Inflammatory arthritis refers to a group of related clinical entities marked mainly by inflammation of the joints, the spine, or both. Rheumatoid arthritis and spondyloarthritis (which includes psoriatic arthritis and axial spondyloarthritis) are the most common forms of inflammatory arthritis. As more studies are conducted, there are accumulating data suggesting the elevated risk of skin cancer, including both melanoma and non-melanoma skin cancer, in inflammatory arthritis compared with the general population. In this context, the question of whether screening for skin cancer should be recommended in individuals with inflammatory arthritis is more relevant than ever. In this Review, we discuss the current knowledge on the risk and possible associations of melanoma and non-melanoma skin cancer in inflammatory arthritis with the aim of raising awareness within the rheumatology community about the risk of skin cancer, screening, and guidance.

Physical activity is internationally recommended as an effective component of inflammatory arthritis (IA) care. It contributes to managing IA symptoms, enhancing quality of life, and reducing cardiovascular disease risk. However, many individuals with IA are insufficiently active to realize these multi-faceted benefits. Supporting physical activity behavior change remains a major challenge within IA care. Therefore, we conducted an umbrella review to understand current evidence on: (1) physical activity levels and associated patient characteristics, (2) barriers and facilitators, and (3) effectiveness and characteristics of physical activity behavior change interventions.

Osteoarthritis (OA) is a painful disorder of the synovial joints characterized by dysfunctional cellular metabolism and extracellular matrix degradation that activates maladaptive repair responses, including pro-inflammatory pathways of innate immunity. OA has historically been viewed as an unavoidable consequence of ageing owing to wear-and-tear of the joint. Most strategies to mitigate OA have primarily focused on the articular cartilage and, more recently, other specific joint tissues, which limits understanding of OA as a systemic disease beyond the joint. Preclinical and clinical data support a paradigm shift in understanding OA as a disease of the whole person, focusing on changes throughout the body that both promote and are caused by OA. This shift provides novel insights into why preclinical research findings have not been successfully translated into clinical therapies. Moreover, a viable strategy for OA drug development could be to treat pain separately from OA structural damage. Challenging classically held views that lack evidence or have been disproven is required for progress. We explore some key emerging questions that should be carefully considered in future OA studies. Adapting and integrating new technologies, techniques, and tools into the rapidly evolving understanding of OA could lead to the development of drugs that might not only treat OA but also provide mechanistic insight into other conditions that result from the dysregulation of systemic factors or from the communication breakdown in inter-organ crosstalk. Such developments would reposition OA researchers from adapting approaches from other fields of science and medicine to leaders in the fight against chronic disease.

The role of autoantibody-producing B cells in connective tissue diseases (CTD) has recently been highlighted by the successful treatment with CD19-targeting CAR T cells. Detrimental effects of autoantibodies are linked to the formation of deposited IgG complexes and the activation of immune cells via Fcγ receptors (FcγRs). The role of circulating immune complexes (cICs) as a link between adaptive and innate immunity has remained understudied. Clinical testing of cICs has been hindered by the lack of reliable detection methods. The aim of this study was to determine the potential of IgG-containing cICs to activate FcγRs (their bioactivity) using a new detection method.

Insulin resistance (IR) is frequently observed and associated with complications of cardiovascular disease among the RA population. Triglyceride-glucose (TyG)-related indexes, serving as surrogates for assessing IR, have been significantly associated with mortality in some chronic diseases. However, their prognostic roles in the RA population have not been validated to date.

Idiopathic inflammatory myopathy (IIM) is increasingly recognized as a systemic disorder with frequent subclinical myocardial involvement. However, its coexistence with heart failure with preserved ejection fraction (HFpEF) remains poorly understood. This study aimed to comprehensively characterize the clinical, serological and radiological features of IIM patients with HFpEF and assess the prognostic utility of the HFA-PEFF score in this setting.

To evaluate the clinical features and diagnostic work-up of patients with Chronic Nonbacterial Osteomyelitis (CNO) followed at a tertiary referral center, and to contribute real-life data to the existing literature. We also aimed to compare our treatment approach to the EULAR recommendations for CNO.

