What is rheumatology? |

Science and Profession

Rheumatology is concerned with the major diseases of bones and joints: arthritis, osteoarthritis, other arthritic disorders such as gouty arthritis, and ankylosing spondylitis, among a host of others.

The onset of rheumatoid arthritis is usually in middle age. It strikes three times as many women as men. To understand the disease, it is necessary to understand the body’s skeletal system—the bones and bone structures, as well as the tissues between and around bones and joints.

There are 206 bones in the human body. Some function as support mechanisms that hold the body erect and support the weight, such as the spine and the bones of the hips and legs. Some bones form defensive “cages” that protect body organs, such as the skull and the ribs. Some bones are involved in movement, specifically the bones in the spine, shoulders, arms, hands, hips, legs, and feet.

Bones are composed of three main sections. The tough membranous tissue that covers the bone, the periosteum, contains the blood vessels that nourish bone cells and the nerve fibers that sense pain and pressure. The outer layer of the bone itself is called compact bone; it forms the hard exterior. Inside is a spongy inner structure called cancellous (chambered) bone. Cancellous bone contains the marrow that manufactures blood cells, and it also stores fat cells.

When bones meet, the structure formed is called a joint, or articulation. Some joints are fixed, such as the ribs and the bones of the skull; they are called fibrous joints because a tough, fibrous adhesive material connects them, prohibiting movement and maintaining the integrity of the protective cage.

Some joints are capable of motion. Moving joints are of two types: synovial joints and cartilaginous joints. An example of the latter is the spine, where each vertebra is connected to its neighbor by a spinal disk made of cartilage. Cartilaginous joints are capable of movement, but they have nowhere near the mobility of the synovial joints, so called because they are filled with synovial fluid, a liquid resembling the white of an egg.

There are six kinds of synovial joints: ball-and-socket, ellipsoidal, hinge, pivot, saddle, and gliding joints. Ball-and-socket joints are found in the shoulders and hips. In these joints, a long bone—the femur in the leg and the humerus in the arm—end with a ball-shaped structure that fits neatly into a round, concave socket. Ball-and-socket joints are capable of the widest range of movement. Ellipsoidal joints are modifications of the ball-and-socket structures, where the bones are not round but oval. They are found in the wrists and ankles. The elbows and knees are hinge joints, which permit only bending and extending motions, up and down or side to side, as with a common door hinge. In pivot joints, one bone contains a small cup or arch that accepts a point of another bone, permitting it to rotate on its axis. The two bones at the top of the spine, which govern the range of motion of the head, are examples. A saddle joint consists of two bones, shaped rather like saddles; they fit snugly into each other and allow a wide range of movement. The joint connecting the thumb to the rest of the hand is the only saddle joint in the human body. The bones of gliding joints are almost flat; their surfaces slide over one another, permitting limited motion forward and back or from side to side. Some of the wrist bones are gliding joints.

The synovial joints are the most intricate and mobile of all the joints, and they are also the most prone to disease. The synovial joint capsule is a complex structure that encloses the moving bones and other tissues. It consists of the capsular ligament, which forms the joint capsule; the joint cavity, an open space between bones that allows free mobility; and the synovial membrane, a thin, smooth tissue that secretes synovial fluid. The synovial fluid fills the joint cavity and lubricates bone surfaces. Bones do not actually rub against each other; they are too rough and would become abraded. They are separated by a covering of smooth, white tissue called articular cartilage that permits smooth movement and absorbs impact. Just outside the joint capsule are bursae, small pouches that store synovial fluid.

In rheumatoid arthritis, the first signs of disease are pain and inflammation in the synovial joint capsule. This initial manifestation may be attributable to a number of factors, such as bacterial infection or injury. The reasons that an acute episode of pain and inflammation in the synovial joints progresses to chronic rheumatoid arthritis are unknown. It is suspected that genetic factors may be involved; the disease often runs in families. Blood components called rheumatoid factors are present in the majority of rheumatoid arthritis patients. The role of these factors in the development of disease, however, is unclear because rheumatoid factors are also found in people who do not develop rheumatoid arthritis.

