This might sound like military lingo, but treating rheumatoid arthritis is similar to winning a war: It requires strategic planning, intelligence and state of the art fighting power. 

Rheumatoid arthritis is a chronic progressive inflammatory arthritis and autoimmune disease, which affects one to three percent of the world's population.  This disease occurs when our immune system goes astray, mistaking our own joint tissue for a foreign invader, attacking it and causing inflammation.  When the inflammatory process advances, chemical mediators released from white blood cells can damage cartilage, bone and ligament, causing a joint to become deformed and impairing its function.  Usually more than eighty percent of its victims will become partially disabled within twelve years of diagnosis and sixteen percent will become completely disabled.    

Since corticosteroids were discovered in 1948, its long-term side effects and inability to prevent bone and joint damage, have tarnished its reputation and forced scientists and physicians to continuously explore new drugs to fight against RA. 

Over the years, many studies have demonstrated that Methotrexate (MTX), Leflunomide, Sulfasalazine, Gold, and Hydroxychloroquine are effective in the treatment of RA.  These drugs affect the activity of RA to a greater extent than drugs such as aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs).  These drugs appear to modify our body's immune system in some way that helps slowdown the inflammatory process.  Therefore, this group of drugs is called disease-modified anti-rheumatic drugs (DMARDs).    

The strategic plan in treating RA has changed from a conventional process of using NSAIDs and corticosteroids to control symptoms, to a more biological modifying process by adding DMARDs to the preceding to alter the inflammatory process and prevent joint damage.  This is one of the milestones in the treatment of RA. 

Since the mid-1980s, MTX has become the more popular treatment for RA because of its effectiveness and ability to work more rapidly than other DMARDs.  Not only is MTX used to treat RA, but it can also be used to treat some forms of cancer.  However, the dose, side effects and administration are quite different when treating arthritis versus cancer.  Therefore, the use of DMARDs in the treatment of RA is not regarded as a form of “chemotherapy".  Leflunomide is a new promising DMARD and has a similar effectiveness and safety profile as MTX. 

Since DMARDs often take from several weeks to several months to work, trying them requires patience, commitment, and time.  Once your symptoms have subsided, you may have to stay on DMARDs for a long period of time, though your doctor may try to decrease the dosage.  While side effects can result from the use of DMARDs, severe ones are uncommon and are usually reversible once the drug is discontinued.  Frequent laboratory monitoring will largely keep side effects from occurring. 

Despite the powerfulness of DMARD drugs, only 60-70 percent of patients respond to treatment.  Even though they can slow down the progression of joint damage, the results are still unsatisfactory.    

In the past few years, due to breakthroughs in genetic engineering and a better understanding of chemical mediators in RA inflammation, TNF and IL-1 have proven to be the key chemical mediators which initiate, maintain and perpetuate inflammation and cause joint damage.  If the action of these chemical mediators can be blocked, joint pain and damage can be impeded and even prevented.    

Finally, a state of the art weapon called biologic response modifiers (BRCMs), which can effectively block chemical mediators has been developed.  Two such drugs, which have been approved by the FDA for treatment of RA, are etanercept (Enbrel) and inflximab (Remicade).  BRCMs are also called biologic agents which mean that the materials from which it is derived are living organism instead of chemical. 

Enbrel and Remicade, through different chemical actions, make TNF molecules unavailable for use in the inflammatory process.  As a result, these drugs impede the inflammatory response, ease joint pain and swelling and effectively reduce and slow down the bone and cartilage damage.  Some inflammation caused by RA can even be ceased.  Think of these drugs as anti-missiles: they can lock in on a precise target and they have the ability to counter attack and block the enemy's offensive maneuvers. 

The mechanism of DMARDs in RA inflammation is broad and ill defined.  New BRCMs are being designed to target specific key steps in the inflammatory course, as they are more powerful, more effective and less likely to create side effects than DMARDs in controlling RA.  A combined treatment of DMARDs and BRCMs is particularly effective for patients with severe RA.