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Define Rheumatoid Arthritis
Rheumatoid Arthritis
Introduction
Rheumatoid arthritis (RA) is a systemic inflammatory disease defined by its (joint) manifestations. The arthritis of RA is an inflammatory, symmetrical, progressive, destructive process that attacks primarily the small proximal joints of the upper and lower extremities, although all joints in the body, except for those of the thoracic and lumbosacral spine, can be affected. The disease afflicts about 1.5% of the North American population, meaning that approximately 4.5 million Americans have RA. Women are affected three times as often as men. The disease usually begins during the childbearing years, but because it is a chronic, incurable disorder, the peak prevalence is seen in the seventh decade of life. Although RA is often considered to be simply a painful, debilitating arthritis, it is, in fact, a systemic disorder that has a significant impact on mortality. Only 30 years ago the 5-year survival for patients with RA was the same as that for stage IV Hodgkin's disease or triple vessel coronary artery disease (1). Fortunately, the past 3 decades have seen significant advances in the diagnosis and treatment of RA. Although the disease is not yet curable, the painful, inflammatory arthritis can almost always be controlled, and the likelihood of joint deformities has dramatically decreased, as has the incidence of internal organ involvement and non-articular tissue damage. The long-term outlook for patients with RA is now far better than it was just a few short decades ago.Etiology
Genetics play a major role in the etiology of RA (2). The incidence of the disease is different in different populations. Although RA is seen in 1.5% of Caucasians it affects over 5% of certain Native American populations, occurs in only 0.2% of the population of Japan and China, and affects less than 0.1% of rural Africans. Part of the difference in prevalence is due to differences in specific major histocompatibility (MHC) genes that determine the surface characteristics of immune and inflammatory cells throughout the body. The products of these genes, termed Human Leukocyte Antigens (HLA), affect the ability of immune cells, or immunocytes, to recognize and bind to foreign or invading substances and to communicate with other immunocytes. In Western European populations the presence of certain subsets (called alleles) of the HLA-DR4 gene imparts an increased susceptibility to RA, while in Israeli populations alleles of the HLA-DR1 gene appear to be most important. The precise role that these genetic factors play in the causation of RA is still not known.Since most people with the genes that make them susceptible to RA do not contract the disease, non-genetic factors must also play a role in disease causation. The disparity in the sexual prevalence suggests that hormonal factors may play a role in the initiation of the disease. However, it is not just the presence of female hormones that causes the sexual disparity, because frequently women with active RA go into remission during pregnancy, when the concentrations of most female hormones are at their highest. It is now clear that smoking tobacco can both trigger the development of RA and make it worse in patients who have the disease (3). Tobacco is thought to stimulate immune reactions in the lungs that lead to the production of abnormal peptides (cyclic citrullinated peptides) that, in turn, lead to the production of antibodies that may cause disease. Lastly, experimental evidence suggests that bacterial or viral antigens (substances found in microbes that can stimulate an immune response) may play a role in RA. Certainly, several viral infections, such as Parvovirus B19 infection or hepatitis C, can cause arthritic conditions that mimic RA. To date, however, no specific infectious agent has been shown to actually cause RA.
Pathogenesis
The inflammation seen in RA is due to a complex interaction of cellular and humoral factors (circulating serum proteins or enzymes) (4). The process is felt to begin when certain cells, called macrophages, ingest an as yet unidentified antigen. The macrophage then processes and presents this antigen to special lymphocytes, called T-lymphocytes, which initiate an immune response. For unclear reasons, this response is directed at normal joint structures. The immune response is mediated by numerous types of cells, including B-lymphocytes, which produce abnormal antibodies, and both effector T-lymphocytes and macrophages, which directly invade and attack target tissues. These immune cells, or immunocytes, produce numerous humoral factors, called cytokines, that damage and even digest articular and periarticular structures. The major target tissue of the immune response is the synovium, or lining of the joint. When the synovium becomes inflamed, it can invade and destroy the cartilage (the cushioning structure of the joint). Certain types of bone cells, called osteoclasts, are activated and begin to erode the bones of the joint. Physicians and scientists are just now beginning to understand the complex interactions of the many cellular and humoral mediators of the immune reaction. Understanding these interactions has already led to the development of new therapeutic interventions that inhibit specific cytokines and decrease the inflammatory process.Clinical Manifestations
Articular manifestations
RA usually presents as a polyarthritis (an arthritis affecting more than 3 joints) with a predilection for the wrists, the metacarpophalangeal joints (the "knuckles"), and the proximal interphalangeal joints (the finger joints closest to the knuckles) (5). Being symmetrical it tends to affect the same joints on both hands, and, because it is an inflammatory process, the joints are red, swollen, painful, and tender. One of the major components of the inflammation seen in RA is morning stiffness that lasts at least an hour. In untreated patients the stiffness may last all day. The stiffness is usually associated with the "gelling" phenomenon, which is daytime stiffness that occurs whenever a patient sits, lies down, or otherwise remains inactive for too long. With mild to moderate exercise, the pain and stiffness of RA actually improves. However, too much exercise, particularly in acutely inflamed joints, will worsen pain and may increase damage to articular and periarticular (around the joint) supporting structures. Although we define the process by involvement of the small proximal joints of the upper extremities, in fact, virtually every joint in both the upper and lower extremities, including the elbows, shoulders, hips, knees, ankles, feet, and toes, can be affected. Even the cricoarytenoid joints of the vocal cords can become arthritic. Thirty percent of patients will develop cervical spine disease, particularly at the articulation of the first and second cervical vertebrae. Inflammation of the joints of the neck may lead to laxity of the ligaments that stabilize the cervical spine, rendering RA patients susceptible to catastrophic misalignments of the spine, with damage to the spinal cord and radicular nerves. The thoracic and lumbosacral spine, as well as the sacroiliac joints, are, for unknown reasons, spared.The damage done to the joints and periarticular supporting structures can lead to characteristic permanent deformities. The damage is caused by cellular and humoral inflammatory processes that erode cartilage and bones and digest the joint capsule and the periarticular soft tissues. Infla
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