Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation and progressive destruction of the joints. Understanding its pathophysiology is crucial for developing effective treatment strategies.
Understanding the pathophysiology of RA is fundamental for developing effective treatment options. Biological therapies targeting specific immune pathways, as well as disease-modifying antirheumatic drugs (DMARDs), are currently used to suppress inflammation, slow joint damage, and improve patient outcomes.
Rheumatoid arthritis (RA) is a chronic autoimmune disease primarily affecting the synovial joints. Its pathogenesis involves a complex interplay between genetic susceptibility, environmental factors, and immunologic dysregulation (1). The central event in RA is the activation of the immune system against components of the synovial joint, leading to inflammation and tissue damage.
Rheumatoid arthritis (RA) is a complex autoimmune disease characterized by immune dysregulation, synovial inflammation, cartilage and bone damage, and systemic manifestations. Understanding the pathophysiology of RA is crucial for developing effective treatment strategies.
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