Rheumatoid arthritis: causes, targets and triggers

If you (or a loved one) has recently been diagnosed with rheumatoid arthritis, get informed about what causes it and triggers it for optimum health.

• The causes of rheumatoid arthritis' key feature — chronic inflammation — are not known. However, scientists do know that a glitch in the immune system is involved.
• Like psoriasis, lupus, multiple sclerosis and type 1 diabetes, RA is an autoimmune disease, meaning that the body's immune system mistakenly attacks healthy tissue as if it were a foreign invader.

• This autoimmune attack is directed against the joint's synovial membrane. It inflames the joint and causes pain, warmth, stiffness and swelling — symptoms common to many types of arthritis.
• What makes RA different from other forms of inflammatory arthritis is the potential for the inflamed synovial membrane to severely damage the joints.
• If that's not enough, RA's inflammation may spread beyond the joints to affect other parts of the body.
• Fortunately, new disease-modifying drugs can block RA's spread by inactivating the immune system components that attack the body's own tissues.
• Researchers have identified risk factors that make some people more likely to develop RA than others.
• Chief among these risk factors is a person's genetic makeup.

• Patients who have this genetic marker usually have more severe RA than those patients without it.
• However, fully one in four people who have the marker never develop RA, which shows that having "RA genes" isn't sufficient to bring on the condition.
• Instead, researchers believe something must be present to trigger RA in susceptible people.

• For a century now, researchers have searched for a link between the onset of RA and literally dozens of infectious agents.
• It used to be that bacteria were the prime suspects: Since they were implicated in causing some types of arthritis (Reiter's syndrome, for instance), it made sense that bacteria could be involved in RA as well.
• In 1912, an American rheumatologist proposed that RA occurred when bacterial toxins from localized infections in the tonsils, gums, teeth or gallbladder were carried to the joints via the bloodstream.
• This focal infection theory failed to hold water, but for the next 30 years unfortunate RA patients had their tonsils removed or all their teeth pulled in a vain effort to halt the progress of the disease.
• To see if RA was contagious, researchers in 1950 took fluid from the joints of people with RA and injected it into the joints of healthy volunteers.
• None of the volunteers developed RA — conclusive evidence that RA does not involve a persistent infection of the joints.In recent years, viruses have received the most attention as possible culprits in triggering RA.
• One prime suspect for more than a decade has been the Epstein-Barr virus, which causes mononucleosis. Studies show that susceptible people — those with any one of three genes associated with RA — tend to have an abnormal immune response to Epstein-Barr infections, which may trigger RA.
• Many arthritis experts remain convinced that infections can initiate RA. So far, the strenuous efforts to link a bacterium, virus or some other infectious agent to the condition have all failed. But even if some microbe is eventually implicated in causing RA, one thing seems certain: You can't catch RA from someone else.
• Rheumatoid arthritis can affect any of the body's freely movable joints, but most commonly involves the hands, wrists, shoulders, elbows, knees, ankles and feet.