Rheumatoid Arthritis

Definition. This condition is sometimes called “crippling arthritis,” which is a misnomer. “Rheumatoid” means “of the nature of rheumatism.” “Rheumatism” means pain in muscles or joints. In short, the name of this disease tells very little except that it involves pain and inflammation of the joints.

Demographics. This disease affects 2.1 million Americans, and women are affected about three times more frequently than are men. Statistics indicate that it is most common among 20- to 40-year-olds, but it can strike anyone, including children and adolescents. It tends to run in families, and a genetic marker has been identified. This marker, however, only identifies persons at risk for the disease. Most people who bear the gene do not develop rheumatoid arthritis (RA).

Etiology. RA is an autoimmune disease. This condition is brought about by a mistake in the vastly complex and usually very effective immune system: Normal, healthy tissues are misidentified as threatening invaders, and attacked by immune system agents. Autoimmune diseases are triggered by pathogens that closely resemble some part of the body’s own proteins. A pathogen’s protein coat needs to have only five amino acids in the same order as some normal, healthy part of the body to trigger an autoimmune disease response. 

In RA, an immune system attack is targeted for a specific protein, but that protein isn’t on an invading microbe; it’s in the synovial membranes. This leads to all the cardinal signs of inflammation: heat, pain, redness, swelling and loss of function. In later stages, the antibodies may also attack the heart, blood vessels, lungs and fascia.

Several pathogens have been identified that may initiate RA. They include a variety of Streptococcus bacterium, Borellia (the same bacterium that causes Lyme disease) and some retroviruses. Contracting and sustaining damage from RA begins with exposure to one of these pathogens. Here is an example of a typical progression of RA:

  • A person has a bout with strep throat. She goes through the usual process of producing T cells, B cells and antibodies. She wins the fight, and the bacterium is vanquished, but now she has a regiment of memory cells and antibodies in circulation, looking for any remnants of the invading microorganisms.
  • Her antibodies get confused. The proteins in synovial membranes have enough in common with the proteins in the strep molecules that her immune system raises the alarm and launches a full-scale attack. This is where genetics may play a role; this person’s antibodies are actually programmed to be “auto-antibodies.”
  • The synovial membrane thickens and swells. Fluid inside the joint capsule begins to accumulate, which causes pressure and pain.
  • The inflamed tissues release enzymes that erode cartilage, eventually right down to the bone. This is the process that causes the telltale deformation of the joint capsules, and “gnarled” appearance of RA. (See Figure 2, page 36.)
  • Fibrous scar tissue develops to connect the raw ends of the bones.
  • The scar tissue ossifies, and the joint is permanently fused.


Figure2. X-rays shows
the deformed joint capsules
in rheumatoid arthritis.

Actually, the disease doesn’t always progress all the way to the final two steps. As serious a condition as RA could be, it seldom fulfills the worst of its promises. After coping with the disease for 10 to 15 years, about 20 percent of affected people are in remission. Most are able to retain full-time employment. After 15 to 20 years of living with RA, only about 10 percent of affected persons are permanently disabled.

Signs and Symptoms. Symptoms of RA vary considerably at the onset of the disease. For many people there is a period of weeks or months when they experience a general feeling of illness: lack of energy, lack of appetite, low-grade fever and vague muscle pain, which gradually becomes sharp, specific joint pain. About 10 percent experience a sudden onset with joint pain alone. Rheumatic nodules, small, painless bumps that appear around fingers, elbows, and other pressure-bearing areas, are also common indicators of the disease.

In the acute stage, the affected joints are red, hot, painful and stiff, although they improve considerably with moderate amounts of movement and stretching. The joints RA most often attacks are the knuckles in hands and toes. It can also appear in ankles and wrists; knees are less common, and one of the rarest (and most serious) places to get it is in the neck. It generally affects the body bilaterally, although it will sometimes be worse on one side than the other.

Complications. If someone has rheumatoid arthritis, it means her immune system is confused about what it should be fighting off. Synovial membranes are just one of the types of tissue that may be attacked. Other possibilities include:

  • Rheumatic nodules on the sclera (“whites”) of the eyes;
  • Sjögren’s syndrome (pathologically dry eyes and mouth);
  • Pleuritis, which makes breathing painful and increases vulnerability to lung infection;
  • Pericarditis, or inflammation of the pericardial sac, around the heart;
  • Vasculitis, or inflammation of blood vessels. This complication carries another set of risks: Raynaud’s phenomenon, skin ulcers, bleeding intestinal ulcers and internal hemorrhaging.