In some patients, rheumatoid arthritis is relatively benign, with pain and inflammation that can be controlled by medication and other support techniques. In other patients, the disease progresses to devastating bone deformities and complete loss of mobility in the affected joints. How this degeneration occurs is related to a disruption in the body’s normal reaction to infection or injury. Pain and inflammation are protective mechanisms with which the body attempts to compensate for a disease or disorder. The following sequence of events is what normally occurs when a synovial joint is damaged by infection, physical injury, or a toxic substance.

Tissue injury—from trauma or infection—causes the release of chemical mediators from surrounding cells. These chemicals include prostaglandins, leukotrienes, histamine, serotonin, and bradykinin. Collectively, they cause the local blood vessels to enlarge (vasodilate), increasing blood flow to the affected area and causing redness and heat.

Ordinarily, the capillaries, the tiny blood vessels that supply nutrients to the cells, have openings in their walls so small that only tiny bits of matter can get through. During inflammation, they become more permeable; that is, the openings in the capillary walls enlarge so that the capillaries can deliver larger substances to the affected area. This group of substances forms the capillary exudate, and it flows copiously into the affected area, causing swelling. The exudate consists of lymphocytes, which produce antibodies to fight infection; neutrophils; and macrophages, specialized white blood cells that facilitate the removal of tissue debris, dead cells, and other material. These white blood cells can also release other substances, such as superoxide, an agent used by white blood cells to kill bacteria but which can also damage healthy tissue. Another is interleukin-1, an agent that promotes healing and stimulates lymphocytes to produce antibodies. The spread of inflammation is prevented by a third agent released by the white blood cells, fibrinogen, which effectively closes off the area of inflammation.

In normal situations, the agent causing the inflammation is neutralized, the capillaries return to their normal size, certain white blood cells remove the protective shield, and the healing process begins. In rheumatoid arthritis, the orderly process that begins with pain and inflammation and ends with healing is disrupted by various events. Instead of neutralizing the trauma, the anti-inflammatory phase can set off a chain of events that makes the condition progressively worse.

Why this disruption occurs is not yet known, but four major theories have been suggested. The first is the theory of genetic predisposition to the disease, a factor which may or may not relate to the other three. The second theory is that rheumatoid arthritis is an immune-complex disease. Ordinarily, when the body fights an infectious microorganism that has invaded the body, lymphocytes produce antibodies that combine with the antigens characteristic of the microorganism. This antigen/antibody combination is the immune complex, and it is removed by other white blood cells. In this theory, the process is altered. Instead of being removed by white blood cells, the immune complex lodges in the synovial membrane and causes continuing inflammation. Capillaries continue to release exudate, whose constituents cause cell proliferation, thickening of the synovial membrane, and destruction of articular cartilage and bone tissue.

The autoimmune theory is similar, but in this case the causative agent is not a foreign substance but something natural within the body. For example, if a specific protein released by a gland finds its way into a joint, it may be regarded as a foreign, infective agent. Thus it will set off an immune response and cause inflammation, initiating the same process described above.

The fourth theory links rheumatoid arthritis to viral or bacterial infection. It has been noted that fever, malaise, and enlarged lymph nodes—common symptoms of infection—are often seen in patients with rheumatoid arthritis. Furthermore, rheumatoid arthritis sometimes occurs simultaneously with bacterial pneumonia, tuberculosis, hepatitis, and sexually transmitted diseases, as well as with diseases caused by viruses, such as mumps and measles.

