悪性関節リウマチ

OBJECTIVE: Aim: The aim of this study is to analyze current data on the molecular and cellular mechanisms underlying the development of degenerative-dystrophic diseases of the temporomandibular joint (TMJ). The article explores the potential of collagen therapy as a pathogenetically substantiated approach to the comprehensive treatment of this disease. PATIENTS AND METHODS: Materials and Methods: A systematic review of the scientific literature over the past 20 years was conducted, indexed in PubMed/MEDLINE, Scopus, Web of Science, the Cochrane Library, RCSB Protein Data Bank until March 2026. A comprehensive literature search identified 14,865 publications. Following a sequential analysis of titles, abstracts, and full texts based on predefined inclusion criteria (original experimental and clinical studies, systematic reviews and meta-analyses that revealed the molecular and cellular mechanisms of TMJ osteoarthritis, the therapeutic impact of types I and II collagen on joint and bone regeneration) and exclusion criteria (irrelevant papers, duplicates, TMJ rheumatoid arthritis, septic arthritis, systemic vasculitis). Ultimately, 37 primary sources were selected for the final review. CONCLUSION: Conclusions: The authors summarized current data on the pathogenetic mechanisms of TMJ osteoarthritis, analyzed data on the use of collagen in the treatment of TMJ. The biological role of collagen types I and II as key structural components of fibrocartilage and subchondral bone is examined. Special attention is given to the feasibility of using injectable tropocolagen to stimulate reparative processes in the TMJ.

Artificial intelligence (AI) and machine learning (ML) are transforming the landscape of rheumatological and systemic inflammatory disease management, offering unprecedented capacity to integrate complex, multidimensional data for diagnostic support, disease monitoring, and therapeutic decision-making. This comprehensive narrative review, based on a non-systematic literature search of PubMed/MEDLINE and Google Scholar combined with the authors' clinical expertise, provides a clinically oriented synthesis of current and emerging AI applications across the full spectrum of immune-mediated inflammatory diseases-including rheumatoid arthritis, systemic lupus erythematosus, vasculitis, inflammatory bowel disease, psoriatic arthritis, systemic sclerosis, inflammatory myopathies, and sarcoidosis-with particular attention to applications that have demonstrated or are approaching clinical utility. We discuss deep learning-based image analysis, natural language processing of electronic health records, multi-omic biomarker discovery, and the application of Fourier transform-based signal processing to biological time series as a novel approach to continuous disease monitoring. Fourier transform methods-already foundational in MRI reconstruction, cardiac electrophysiology, and clinical neurophysiology-are here systematically extended to rheumatological and inflammatory disease signals, including accelerometry, electromyography, heart rate variability, and longitudinal biomarker time series. The phenomenon of large language model hallucination-particularly critical in rare inflammatory diseases-is addressed alongside retrieval-augmented generation as a mitigation strategy. We further argue that AI-driven methods do not merely improve the interpretation of clinical data, but fundamentally expand what is observable-with profound epistemological implications for clinical knowledge transmitted through generations of medical tradition. Ethical considerations and future directions toward precision inflammatory disease medicine are outlined.

Aortopathies in autoimmune rheumatic diseases (ARD) include a spectrum of aortic pathologies-including aortitis, aneurysms, dissections, and insufficiency-primarily caused by systemic inflammation. This comprehensive review investigates the clinical manifestations, pathophysiology, diagnostic modalities, and management strategies across various rheumatic diseases associated with aortopathies such as large vessel vasculitis (e.g., Takayasu arteritis, giant cell arteritis), connective tissue diseases (e.g., systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, systemic sclerosis) and less common conditions (e.g., relapsing polychondritis, Cogan's syndrome, Behçet's disease, IgG4-related disease). Disease-specific pathophysiologic mechanisms of aortic wall inflammation and remodeling, including granulomatous and lymphoplasmacytic patterns and mixed inflammatory infiltrates, are described. Diagnostic imaging modalities-such as CTA, MRI, and PET/CT-are evaluated for their roles in detecting active inflammation, assessing structural complications, and guiding clinical decision-making. Histopathological findings provide insight into disease-specific vascular changes. Management strategies focus on the use of glucocorticoids, disease-modifying antirheumatic drugs (DMARDs), and biologics, including IL-6 and TNF-α inhibitors, with an emphasis on patient-centered approaches, multidisciplinary care, and timely surgical intervention for complications. Evidence gaps include optimal screening intervals and the role of novel biomarkers in risk stratification and in monitoring disease progression, highlighting the need for early recognition, frequent monitoring, and aggressive management of aortic involvement in rheumatic diseases to prevent life-threatening complications.

