Rheumatoid arthritis (RA) is a chronic disease characterized by inflammation and destruction of the synovial joints (Wollheim, 1998) resulting in marked disability and morbidity. With an estimated adult prevalence in the UK of around 1% for females and half that for males (Symmons et al., 2002) the potential social and economic impact of this disease is tremendous. It is estimated that after 20 years of disease, up to 80% of patients with RA are considered disabled (Jantti et al., 1999). The disease is also associated with an increased and early mortality, with standardized mortality ratios two to three times that of the general population (Wolfe et al., 1994).
The goals of treatment for RA are to control pain and other symptoms, to slow or arrest the destruction of cartilage and bone, minimize physical disability, and maximize quality of life. This treatment of RA dates back to antiquity, when it was found that ingestion of willow bark, a substance that contained the same active ingredient as acetylsalicylic acid (ASA), could relieve the fever and pain associated with arthritis. Since the 1920s, a progression of numerous drugs, known collectively as disease modifying anti-rheumatic drugs (DMARDs), have been used in an attempt to control disease activity and slow the progression of joint destruction. Examples include gold, methotrexate, azathioprine, sulphasalazine, and leflunomide. The effectiveness of each has been variable, and to date, no single drug has had the ability to consistently and completely stop the underlying inflammatory process. These medications have also been associated with a whole array of associated toxicities. Some side effects are as benign as rash or nausea and disappear after the drug has been discontinued. However, the potential for life-threatening infections, or even