Abstract
Rheumatoid arthritis (RA) is a chronic polyarthritis leading to joint destruction and remarkable disability. Current therapies have various degrees of efficacy, but toxicity frequently limits their long-term use. Although the etiology of the disease remains unknown, our increasing knowledge of the mechanisms underlying pathogenic events in rheumatoid synovitis has enabled selective targeting of the pathogenic elements of disease. Several new drugs have recently been introduced for the treatment of RA. These include cyclooxygenase type 2 inhibitors, adhesion molecules, T cells, B cells, cytokine/receptor, chemokines, angiogenesis, oral tolerance antigens, costimulatory molecules, and new disease-modifying antirheumatic drugs. Continuing research into the pathogenesis of RA will undoubtedly identify even more effective therapeutic approaches for the management of this disease in the future. In conclusion, the proof of principle has been established that selective targeting of pathogenic elements of disease results in substantial improvement in signs and symptoms as well as disease progression. Improved efficacy is expected with more aggressive targeting of the pathogenic elements.
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