UNLABELLED: Autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, and systemic vasculitis, are associated with increased risk of thrombosis, accelerated atherosclerosis, cardiovascular-events, and premature mortality. Heparin-induced thrombocytopaenia and vaccine-induced thrombocytopaenia and thrombosis (VITT) or VITT like syndrome are autoimmune thrombotic disorders that do not have additional features of autoimmune diseases. We summarise the epidemiology, pathophysiology, diagnosis, and management of autoimmune thrombosis. Key mechanisms include autoantibody-mediated coagulation activation, endothelial dysfunction, complement activation, platelet activation, neutrophil extracellular-trap formation, and thrombo-inflammation, promoting thrombin generation, impaired fibrinolysis, and vascular injury. Traditional cardiovascular risk factors, such as smoking, obesity, hypertension, diabetes mellitus, and infection, further amplify thrombotic risk. Management requires integrated strategies combining anticoagulation, immunomodulatory therapy, cardiovascular-risk reduction, and long-term surveillance. Autoimmune thrombosis is an under-recognised contributor to cardiovascular disease and premature mortality across Europe. Earlier diagnosis, improved risk stratification, multidisciplinary care, and integration of autoimmune diseases into European cardiovascular prevention and health-system strategies are essential to reduce morbidity and premature mortality. FUNDING: DJA is funded by Medical Research Council UK (MR/Z505274/1) and infrastructure support was provided by the NIHR Imperial Biomedical Research Centre.

IMPORTANCE: Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation and destruction of cartilage and adjacent bone and can lead to irreversible disability. Rheumatoid arthritis affects 0.53% of adults worldwide and 0.74% of US adults. OBSERVATIONS: Rheumatoid arthritis is more common among females than males (2:1) and has a peak incidence at ages 55 to 75 years. Rheumatoid arthritis can affect all synovial joints, and extra-articular involvement may include rheumatoid nodules, vasculitis, and rheumatoid lung disease. At diagnosis, approximately 40% to 60% of patients have autoantibodies (eg, rheumatoid factor and/or anticitrullinated peptide antibodies). There are no formal diagnostic criteria for RA, so the diagnosis is based on clinical history, characteristic joint swelling in proximal interphalangeal, metacarpophalangeal, and/or wrist joints and often presence of autoantibodies and elevated C-reactive protein levels. Early diagnosis, ideally within 6 weeks of symptom onset, allows rapid initiation of therapy with disease-modifying antirheumatic drugs (DMARDs), which inhibit inflammation and decrease the risk of joint destruction. The goal of treatment is to achieve at least 50% improvement in disease activity by 3 months and remission or low disease activity at 6 months, measured by validated indexes such as the Clinical Disease Activity Index (CDAI). The European Alliance of Associations for Rheumatology recommends starting treatment with methotrexate, 7.5 mg to 10 mg orally weekly, increasing to 20 mg to 25 mg weekly within 4 to 8 weeks, and considering addition of short-term glucocorticoids (eg, prednisone, 5-7.5 mg/d), tapered and discontinued within 3 months, or 1 intramuscular injection of 80 mg to 160 mg depot methylprednisolone. For patients with contraindications to methotrexate, sulfasalazine (2-4 g/d) or leflunomide (20 mg/d) is recommended. With treatment, about 40% of patients with newly diagnosed RA achieve CDAI remission within 6 months. Patients who do not achieve remission with first-line DMARDs should be prescribed biological DMARDs (eg, tumor necrosis factor α inhibitors, costimulation inhibitors, interleukin 6 receptor inhibitors, anti-CD20-targeting B cells), or Janus kinase (JAK) inhibitors (in patients not at high risk of thromboembolism, cardiovascular disease, or malignancy). With addition of biological DMARDs or JAK inhibitors to first-line DMARDs, overall remission or low disease activity rates increase to approximately 80%. CONCLUSIONS AND RELEVANCE: Rheumatoid arthritis is a chronic autoimmune disease that causes joint destruction. First-line initial therapy is methotrexate, with consideration of glucocorticoids as additive therapy. For patients who do not achieve remission with this initial treatment, adding biological DMARDs or JAK inhibitors increases overall remission or low disease activity rates to 80%.