To develop and validate a model to predict serious infection risk in rheumatoid arthritis (RA) patients initiating biologic or targeted synthetic DMARDs (b/tsDMARDs), and to implement it as an interactive tool (RAISE).

To determine the frequency of axial SpA (axSpA) patients fulfilling the recently proposed Assessment of SpondyloArthritis International Society (ASAS) definitions for difficult-to-manage (D2M) and treatment-refractory (TR) axSpA, and to characterize these patients at initiation of their first advanced therapy.

Immune-checkpoint molecules have essential roles in regulating immune responses, which maintain the delicate balance between physiological immune reactions and autoimmunity. The clinical success of immune checkpoint blockade for cancer therapy, and the occurrence of immune-related adverse events during cancer immunotherapy, highlight the profound effect of modulating these receptors on both tumour-specific and 'self'-specific responses. As a result, interest in exploring how these molecules can be targeted to treat autoimmune and rheumatological diseases is expanding. Targeting of the immune-checkpoint molecules PD-1, B and T lymphocyte attenuator (BTLA) and T cell immunoreceptor with Ig and ITIM domains (TIGIT) to induce immune tolerance has shown therapeutic promise in pre-clinical models and, in some instances, clinical trials. A comprehensive understanding of how these receptors function in various immune cell populations, particularly T cells, and across different diseases is crucial for the successful translation of these findings to clinical applications.

To evaluate the performance of non-invasive screening tools in identifying metabolic dysfunction-associated steatotic liver disease (MASLD) causing clinically significant liver disease (CSLD) in PsA patients at high risk for liver disease, and to identify factors associated with CSLD.

To investigate cellular immune responses to the herpes zoster (HZ) subunit (HZ/su) vaccine in patients with rheumatoid arthritis (RA) treated with Janus kinase inhibitors (JAKis).

Systemic lupus erythematosus (SLE), an autoimmune disease, damages multiple organs. Studies showed higher all-cause mortality in SLE patients compared to the general population. However, it remains unclear whether the persistent immunodeficiency and organ damage exacerbate the prognosis of intensive care for patients with comorbid SLE.

The objectives of this study were to evaluate NSAID use over time in patients with axial spondyloarthritis (axSpA) receiving biologic therapy, to determine the prevalence of axSpA remission without NSAIDs, and to identify factors associated with continued NSAID use after one year of follow-up.

Previous research has suggested that the incidence of haemophagocytic lymphohistiocytosis is increasing in Europe. We aimed to examine rates of mortality due to haemophagocytic lymphohistiocytosis across 29 European countries from 2011 to 2021.

The disappointment stemming from IL-23 inhibition failure in axial spondyloarthritis has resulted in expert panels extrapolating these results to axial psoriatic arthritis, with recommendations against the use of IL-23 inhibitors in this setting. However, post-hoc analyses of clinical trials show clinical improvements in axial psoriatic arthritis following treatment with ustekinumab, guselkumab, and risankizumab. A growing body of real-world evidence also shows substantial amelioration of spinal pain, related outcome measures, and imaging-detected inflammation. Despite negative trials, IL-23 inhibition was associated with C-reactive protein reductions and some improvement in MRI scores in ankylosing spondylitis, indicating some modicum of potential benefit. Furthermore, inadequate response to biological therapies in axial spondyloarthritis was associated with absence of MRI-determined bone marrow oedema, whereas responses to secukinumab in axial spondyloarthritis were independent of bone marrow oedema, pointing to divergent pathophysiological processes. The growing recognition of clinical, microanatomical, and immunological differences between axial spondyloarthritis and axial psoriatic arthritis suggests differential IL-23 pathway dependence. This Personal View aims to provide a deeper examination of these distinctions as a basis to propose reconsidering the current moratorium on IL-23 inhibitors-particularly in phenotypes not linked to HLA-B27-and to potentially expand therapeutic options.

To examine the influence of demographics on organ damage in a broad, multiethnic cohort of patients with Behçet's syndrome (BS).