Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects nearly 0.5%–1% of the world’s population. It is characterized by synovial tissue inflammation with symmetric polyarticular distribution. Along the disease course, it is possible to identify a preclinical phase before any clinical manifestation, during which the loss of immunological tolerance is promoted by different trigger factors with the development of disease-specific autoantibodies (anticitrullinated peptide antibodies and rheumatoid factor). Among them, the complex interplay between the innate and adaptive immune system has a critical role in the onset and perpetuation of synovial tissue inflammation in RA. RA pathophysiology is characterized by inflammation of the synovial tissue which displays as synovial lining layer hyperplasia, sublining infiltration with mononuclear cells, increased vascularity, and fibrin deposition. These features can be very heterogeneous among RA patients from pauci-immune or diffuse infiltrate till the formation of lymphoid structures within the synovium. RA primarily involves synovial joints with symmetrical synovitis that usually leads, if uncontrolled, to their destruction because of erosion of cartilage and bone. This process causes joint deformities, resulting in significant disability in patients who do not start or fully respond to pharmacological treatment. Thus, an early diagnosis is of crucial importance despite the fact that recognizing the clinical features of early RA can be challenging. Multiple studies have showed the value of early diagnosis in RA patients, which avoids the development of irreversible joint damage and functional disability. The last decades of research have dramatically increased our knowledge about RA pathogenesis and disease course. This has led to the development of potent new biologic and small molecules therapies. In this chapter, the physiopathology, clinical, and laboratory characteristics of RA will be described with an overview of the therapeutic management with conventional and biological disease-modifying antirheumatic drugs.

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