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Chronic inflammation of the synovium may cause sensory and sympathetic nerve fiber depletion. The synovium is a membrane found in joint cavities, which secretes fluids. Researchers induced arthritis in rats by three different methods. Afterwards, the rats' synovia were analyzed for signs of inflammation and nerve depletion. Rats with latex-induced arthritis showed mild inflammation in the synovium with no signs of nerve depletion. Those with antigen-induced and hydrogen peroxide-induced arthritis showed signs of inflammation and nerve depletion. Only areas of inflammation had evidence of nerve depletion. The inflamed areas had evidence of macrophage and lymphocyte infiltration. These findings suggest that lymphocytes and macrophages, both part of the immune system, have a role in the depletion of nerve fibers.

The enzyme thrombin appears to have a role in both the inflammatory and healing process of rheumatoid arthritis (RA). RA is a systemic disease usually affecting the joints. Thrombin aids in the formation of blood clots. It causes plate aggregation leading to blood coagulation. Thrombin contributes to the inflammatory process by upregulating the synthesis of arachidonic acid. This leads to the proliferation of synovial cells in joints affected by RA. Fibroblasts may inhibit the inflammatory effects by releasing the thrombin inhibitor PN-1 in a dose-dependent relationship. In addition, thrombin and basic fibroblast growth factors can collectively initiate healing through cellular proliferation and angiogenesis, the development of blood vessels.

The lymphocytes of patients with certain autoimmune diseases may be more vulnerable to reactive species of oxygen than those from healthy individuals. This may result in more damage to DNA and higher susceptibility to killing by hydrogen peroxide. Autoimmune diseases are characterized by an immune response against the body's own tissues. Oxidative damage to DNA was examined in lymphocytes from patients with various autoimmune diseases and from healthy individuals (control group). Significantly more oxidative damage to DNA was found in the lymphocytes of patients with autoimmune diseases than in those of the control group. The toxic effects of hydrogen peroxide were greater in the lymphocytes of patients with systemic lupus erythematosus and rheumatoid arthritis. Increased susceptibility to hydrogen peroxide was not observed in the lymphocytes of scleroderma patients.

Foam cells that contain oxidized low density lipoprotein (LDL) may be present in the synovial membranes of patients with rheumatoid arthritis (RA). RA is a inflammatory disease that affects the joints. The synovial membrane lines the inside of the joint cavity. Researchers examined the presence of foam cells with oxidized LDL in synovial membrane specimens from RA patients and patients without RA who had had knee injuries. Macrophages with the characteristics of foam cells were found in close proximity to blood vessels in the specimens from RA patients. Scattered foam cells were also found in conjunction with deposits of fibrin. Foam cells were not found in the specimens from patients without RA. The development and progression of RA may have certain similarities to that of atherosclerosis. Foam cells may play an important role in the formation of atherosclerotic plaques.

Patients suffering from rheumatoid arthritis often develop anemia. Rheumatoid arthritis is an inflammatory disease that affects the joints. Anemia in patients with rheumatoid arthritis is caused by abnormalities in iron metabolism. These abnormalities result in decreased blood levels of iron and hemoglobin but increased blood levels of ferritin, the iron storage protein. Decreased blood levels of iron may be caused by abnormalities in the release of iron from cells of the reticuloendothelial (RE) system. The RE system plays a central role in iron storage and release in the body. Ferritin often is deposited in the joints of patients with rheumatoid arthritis. This accumulation of ferritin in the joints may be associated with the level of anemia. The level of disease activity may also be determined by the amount of ferritin accumulated in the joints.

Endothelial cells form the smooth lining of blood vessels. Previously these cells were thought to function only as a permeability barrier, allowing selected molecules to cross from blood into tissues. Now, however, these cells are known to be very active, producing regulatory hormones and molecules, and contributing to the control of processes such as coagulation (clotting), platelet activity, blood vessel tone (extent of constriction) and growth, and white blood cell (leukocyte) traffic. Endothelial cells can be activated to perform new functions, such as increasing adhesion of particular leukocytes to the endothelium. This is important to arthritis because increased movement of inflammation-associated leukocytes into joint tissues may be an important step in the development of synovitis (joint inflammation). Adhesion between neutrophils, a type of leukocyte, and endothelial cells is increased over hour-long periods by cytokines, hormones made by immune cells. Adhesion of lymphocytes, a type of immune cell, to particular types of endothelium is also enhanced by local molecules produced in response to cytokines. Improved techniques have shown the presence of some cytokines in synovial fluid taken from patients with rheumatoid arthritis. This work is only the beginning of understanding the relationship between activated endothelium and the inflammation of rheumatoid arthritis. Results from studies using cultured (laboratory-grown) endothelial cells will continue to be valuable. (Consumer Summary produced by Reliance Medical Information, Inc.)

An enzyme called thrombin may be an important factor in initiating the inflammation process in the joints of patients with rheumatoid arthritis. The presence of thrombin receptors was determined in tissue samples from 4 normal joints, 16 joints with osteoarthritis, and 20 joints with rheumatoid arthritis. All of the samples from patients with rheumatoid arthritis had many cells with thrombin receptors while only a few of the other sample cells contained these receptors. Receptors for a non-specific enzyme called esterase were also present in some samples from patients with rheumatoid arthritis.