Volume 12 Issue 2, February 2016

Since glucocorticoids were first used to treat patients with rheumatoid arthritis in 1949, they have become the most common therapy for inflammatory disorders; however, their use is associated with major metabolic adverse events. Here, we review three 2015 reports with clinical and fundamental implications for the use of glucocorticoid therapy in rheumatology.

Key advances in lupus research in 2015 highlight the contribution of T cells to the pathogenesis of the disease. The findings not only shed light on the regulation and activity of these cells, but also suggest several novel therapeutic targets.

In 2015, a EULAR task force released evidence-based recommendations on the use of imaging in the clinical management of spondyloarthritis, including psoriatic arthritis. These recommendations, together with articles dealing with tight control strategies and use of the IL-17A inhibitor secukinumab, have consolidated progress in the management of psoriatic arthritis.

Novel therapies to reduce the progressive and destructive nature of inflammatory joint disease are always welcome, provided that safety is not compromised. Among the many 2015 studies in the field, we highlight a targetable mechanism of uric-acid-induced inflammation in gouty arthritis and the expected efficacy — but unforeseen safety concerns — of anti-IL-17 antibodies.

Several genetic associations have been identified in patients with spondyloarthropathies, particularly ankylosing spondylitis (AS). The most recent associations uncovered which involve genes in the IL-17/IL-23 pathway enabled a better understanding of the aetiology of spondyloarthropathies, and informed the use of previously existing drugs to treat patients with these diseases—an example of how translation of hypothesis-free medical research can yield new therapeutic strategies.

Osteoarthritis (OA) is a chronic condition that is associated with pain and disability. In this Review, Roos and Arden consider the strategies that are available for modification of risk factors contributing to the development of knee OA. Interventions for prevention and early care of knee OA could help to avoid joint-replacement surgery.

Anti-DNA antibodies are serological hallmarks of systemic lupus erythematosus, but many questions remain unanswered regarding their origins and pathological properties, as well as the relative merits of different assay formats. Understanding the mechanisms of DNA binding and pathogenesis relating to anti-DNA antibodies can aid the development of diagnostic and theranostic assays.

Proangiogenic signalling pathways are activated in chronic inflammation, but although antiangiogenic treatments are routinely incorporated into cancer therapy, surprisingly few clinical trials have investigated this approach in patients with chronic inflammatory diseases. However, this situation could soon change — a wide range of small-molecule inhibitors with improved specificity, and techniques to target such inhibitors to specific cell types, are currently undergoing clinical and preclinical development.

Lipopolysaccharide derived from gastrointestinal microbiota contributes to systemic inflammation and obesity. Huang and Kraus propose that lipopolysaccharide is a major risk factor for osteoarthritis (OA), and suggest that therapeutic strategies for the reduction of systemic levels of lipopolysaccharide should be considered for prevention and treatment of OA.