NSAIDs work by inhibiting the activity of cyclooxygenase (COX) enzymes involved in prostaglandin (PG) synthesis. Standard treatment for patients with RA include non-steroidal anti-inflammatory drugs (NSAIDs). This leads to an increased destruction of bone by synoviocytes, causing joints to become unstable and painful. Over time, the cartilage and elastic tissue that covers the end of bones can also become damaged due to antigen-activated CD4+ T cells which amplify the immune response. The inflammation and production of pro-inflammatory cytokines causes the synovium, which lines the inside of joints, to thicken, especially in the wrists, fingers, feet, and ankles. The exact cause is still unknown but genetic and environmental factors are thought to contribute. Rheumatoid arthritis (RA) is a chronic, progressive disease which causes inflammation in the joints, resulting in reduced mobility and painful deformities.
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