STAGES OF RA (RHEUMATOID ARTHRITIS): STAGES 1 AND 2

Stage 1 (normal). In this stage, people with RA have no symptoms of arthritis, and their joints appear normal. Some of these people may be genetically susceptible to arthritis. Having the HLA-DR4 gene alone is not sufficient to cause someone to develop RA, however. It is presumed that some unknown trigger initiates the development of arthritis in the genetically susceptible person; that is, an unknown factor triggers the inflammatory process, and other unknown factors keep it going, apparently blocking normal resolution. One theory is that in RA, the communication between cells is disturbed in some way, allowing ongoing inflammation to occur.
Stage 2. This is the stage during which people with RA first have symptoms. Early in the course of arthritis, small lymphocytes migrate to the synovial lining, causing what is called synovitis or “inflammation of the synovium”. The macrophages and lymphocytes continue to promote inflammation by producing cytokines, the chemical signals that are sent from one cell to another. There are several cytokines being studied, and new ones are discovered all the time. We are just starting to appreciate their individual roles and how they help produce the symptoms of RA. Cytokines can induce an increase in the number of blood vessels going to the synovium, and with increased blood flow, the joints become warm. The leakage of cytokines into the bloodstream may also contribute to the fatigue that is so common in RA. Other cytokines are partially responsible for stimulating cells to produce prostaglandins and leukotrienes, both of which are potent producers of inflammation. Continued production of cytokines, prostaglandins, leukotrienes, and other substances leads to swelling, warmth, and pain in the joints.
It is also during this stage that В lymphocytes are transformed into another type of white blood cell, the plasma cell, which manufactures antibodies. Antibodies, also referred to as immunoglobulins, are distinctive proteins that the body normally produces to fight against foreign viruses and bacteria. In RA, for reasons that are unclear, the body appears to produce an excessive amount of antibodies. One particular antibody often found in the blood of people with RA is called the rheumatoid factor.
The production of rheumatoid factor exacerbates the inflammatory process.
Stage 3. In this stage there is a marked increase in the number of cells in the synovium, possibly stimulated by the presence of different cytokines. The synovium becomes much thicker, or hypertrophied, and this makes the joint feel doughy or spongy. An increase in the amount of synovial fluid in the joint adds to the stiffness and limitation of motion of the joints. (Accumulation of joint fluid is known as joint effusion.)
With RA there is also an increase in hyaluronic acid, the lubricating substance in the synovial joint fluid. Many people believe that increased hyaluronic acid is responsible for morning stiffness (or morning gelling) and stiffness experienced after sitting for a prolonged period of time without moving (gelling phenomenon).
Joint fluid contains inflammatory white blood cells called neutrophils (or polymorphonuclear leukocytes). (Why lymphocytes reside in the synovial lining and neutrophils appear in the synovial fluid is unclear.) In the joint affected by RA, neutrophils join lymphocytes in perpetuating the inflammatory process. In testing for RA, the physician may remove a sample of fluid from the joints to determine the relative proportions of these cells present. This helps the physician differentiate RA from other forms of arthritis.
A person in any one of the three earliest stages of RA may experience significant joint symptoms including pain, heat, swelling, stiffness, and loss of motion. All of these inflammatory changes are potentially reversible with proper medical therapy.
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