Bursitis and anemia are also common complications of RA, especially when onset of the disease occurs in childhood.

Advanced structural damage also brings a set of complications. Deformed and bone-damaged joints may dislocate or even collapse, rendering them useless. The tendons that cross over distorted joints sometimes become so stretched that they snap. If the disease is at the C1-C2 joint and there is a collapse, the resultant injury to the spinal column may even result in paralysis. 

Diagnosis. There are many clues that help to differentiate RA from osteoarthritis. RA is not a result of age and joint wear and tear. It does not target the weight-bearing joints; it tends to act symmetrically on the body, rather than simply where the most use has worn down a joint. Nonetheless, it can be difficult to distinguish between the two conditions.

RA is typically diagnosed through a description of symptoms, X-rays, and a blood test to check for rheumatoid factor, a substance that is present in most, but not all, cases. Even then, the diagnosis is sometimes not considered conclusive until the patient has been under observation for a long while.

Treatment. Once the presence of RA has been confirmed, the first line of defense is to try to prevent the disease from progressing. New drug therapies have been developed toward this goal. Emotional and physical trauma have also been seen to exacerbate RA attacks; it’s as if the body gets ready to defend itself against something, but it can’t figure out what. Therefore, keeping the patient as healthy and stress-free as possible is important; rest and moderate exercise are key parts of the program.

Other treatment strategies revolve around the goals of minimizing pain and retaining maximum muscle health and joint function. Physical therapists are sometimes recommended to set up exercise programs. Medications may include drugs for pain relief and anti-inflammatories. If the disease continues to get worse, cytotoxic drugs are sometimes used in an effort to reduce white blood cell and antibody activity.

Surgery is seldom considered anything but a last resort for RA patients. If just one joint has been damaged, and if the damage is quite severe, a synovectomy, or removal of the synovial membrane, is sometimes performed. Joint replacements are another option. One fairly new and radical procedure is being used for very extreme cases of RA; it is called plasmapheresis. This procedure was originally developed to aid in the removal of heavy metals and other toxins from the bloodstream. Now it has a broader application. Blood is continually drawn, the aggravating factors (in this case antibodies) removed, and then replaced into the body. It takes several hours at a time, and has a list of serious side effects and complications, so it is seldom used.

Massage? In its acute phase, RA is an inflammatory condition caused by agents in the circulatory system. Anything that increases circulation will also increase the chance that the disease will spread to other joints in the body. In its subacute phase, RA leaves the joints stiff but not inflamed, and the muscles and tendons around them stressed and tight from chronic pain. RA indicates massage in the subacute stage. Massage can improve mobility and the health of the soft tissues surrounding the joints. In addition to the structural benefits it offers, massage can also be an important part of the keep-healthy-and-stress-free part of prevention strategy. If massage can help to balance the autonomic nervous system, it may also help to reduce the incidence of attack.

•••

Adapted from A Massage Therapist’s Guide to Pathology by Ruth Werner and Ben E. Benjamin, published by Lippincott Williams and Wilkins, Baltimore, Maryland.

•••

Figure 1: Reprinted with permission from Eideken J. Roentgen. Diagnosis of Diseases of Bone, Volume 2, 3rd ed. Baltimore: Lippincott Williams & Wilkins, 1981: 841.

Figure 2: Reprinted with permission from Harris JH Jr, Harris, WH, Novelline RA. The Radiology of Emergency Medicine, 3rd ed. Baltimore: Lippincott Williams & Wilkins, 1993: 440.

•••

Ben E. Benjamin, Ph.D. in sports medicine and education, is the founder and president of the Muscular Therapy Institute in Cambridge, Massachusetts. In private practice for more than 35 years, he is the author of dozens of articles.

Ruth Werner, teacher and massage therapist, has taught every aspect of the massage therapy curriculum at the Brian Utting School of Massage in Seattle, Washington.

Click here to return to Journal

© Copyright 2001, American Massage Therapy Association