The progress of rheumatoid arthritis is variable. In some patients, it is characterized by occasional flare-ups (episodes of acute pain and inflammation) and periods of remission (times when the patient is relatively comfortable). In others, the disease causes progressive, insidious destruction of the joint and may involve other organs of the body. Articular cartilage may be destroyed, and the joint may become immobilized, an extremely painful condition. The bones in the joint may fuse together, becoming one solid mass. The bones may also become dislocated. In about 30 to 35 percent of patients, rheumatoid nodules develop. These hard, solid lumps usually occur at the elbows but may also be found at the knees, ankles, and feet. In advanced cases, nodules may be discovered in the heart muscle, the lungs, and other organs where they could impair organ function.

The diagnosis of rheumatoid arthritis has been codified by the American Rheumatism Foundation. This organization lists seven symptoms and suggests that the presence of any four should confirm the diagnosis of rheumatoid arthritis (although patients with two or more of the symptoms should not be excluded). The seven symptoms are morning stiffness lasting an hour or more; arthritis in three or more joints; arthritis in hands, fingers, or wrists; arthritis occurring symmetrically (for example, in both hands, elbows, or knees); rheumatoid nodules; the presence of rheumatoid factor; and x-ray evidence of bone deterioration.

Diagnostic and Treatment Techniques

Once a patient is suspected of having rheumatoid arthritis, the physician may wish to conduct further laboratory tests to assess the severity of the disease and, from that analysis, develop a treatment regimen. In addition to testing for rheumatoid factor, the physician will check the patient’s erythrocyte (red blood cell) sedimentation rate (ESR). This test helps to determine the presence of inflammatory activity. Another blood test looks for C-reactive protein (CRP). CRP also indicates inflammatory activity; levels rise during an acute attack and fall during a period of remission. Synovial fluid is analyzed to discover changes that occur during inflammation. For example, during inflammatory episodes, the color of the fluid becomes significantly darker, turning yellow or green. Ordinarily quite clear and viscous, it becomes cloudy and thinner in consistency. Many more tests are available to the physician to help him or her evaluate the severity of the disease, including an analysis of the various substances involved in the immune process.

There is no cure for rheumatoid arthritis, but most patients can be helped with the therapies available. In spite of treatment, however, 5 to 10 percent will eventually be disabled by bone deterioration and destruction.

Treatment depends on the severity of the condition. The regimen can simply involve rest and immobilization of the affected joint, or it may include any of a wide range of medications, from aspirin to potent, often toxic compounds. In advanced cases, joint deformity may be so severe as to require surgery or prosthetic implants.

The goals of therapy are to relieve pain, reduce inflammation, and maintain the function of the joint. Ideally, the physician would also like to halt the progress of the disease. Some medications in use today promise to slow or stop the progress of the disease, but nothing is available to cure it.

For the relief of pain, the physician has a large number of medications available, many of which will also reduce inflammation. These include a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs as a class include the salicylates, such as aspirin, ibuprofen, acetaminophen, and at least twenty other drugs currently in use in the United States.

Far and away the largest number of patients with rheumatoid arthritis are being treated with NSAIDs. Many of the NSAIDs are perfectly safe when used in lower doses. At the high doses often required to control the pain of rheumatoid arthritis, however, they can cause significant adverse reactions. A significant percentage of patients given some NSAIDs develop side effects severe enough to warrant stopping the drug. Many develop gastrointestinal (GI) problems ranging from stomachaches to bleeding ulcers, which can be fatal.

One of the ways in which NSAIDs work is to reduce the production of prostaglandins, substances released in the capillary exudate that are partially responsible for the inflammatory process. At the inflamed synovial joint, this attribute of NSAIDs is a desirable one. In the stomach, however, NSAIDs can cause problems. One of the prostaglandins helps to protect the stomach lining from damage by the organ’s highly acid contents. NSAIDs can remove this protection, allowing stomach acids to attack the lining, causing irritation and inflammation. Therefore, some physicians prescribe an NSAID with a prostaglandin analog, such as misoprostol, in the hope of avoiding or reducing GI distress. Misoprostol has problems of its own, however, such as causing severe diarrhea in some patients.

