Several studies recently reported a potentially beneficial effect

Several studies recently reported a potentially beneficial effect of low dose, short term sys temic though glucocorticoids on BMD in RA due to its anti inflammatory effects. Although this study was not designed to address a potential role of disease modi fying anti rheumatic drugs including TNF a inhibitors in the risk of osteoporotic fracture among RA patients, there is some evidence Inhibitors,Modulators,Libraries suggesting a beneficial effect of such drugs on bone loss. The exact effects of glucocorticoids or disease modifying anti rheumatic drugs on the risk of fractures in RA should be further studied. Conclusions Our study found that patients with RA are at an increased risk of osteoporotic fractures across age groups, sex and various anatomic sites. An independent association between the use of oral glucocorticoids and fracture risk was confirmed.

Future research that evalu ates the effect of RA treatments on the risk of osteo porosis would be important. Introduction Rheumatoid arthritis is a chronic systemic autoim mune disease that predominantly affects multiple peripheral synovial joints. The Inhibitors,Modulators,Libraries synovial environment has numerous inflammatory cells such as T cells, B cells, fibroblast like synoviocytes and antigen presenting cells, which can cause the development of RA. FLSs constitute the synovial lining cells that have a key role in pannus formation and destruction of joints. In addition, numerous cytokines have Inhibitors,Modulators,Libraries been implicated in the immune processes that are associated with RA. T cells, the most invading type of lym phocyte in the RA synovium, can contact and activate FLSs.

A variety of in vitro and in vivo models have shown that TNF Inhibitors,Modulators,Libraries dependent networks are involved in critical pathogenic interactions in Inhibitors,Modulators,Libraries RA synovitis. In recent years, new novel cytokines such as IL 17 and IL 32 have been reported to be involved in the pathogenesis or regulation of synovial inflammation. selleck IL 17, a proinflammatory cytokine produced by T helper 17 cells, plays a key role in the propagation of joint inflammation, cartilage destruction and bone erosion, and it is present in both the synovium and synovial fluid. IL 17 participates in the joint inflammation of RA via activation of T cells and FLSs by secreting cytokines and chemokines such as IL 6, IL 8, 1L 16, stromal cell derived factor 1, matrix metalloproteinase 3 and MMP 1. Moreover, IL 17 is well known as a strong inducer of osteoclastogenesis. IL 32, a recently discovered cytokine, was originally described as natural killer cell transcript 4. IL 32 has four splice variants, IL 32a, IL 32b, IL 32 and IL 32g, with IL 32a as the most abundant transcript, and IL 32g as the most active isoform. The expression of TNF a and IL 6 are significantly correlated with IL 32g expression.

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