The endothelium: its role in scleroderma

Article Abstract:

Altered blood vessel, or vascular, activity and anatomy is one of the problems associated with the development of systemic sclerosis, or scleroderma. Damage and dysfunction of endothelial cells, which form the smooth lining of blood vessels, seem to be a primary event. Formerly, these cells were thought to be inactive or to have the function of a selective permeability barrier for the passage of molecules and cells between the blood and tissues. However, endothelial cells are now considered to regulate many events related to blood and blood vessel function. Endothelial cells produce several factors including one that relaxes, or dilates, blood vessels, and another that causes vasoconstriction. Disturbance of the endothelial barrier during inflammation increases permeability to salts and large molecules such as proteins, leading to edema (fluid accumulation). Binding of inflammation-related white blood cells, such as neutrophils, to endothelium increases with inflammation, and this can also augment vascular permeability. Endothelial cells also produce molecules that can block clot formation and enhance clot breakdown. Among other interactions with white blood cells, endothelial cells may enhance the processes leading to antibody production. Most patients with scleroderma have Raynaud's phenomenon, in which the fingers turn white, and possibly blue and then red, in response to cold or emotions. Excessive vasoconstriction is one problem underlying this condition; abnormal loops in capillaries may also be involved. Altered levels of endothelial-derived factors occur, and endothelial damage may be related to the presence of autoantibodies (antibodies inappropriately made against the body's own molecules.) Research suggests that failure of endothelial regulation may contribute to abnormal vascular tone and permeability. Endothelial cells may also mediate immune reactions that may then damage small blood vessels and, eventually, endothelial cells themselves. Further studies are needed before researchers understand how these different mechanisms contribute to the development of scleroderma. (Consumer Summary produced by Reliance Medical Information, Inc.)

Abnormalities, Systemic scleroderma, Scleroderma (Disease), Endothelium

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Vascular endothelium, cytokines, and the pathogenesis of inflammatory synovitis

Article Abstract:

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.)

Cytokines, Vascular endothelium, Synovitis

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Intra-articular pressure profile of the knee joint in a spectrum of inflammatory arthropathies

Article Abstract:

Inflammatory arthritis may cause a loss of control of the pressure of the synovial fluid within the joint and lead to recurring injuries due to local oxygen deprivation. The intra-articular pressure (IAP) in the knees of 33 patients was measured at rest and during leg muscle contractions. One group had knee swelling due to an injury, the other three groups had inflammatory causes for the swelling. The IAP rose significantly with exercise in all but the injury group. This abnormal pressure may prevent blood flow and cause a lack of oxygen to the joint.

Knee, Joint diseases, Synovial fluid

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