For the patient with severe rheumatoid arthritis—defined as painful, debilitating illness that does not respond to NSAIDs and is progressing to deformity—the available medications are both more potent and more toxic. A group of agents called disease-modifying drugs promise to reduce the degenerative processes in rheumatoid arthritis. These drugs include gold compounds, D-penicillamine, drugs used to treat malaria, and sulfasalazine. They appear to alter the course of rheumatoid arthritis, but they do not relieve pain or inflammation, so they must be given with NSAIDs. They all have a high potential for toxicity and must be used carefully, with constant monitoring, to avoid serious side effects.

In some cases, physicians find it necessary to prescribe corticosteroids to patients with rheumatoid arthritis. These drugs present a problem, because rheumatoid arthritis is a lifelong condition, and toxicity and physical changes often occur with long-term steroid therapy. Sometimes corticosteroids are given as short-term therapy to achieve a rapid reduction of inflammation. In this case, there is a danger of a severe rebound reaction when the drug is stopped. A corticosteroid may be administered as an injection into the joint, which is an effective short-term procedure to bring fast relief of pain and inflammation in an acute situation.

Immunosuppressive therapy is sometimes prescribed for patients with rheumatoid arthritis. Immunosuppressive agents have the potential to be highly toxic, and their use is reserved for patients who have not responded to other treatments.

Exercise and physical therapy are useful to the patient with rheumatoid arthritis. During acute inflammation, passive exercise within pain limits, with the limb manipulated by another person or the patient, will help keep the joint mobile and prevent muscle tightening. After the inflammation has subsided, active exercise is recommended to maintain muscle mass and mobility, but the activity should never be strenuous or fatiguing.

Flexion contracture, a condition in which the muscles that move the joint become stiff and shortened, may respond to exercise. If the contracture has become established, however, then more intensive exercise, splinting, or orthopedic treatment may be necessary.

Orthopedic surgery to correct fused or dislocated joints can be performed on any joint in the body, and in some cases, a fused or badly deteriorated joint can be replaced with an implant of metal or plastic (arthroplasty). The two most successful implant procedures are total replacement of the hip or knee. When a hip is replaced, the surgeon reveals the joint where the ball of the femur nests in the socket of the acetabulum, a cavity in the hipbone. The ball of the femur is replaced by a metal or plastic ball attached to a shaft that is anchored inside the femur. The socket is replaced as well, usually with a plastic cup that is anchored into the hipbone. The implant can give the patient instant relief from pain and restore mobility. The length of time that the hip replacement will last varies, but many patients receive years of relief from a single operation. A similar procedure is used to replace the hinge joint of the knee, and, although knee replacement is not as successful as hip replacement, it has helped many patients.

Perspective and Prospects

Rheumatoid arthritis afflicts about 1 percent of all populations. While the disease is not life-threatening, it is one of the most significant crippling disorders in the world. Most patients can be treated successfully by medication, exercise, and other support measures. The disease is progressive in most patients. After ten years, 80 percent of patients will have some degree of deformity, ranging from minor destruction of bone and cartilage to complete fusion of the joint.

Some patients medicate themselves with over-the-counter painkillers and rarely, if ever, see a physician. It is to be expected that, in these patients, the disease is mild, with acute episodes occurring only sporadically. The majority of patients with moderate-to-severe rheumatoid arthritis are seen by physicians.

Currently, there is no perfect therapy for rheumatoid arthritis, in the sense that there is no one agent or family of agents that promises to be safe and effective in all patients. The danger of significant adverse reactions exists with most drugs that are effective, particularly in those patients who require high doses to control the pain and inflammation of the most severe forms of the disease.

Pharmaceutical science continues to search for new medications that will relieve pain and inflammation without damaging side effects. New drugs that will stop the progress of the disease safely and effectively are also sought. There is also the hope that rheumatoid arthritis will be curable or preventable one day.

Orthopedic surgeons continue to improve the techniques for alleviating the effects of bone and joint destruction that occur in some patients. New prosthetic appliances are designed and produced constantly in an effort to widen the range of joint replacement procedures.

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