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Cover image supplied by Dr Jan Hohe, Dr Wolfgang Wirth and Prof Felix Eckstein from the Institute of Anatomy, Paracelsus Medical University, Salzburg, Austria, and from Chondrometrics GmbH, Ainring, Germany. The image shows a lateral view of a 3D reconstructed knee from sagittal magnetic resonance images (MRIs). The tibial condyles and tibial plateau cartilages are depicted at the bottom, the (transparent) femoral bone at the top left, and the patella bone and cartilage at the top right. The thickness distributions of the tibial and patellar cartilages are colour-coded. This MRI-based analysis of knee cartilage thickness was performed as part of a project that investigated longitudinal cartilage loss in knee osteoarthritis, as a sensitive measure of structural disease progression.
Given the known involvement of IL-36 in psoriasis it might be surprising that the latest mouse models show that inhibiting IL-36 signalling does not alter the course of inflammatory arthritis. Can we now add IL-36 to the list of inflammatory mediators that are not viable DMARD targets?
Macrophage activation syndrome (MAS) in systemic juvenile idiopathic arthritis (sJIA) is difficult to distinguish from active sJIA or sepsis. A collaborative effort scoring the performance of different clinical diagnostic criteria provides valuable guidance to clinicians, but challenges in the diagnosis of sJIA-related MAS remain.
A lack of universally accepted classification criteria for patients with juvenile spondyloarthritis (SpA) has hindered efforts to develop tools to assess the severity and progression of this disease. With the publication of a new juvenile SpA disease activity index, has this gap now been bridged, and is it a comprehensive tool for the clinic?
Autoantibodies towards citrullinated proteins define a distinct clinical subtype of rheumatoid arthritis (RA). Here, the authors describe events triggering immunity against citrullinated proteins and argue that this immune response might be initiated outside the joint, pointing to the lungs as a possibly important site of initiation of these events.
Elevated serum uric acid levels and gout are linked with the development of several comorbid conditions including hypertension, metabolic syndrome, chronic kidney disease and cardiovascular disease. In this Review, the authors explore the mechanisms underlying these associations and discuss the potential of appropriate treatment strategies to improve cardiovascular and renal outcomes in patients with hyperuricaemia and gout.
Although paraneoplastic syndromes are rare, it is important that rheumatologists can recognise the typical clinical patterns of these syndromes in their rheumatic disease patients to allow for timely diagnosis and potentially life-saving therapy. Here, the authors focus on well-defined paraneoplastic musculoskeletal syndromes for which the evidence of a causal relationship to an underlying tumour is not only based on a temporal relationship but also on underlying pathomechanisms.
Systemic sclerosis (SSc) is a complex autoimmune disease. Here, the authors describe the current understanding of the genetics of SSc and how genetic risk factors can influence disease pathogenesis. Available evidence of the role of epigenetic factors (including microRNAs and DNA methylation patterns) in disease development is also discussed.
Treatment of children with juvenile idiopathic arthritis (JIA) is often marred by therapeutic inefficacy and considerable adverse effects. In this Review, the authors highlight the importance of identifying new pharmacogenomics biomarkers by applying modern genome analysis to large cohorts of JIA patients, with the objective of improving safety of existing therapies and providing new drug targets for the treatment of JIA.
Rheumatoid arthritis (RA) and metabolic syndrome share several pathologic characteristics, such as changes in body composition, lipid levels and insulin sensitivity, that may increase cardiovascular mortality. Here, Kerekes and co-authors discuss associations between these components in RA and metabolic syndrome and propose that optimal therapeutic control of RA might attenuate adverse effects of metabolic syndrome in patients with RA.