after exercise minimizes painful symptoms. Studies are being done on different types of connective tissue collagen, to better understand and reduce RA disease activity. Lastly, with the scientific advancements and enhanced understanding of the molecular mechanisms, newer and better treatment options should become available in the near future [50–55]. Conclusion RA is a debilitating, chronic, inflammatory disease, capable of causing joint damage as well as long-term disability. Early diagnosis and intervention are essential for the prevention of serious damage and loss of essential bodily functions. The treating physician should consider adhering to treat-to-target (T2T) recommendations [56], by first outlining the aims and then implementing the protocols to achieve and assess them. Furthermore, early referral to a specialist can help to ensure better treatment outcomes. With advances in the field of molecular medicine, we have a better understanding of disease mechanisms which can aid in the designing of more effective treatments. Old treatment modalities have been optimized and new ones have been produced. Gene array analysis is proving beneficial in finding out which patients will be more responsive to specific medications. This customization will allow for more rapid treatment as well as decrease the likelihood of disease progression during the experimental phase to seek an appropriate treatment for a particular patient. Gene array analysis is also being used to determine which patients are at greater risk for more aggressive forms of RA. It is foreseen that treatment methods will face tremendous improvements in the management of RA. Disclosure Statement Cochrane systematic review. Innate immunity and the failing heart: the cytokine hypothesis revisited. Circ R Rheumatoid arthritis is a chronic disorder for which there is no known cure. Fortunately in the last few years, a shift in strategy toward the earlier institution of disease modifying drugs and the availability of new classes of medications have greatly improved the outcomes that can be expected by most patients. The goal of rheumatoid arthritis treatment now aims toward achieving the lowest possible level of arthritis disease activity and remission if possible, minimizing joint damage, and enhancing physical function and quality of life. The optimal treatment of RA requires a comprehensive program that combines medical, social, and emotional support for the patient. It is essential that the patient and the patient’s family be educated about the nature and course of the disease. Treatment options include medications, reduction of joint stress, physical and occupational therapy, and surgical intervention.There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: non-steroidal anti-inflammatory agents (NSAIDs), corticosteroids, and disease modifying anti-rheumatic drugs (DMARDs). NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect. DMARDs include methotrexate, sulfasalazine, leflunomide (Arava®), etanercept (Enbrel®), infliximab (Remicade®), adalimumab (Humira®), certolizumab pegol (Cimzia®), golimumab (Simponi®), abatacept (Orencia®), rituximab (Rituxan®), tocilizumab (Actemra®), anakinra (Kineret®), antimalarials (e.g. Plaquenil®). Other immunomodulators are occasionally used including azathioprine (Imuran) and cyclosporine. Because cartilage damage and bony erosions frequently occur within the first two years of disease, rheumatologists now move aggressively to a DMARD agent early in the course of disease, usually as soon as a diagnosis is confirmed. Analgesic drugs are also sometimes helpful in decreasing pain until DMARDs take effect. A summary table of how to monitor drug treatment in rheumatoid arthritis is included. Non-steroidal Anti-inflammatory Agents (NSAIDs) The major effect of these agents is to reduce acute inflammation thereby decreasing pain and improving function. All of these drugs also have mild to moderate analgesic properties independent of their anti-inflammatory effect. It is important to note however that these drugs alone do not change the course of the disease of rheumatoid arthritis or prevent joint destruction. Aspirin is the oldest drug of the non-steroidal class, but because of its high rate of GI toxicity, a narrow window between toxic and anti-inflammatory serum levels, and the inconvenience of multiple daily doses, aspirin’s use as the initial choice of drug therapy has largely been replaced by other NSAIDs. There are a large number of NSAIDs from which to choose, and at full dosages all are potentially equally effective. Likewise, the toxicities of the currently available NSAIDs are similar. However, there is a great deal of variation in tolerance and