Immunologic Aspects of Postmenopausal Osteoporosis

• Main Authors: V.V. Povoroznyuk, N.A. Reznichenko, E.A. Maylyan
• Format: Article
• Language: English
• Published: Zaslavsky O.Yu. 2013-08-01
• Series: Bolʹ, Sustavy, Pozvonočnik
• Subjects: osteoporosis; menopause; estrogens; immu­nity
• Online Access: http://pjs.zaslavsky.com.ua/article/view/82325
• ISSN: 2224-1507; 2307-1133

The most common form of osteoporosis — postmenopausal one, and its main cause is an estrogens deficiency. However, the mechanisms determining bone weight loss in estrogens deficiency are not limited to model of direct control actions of these hormones on bone tissue cells and are considerably more difficult. The findings are the evidence of interrelation between immune system and bone tissue and of significant role of immune mechanisms in pathogenesis of osteoporosis. Scientific studies in recent years show the central and catalytic role in the regulation of osteoclast function of two cytokines — macrophage colony-stimulating factor and receptor activator of nuclear factor κВ ligand (RANKL). Furthermore, the activity of osteoclastogenesis is directly dependent on the production of several cytokines (TNF, IL-1, IL-6), which are called proosteoclastogenic. Estrogens are able to suppress the production of RANKL, TNF, IL-1 and IL-6 due to the effect on cells of the immune system, both directly and indirectly — through the inhibition of IL-7 and the stimulation of the transforming growth factor beta (TGF-β). Furthermore, it was found that estrogen deficiency leads to increased production of IL-17, which is a potent inducer of RANKL, and other proinflammatory cytokines and induces bone loss. Thus, the results of studies in recent years have substantially broadened our understanding of the pathogenesis of postmenopausal osteoporosis. At the moment, at the cellular and molecular level there has been proved important, and perhaps even the key role of immune factors in the development of osteoporosis-related bone disorders with estrogen deficiency.