The results of several retrospective studies have reported that systemic treatment in patients with psoriasis reduces the risk of incident psoriatic arthritis (PsA). Although encouraging from a prevention perspective, such studies are limited in their ability to provide a conclusive understanding of PsA risk, preventing a clear picture from emerging.

Joint distraction, the prolonged mechanical separation of the bones at a joint, has emerged as a joint-preserving treatment for end-stage osteoarthritis, with the gradually growing promise of implementation in regular clinical practice. Joint distraction of the knee has been most extensively studied, with these studies showing prolonged symptomatic improvement in combination with repair of cartilage

Interferon-γ (IFNγ) is a pleiotropic cytokine with multiple effects on the inflammatory response and on innate and adaptive immunity. Overproduction of IFNγ underlies several, potentially fatal, hyperinflammatory or immune-mediated diseases. Several data from animal models and/or from translational research in patients point to a role of IFNγ in hyperinflammatory diseases, such as primary haemophagocytic

Fatigue is a complex phenomenon and an important health concern for many people with chronic inflammatory rheumatic diseases, such as rheumatoid arthritis, psoriatic arthritis, primary Sjögren syndrome and systemic lupus erythematosus. Although some clinical trials have shown the benefits of cognitive behavioural therapy in fatigue management, the effect of this approach is relatively modest, and no

Researchers have created therapeutic implants containing cells engineered to release anti-inflammatory biologic drugs in response to changing endogenous inflammatory signals.

Non-coding RNAs have distinct regulatory roles in the pathogenesis of joint diseases including osteoarthritis (OA) and rheumatoid arthritis (RA). As the amount of high-throughput profiling studies and mechanistic investigations of microRNAs, long non-coding RNAs and circular RNAs in joint tissues and biofluids has increased, data have emerged that suggest complex interactions among non-coding RNAs

New research shows that cartilage engineered from nasal chondrocytes can integrate with osteoarthritic joint tissues in animal models, and provides early evidence of clinical benefits in patients with knee osteoarthritis.

A new study finds that a small-molecule inhibitor of IRAK4 blocks inflammation and pathophysiological processes in rheumatoid arthritis and systemic lupus erythematosus.

A study in Genome Biology reports the fine-mapping of rheumatoid arthritis risk loci in synovial fibroblasts and provides evidence of a causal role for these cells in the heritability of this disease.

Morphological and functional analysis of the microcirculation are objective outcome measures that are recommended for use in the presence of clinical signs of altered peripheral blood flow (such as Raynaud phenomenon), which can occur in systemic sclerosis (SSc) and other autoimmune rheumatic diseases. Several advanced non-invasive tools are available for monitoring the microcirculation, including

A study of human immune-cell populations has shown that IFNγ from synovial natural killer cells can activate a subset of pro-inflammatory HLA-DR+CD90+ synovial fibroblasts that is greatly expanded in rheumatoid arthritis.

Targeted nanoparticles that bind to exposed type II collagen in injured joints and promote localized downregulation of Mmp13 expression represent progress towards a disease-modifying osteoarthritis drug.

A population of FOXP3+ regulatory T cells that express RANKL are capable of promoting osteoclast formation and accelerate bone loss in a mouse model of arthritis.

The ACR have published their first guideline for the management of large vessel vasculitis, which covers giant cell arteritis and Takayasu arteritis. The new guideline differs from the current EULAR recommendations on some important points, but do these different views actually affect patient care?

Blood vessels form a versatile transport network that is best known for its critical roles in processes such as tissue oxygenation, metabolism and immune surveillance. The vasculature also provides local, often organ-specific, molecular signals that control the behaviour of other cell types in their vicinity during development, homeostasis and regeneration, and also in disease processes. In the skeletal

Systemic sclerosis (SSc) is a prototypical inflammatory fibrotic disease involving inflammation, vascular abnormalities and fibrosis that primarily affect the skin and lungs. The aetiology of SSc is unknown and its pathogenesis is only partially understood. Of all the rheumatic diseases, SSc carries the highest all-cause mortality rate and represents an unmet medical need. A growing body of evidence

New research shows that metabolic modulation can restore immune tolerance induction by anti-CD45RB antibodies in lupus-prone mice and reduce systemic lupus erythematosus-like pathology.

Chimeric antigen receptor (CAR) T cell therapy has been used to treat a patient with systemic lupus erythematosus, marking the first time this approach has been successfully used to treat an autoimmune disease.

A study published in Nature shows the effects of ageing on skeletal stem cells (SSCs) and how aged SSCs affect haematopoiesis, bone turnover and fracture repair.

Osteoarthritis (OA) remains the most challenging arthritic disorder, with a high burden of disease and no available disease-modifying treatments. Symptomatic early-stage OA of the knee (the focus of this Review) urgently needs to be identified and defined, as efficient early-stage case finding and diagnosis in primary care would enable health-care providers to proactively and substantially reduce the

New evidence has emerged that DNA can bind to cell surface HLA class II molecules. If true, this surprising interaction could lead to T cell and B cell activation by DNA, and surface DNA could also provide a target for cell killing by anti-DNA antibodies in systemic lupus erythematosus.

