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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.
In 2010, important research into the systemic autoinflammatory diseases has confirmed and extended the role of IL-1 inhibition in hereditary autoinflammatory disorders, demonstrated a novel treatment for a dangerous complication, and expanded the spectrum of systemic autoinflammatory diseases while further implicating autoinflammation in the complications of the metabolic syndrome.
Important advances have been made in gout therapeutics in 2010. In addition to the development of novel biologic agents, progress has been made in the safe prescribing of colchicine. However, colchicine also became the subject of considerable controversy in the USA when one brand of this drug was granted exclusivity.
Novel findings shed light on the role of tumor necrosis factor in ankylosis and inflammation, pointing to new indications for blockade of this cytokine in treating spondyloarthritis. At the same time, the identification of other potential targets for therapy could expand the treatment options for this family of inflammatory disorders.
From evidence pointing to a possible etiologic role for microbes to the development of new strategies and agents to treat early and established disease, 2010 has seen the publication of several interesting findings in the field of rheumatoid arthritis.
How can we optimize the management of osteoarthritis? Recent studies into the efficacy and mechanisms of interventions that target nociceptive mechanisms, lower-extremity musculature and ligament integrity reflect the progress being made in this field.
In several areas of investigation, the results of a bumper year in osteoporosis research are set to stoke rather than settle debate. From the origins of bone health to the use of established and experimental therapies, the new findings will be discussed into 2011 and beyond.
