IMPLICATIONS OF THE RANK/RANKL AXIS IN THE BONE PATHOLOGY

The receptor activator of NF-κB (RANKL) is a member of the tumor necrosis factor (TNF) super-family. Its receptor, RANK, is expressed on the membrane surface of the dendritic cells (DC). RANKL, expressed by mesenchymal cells on bone tissue level, is a direct regulatory factor of osteoclasts formation and of the bone turnover. T and B lymphocytes express RANKL following their activation. On biologic level, various bone disease are mediated by RANKL. Moreover, the proinflammatory cytokines such as interleukines (IL-1, IL-6, TNFα) present high levels in periodontal impaired tissues. The current literature describes an interaction between these cytokines and RANK/RANKL/OPG system. High levels of IL-1 and TNFα determine high levels of RANKL and, consequently, initiate the osteoclastogenesis. Current studies are focused on the research of the inhibitory effects for RANKL in patients with post-menopausal osteoporosis, rheumatoid arthritis, prostate cancer, breast cancer and multiple myeloma.