Rheumatoid arthritis pathogenesis

In the pathogenesis of many chronic inflammatory diseases (e.g., rheumatoid arthritis, glomerulonephritis, colitis ulcerosa, Morbus Crohn, atopic dermatitis, psoriasis) autoimmune processes play an important role, too. Although first of all nonsteroidal antiinflammatory agents or glucocorticoids should be applied, immunosuppressive agents may also be indicated. 

Human chronic inflammatory diseases are characterized by populations of cells with altered regulation and function. A large body of evidence suggests that many of these cellular abnormalities may be linked to an increase in the production of free radicals and/or deficiencies of antioxidant defence systems. Oxygen free radicals attack cell structures, altering their function, and are cytotoxic. They have therefore been implicated in the pathogenesis of rheumatoid arthritis as well as many other human diseases (HaUiwell, 1991). 

Rothschild, B.M. and Masi, A.T. (1982). Pathogenesis of rheumatoid arthritis a vascular hypothesis. Semin. Arthritis Rheum. 12, 11-31. 

Human leukocyte elastase is a protease that degrades elastin and other connective tissue components. It is implicated in the pathogenesis of pulmonary emphysema and other inflammatory diseases such as rheumatoid arthritis and cystic fibrosis. Porcine pancreatic elastase has often been used as a model for HLE. Both enzymes have a small primary binding site Si. 

Goldring SR. Pathogenesis of bone and cartilage destruction in rheumatoid arthritis. Rheumatology (Oxford) 2003 42(Suppl 2) iil 1—6. 

Harris ED Jr. Pathogenesis of rheumatoid arthritis its relevance to therapy in the 90s. Trans Am Clin Climatol Assoc 1990 102 260-8 discussion 8-70. 

Anthony DD, Haqqi TM. Collagen-induced arthritis in mice an animal model to study the pathogenesis of rheumatoid arthritis. Clin Exp Rheumatol 1999 17(2) 240-244. 

Thomas R, MacDonald KP, Pettit AR, Cavanagh LL, Padmanabha J, Zehntner S. Dendritic cells and the pathogenesis of rheumatoid arthritis. J Leukoc Biol 1999 66(2) 286-292. 

A variety of medical conditions are now believed to be caused or exacerbated by overproduction of certain cytokines in the body. A variety of pro-inflammatory cytokines, including IL-6 and IL-8 as well as TNF, have been implicated in the pathogenesis of both septic shock and rheumatoid arthritis. Inhibiting the biological activity of such cytokines may provide effective therapies for such conditions. This may be achieved by administration of monoclonal antibodies raised against the target cytokine, or administration of soluble forms of its receptor which will compete with cell surface receptors for cytokine binding. 

There have been reviews of the mechanisms and adverse effects of glucocorticoids in rheumatoid arthritis (205) and the pathogenesis, diagnosis, and treatment of glucocorticoid-induced osteoporosis in patients with pulmonary diseases (206). Several mechanisms underlie the effect of glucocorticoids on bone, both biochemical and cellular. Effects on calcium are ... 

Increased levels of ROS due to oxidative stress have been consistently found in cardiovascular diseases as atherosclerosis or hypertension [18]. There is certain evidence that the free radicals involved in Parkinson s disease are mainly due to the production of increased levels of free radicals during oxidative metabolism of dopamine [19]. Oxidative stress, manifested by protein oxidation and lipid peroxidation (LP), among other alterations, is a characteristic of Alzheimer s disease [20] and in the pathogenesis of diabetes related complications. Treatment with antioxidants seemed to be a promising therapeutic option for these diseases [21], The inflammatory nature of rheumatoid arthritis implies that a state of oxidative stress may also exist in this disease [22,23]. Also, free radicals have a certain role in Huntington s disease [24,25], age related degeneration [26], and some autoimmune disorders [27],... 

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