Osteoimmunology: immunological mechanisms in pathogenesis of postmenopausal

The most widespread form of osteoporosis is post-menopausal osteoporosis. Its main reason is estrogens defi ciency. However, the mechanisms of bone weightloss at estrogens defi ciency are not limited to model of direct control actions of these hormones on bone tissue cells and are considerably more diffi cult. The data obtained are the evidence of interrelation between immune system and bone tissue and are of essential signifi cance for immune mechanisms in a pathogenesis of osteoporosis.Last year’s scientifi c research showed that the dominant role in a regulation of osteoclasts diff erentiation and activation was given to the two cytokines – amacrophage colony-stimulating factor and a receptor activator of nuclear factor kappa-B ligand (RANKL). In addition, for osteoclasts activity directly depends onthe production of several cytokines (TNF, IL-1, IL-6), which are called proosteoclastogenous cytokines.At that, estrogen is capable to suppress RANKL, TNF, IL-1 and IL-6 by the direct eff ect on T-cells, indirectly – through an inhibition of IL-7 and stimulation of atransforming growth factor beta – TGF-β.It was showed, that estrogens defi ciency led to an increase of IL-17 production. This cytokine induces bone tissue loss by the increase of proosteoclastogenouscytokines (TNF, IL-6 and RANKL) synthesis.Thus, results of the recent research signifi cantly expanded our idea as to pathogenesis of post-menopausal osteoporosis. At present, on a cellular and molecular scale it is proved important and the dominant role of immune factors in the development of osteoporotic violations of bone tissue is likely to be caused by the estrogens defi ciency.