The development of treatments for systemic sclerosis has historically been hampered by the clinical heterogeneity of the disease and limited understanding of its pathogenesis. Encouragingly, advances including the identification of important molecular targets and improvements in clinical trial design have now greatly increased the number of investigative therapies.

New research demonstrates that antibodies from patients with fibromyalgia induce sensory hypersensitivities in recipient mice, suggesting an autoimmune basis for the disease as well as new therapeutic possibilities.

Limited data suggest associations between air pollution and rheumatic disease risk and outcomes. More sophisticated research is needed to clarify the conditions under which air pollution might influence the health of people with rheumatic disease, including their response to biologic drugs.

An anti-CD38 monoclonal antibody and an in vivo gene-editing approach show promise for the treatment of different forms of systemic amyloidosis in separate clinical trials.

Interactions between lymphocytes and stromal cells have an important role in immune cell development and responses. During inflammation, stromal cells contribute to inflammation, from induction to chronicity or resolution, through direct cell interactions and through the secretion of pro-inflammatory and anti-inflammatory mediators. Stromal cells are imprinted with tissue-specific phenotypes and contribute

Systemic lupus erythematosus (SLE) is an autoimmune disease with protean manifestations that predominantly affects young women. Certain ethnic groups are more vulnerable than others to developing SLE and experience increased morbidity and mortality. Reports of the global incidence and prevalence of SLE vary widely, owing to inherent variation in population demographics, environmental exposures and

Most rheumatic and musculoskeletal diseases (RMDs) can be placed along a spectrum of disorders, with autoinflammatory diseases (including monogenic systemic autoinflammatory diseases) and autoimmune diseases (such as systemic lupus erythematosus and antiphospholipid syndrome) representing the two ends of this spectrum. However, although most autoinflammatory diseases are characterized by the activation

Gout and chronic kidney disease (CKD) frequently coexist, but quality evidence to guide gout management in people with CKD is lacking. Use of urate-lowering therapy (ULT) in the context of advanced CKD varies greatly, and professional bodies have issued conflicting recommendations regarding the treatment of gout in people with concomitant CKD. As a result, confusion exists among medical professionals

New research shows that combination therapy for septic arthritis in mice considerably reduces intracellular bacteria in synovial tissue and protects against joint damage.

New research shows that platelets inhibit regulatory T cell immunosuppressive activity in systemic lupus erythematosus via P-selectin–PSGL1 interaction.

Osteoarthritis (OA) is a whole-joint disease characterized by subchondral bone perfusion abnormalities and neovascular invasion into the synovium and articular cartilage. In addition to local vascular disturbance, mounting evidence suggests a pivotal role for systemic vascular pathology in the aetiology of OA. This Review outlines the current understanding of the close relationship between high blood

Photothermal therapy using gold nanorods targeted to nerve growth factor shows promise for relieving pain in a mouse model of osteoarthritis.

In patients with axial spondyloarthritis (axSpA), pain, functional and structural impairments, reduced mobility and potential deformity of the axial skeleton are the most prominent health concerns. Limitations in physical function and spinal mobility are caused by both inflammation and structural damage, and therefore restrictions to physical function must be monitored throughout a patient’s life.

A new study describes an anti-inflammatory signalling pathway mediated by TNFR2 and the signalling molecule 14-3-3ε and the effects of this pathway on macrophage polarization.

Short telomere length is implicated in lung diseases and can be caused by mutations in telomere genes. Acquired autoimmunity directed against components of the telomere system is now reported in some patients with systemic sclerosis or idiopathic pulmonary fibrosis, suggesting a novel explanation for short telomeres in these diseases.

The 2021 ACR guideline for the treatment of rheumatoid arthritis provides an update on several important topics, including the use of targeted synthetic DMARDs (tsDMARDs). But how does the new guideline compare to EULAR recommendations, and is the growing importance of tsDMARDs adequately accounted for?

A new study implicates the tumour protein LASP1 in the aggressive phenotype of fibroblast-like synoviocytes in rheumatoid arthritis.

Wnt mimetics designed to activate the Wnt signalling cascade induced rapid and robust bone growth in models of osteoporosis, ageing and fracture.

Infectious agents can trigger autoimmune responses in a number of chronic inflammatory diseases. Lyme arthritis, which is caused by the tick-transmitted spirochaete Borrelia burgdorferi, is effectively treated in most patients with antibiotic therapy; however, in a subset of patients, arthritis can persist and worsen after the spirochaete has been killed (known as post-infectious Lyme arthritis). This

An engineered protein that blocks CCR6–CCL20 signalling was able to prevent and treat skin, joint and entheseal inflammation in an IL-23-dependent mouse model of psoriatic arthritis.

Treatments that block tumour necrosis factor (TNF) have major beneficial effects in several autoimmune and rheumatic diseases, including rheumatoid arthritis. However, some patients do not respond to TNF inhibitor treatment and rare occurrences of paradoxical disease exacerbation have been reported. These limitations on the clinical efficacy of TNF inhibitors can be explained by the differences between

Infection with malaria parasites can prevent progression to severe kidney disease in lupus-prone mice by preventing the migration of CCL17-producing dendritic cells to the kidneys.