregulatory cytokines they produce, and discuss whether inducing differential cytokine responses in these cells could be exploited to develop cell-based therapies.

Osteoporosis is a highly prevalent disease that leads to bone fragility and subsequent fracture, most commonly at the hip, spine and wrist. This article reviews the epidemiology of this potentially devastating disease, highlighting the incidence and prevalence of osteoporotic fractures, the resulting morbidity and mortality and the associated costs both to the individual and to society as a whole.

Asian researchers have been at the forefront of many topics in the field of Rheumatology, from the identification of disease entities that were first observed in the region to the establishment of the field of osteoimmunology. In this Review, Yamano and Nishioka highlight the ongoing contribution of Asian researchers to our understanding and treatment of rheumatic diseases.

Autoantibodies—predominantly antinuclear antibodies—are strong predictors of disease outcome and the pattern of organ complications in patients with systemic sclerosis (SSc). In conjunction with improved methods to detect and evaluate autoantibodies, this strong association offers a real chance for risk stratification and disease assessment in patients with SSc.