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Mediators of Inflammation
Volume 2015 (2015), Article ID 782382, 10 pages
Review Article

The Role of IL-1β in the Bone Loss during Rheumatic Diseases

1Department of Biotechnological and Applied Clinical Sciences, Rheumatology Unit, University of L’Aquila, Delta 6 Building, 67100 L’Aquila, Italy
2Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila, Italy

Received 31 December 2014; Revised 15 February 2015; Accepted 4 March 2015

Academic Editor: Nina Ivanovska

Copyright © 2015 Piero Ruscitti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Several inflammatory diseases have been associated with increased bone resorption and fracture rates and different studies supported the relation between inflammatory cytokines and osteoclast activity. The main factor required for osteoclast activation is the stimulation by receptor activator of nuclear factor kappa-B ligand (RANKL) expressed on osteoblasts. In this context, interleukin- (IL-) 1β, one of the most powerful proinflammatory cytokines, is a strong stimulator of in vitro and in vivo bone resorption via upregulation of RANKL that stimulates the osteoclastogenesis. The resulting effects lead to an imbalance in bone metabolism favouring bone resorption and osteoporosis. In this paper, we review the available literature on the role of IL-1β in the pathogenesis of bone loss. Furthermore, we analysed the role of IL-1β in bone resorption during rheumatic diseases and, when available, we reported the efficacy of anti-IL-1β therapy in this field.