Articles in 2012

That primary osteoarthritis (OA) is an age-related disorder is undoubted, but how aging contributes to OA is poorly understood. New insights from 2011 offer potential explanations, novel models for study, and the suggestion that a deeper understanding of what 'aging' actually is might pave the way to everlasting joints.

In 2011, the year that subtypes of ANCA-associated vasculitis (AAV) were officially renamed according to key pathological characteristics, important progress was made not only in differentiating these subtypes, but also in understanding—and treating—their eponymous manifestations.

In 2011, new treatment recommendations for juvenile idiopathic arthritis (JIA) were proposed, inroads were made towards understanding the heterogeneity of this disease, and data were presented demonstrating the potential efficacy of DMARD combination therapies for JIA treatment. These advances hold promise for improved management of JIA in 2012 and beyond.

Evidence presented in 2011 suggests that rheumatoid arthritis might comprise two separate diseases—each with different etiological underpinnings—and that kinase inhibitors could soon be added to the therapeutic armamentarium. Together with new definitions of remission, these advances could aid the development of personalized, treat-to-target strategies.

Findings from ongoing studies of imatinib in systemic sclerosis (SSc) were eagerly awaited in 2011, but results from these clinical trials have so far been disappointing. However, progress in the understanding of the mechanisms that underlie SSc pathogenesis could provide clues to novel targets for 2012 and beyond.

From neutrophil extracellular traps to genetic networks that underlie the disease and new targeted therapies, important advances in 2011 improve our understanding of the pathogenesis of systemic lupus erythematosus and mark the beginning of our ability to treat it effectively.

Susceptibility to osteoarthritis (OA) is influenced by genetic mutations, many of which occur in genes associated with the development of synovial joints. In this Review, Linda Sandell proposes a theory that these mutations can be placed on a continuum—from obvious alterations that result in mild chondrodysplasia associated with early-onset OA to subtle changes that predispose to 'primary OA' later in life. This view is explained in the context of our current etiological understanding of OA, and how this knowledge could improve screening and treatment of patients is discussed.

Advances in the fields of cell biology and imaging have allowed researchers to dig deeper into the underlying mechanisms of joint damage in patients with tophaceous gout. This Review describes some of the recent advances in our understanding of bone erosion and cartilage damage in this disease.