Negative regulation of osteoclastogenesis and bone resorption by cytokines and transcriptional repressors
1 Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY 10021, USA
2 Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Science, New York, NY 10021, USA
Arthritis Research & Therapy 2011, 13:234 doi:10.1186/ar3379
See related review by Braun and Zwerina, http://arthritis-research.com/content/13/4/235Published: 28 July 2011
Bone remodeling in physiological and pathological conditions represents a balance between bone resorption mediated by osteoclasts and bone formation by osteoblasts. Bone resorption is tightly and dynamically regulated by multiple mediators, including cytokines that act directly on osteoclasts and their precursors, or indirectly by modulating osteoblast lineage cells that in turn regulate osteoclast differentiation. The critical role of cytokines in inducing and promoting osteoclast differentiation, function and survival is covered by the accompanying review by Zwerina and colleagues. Recently, it has become clear that negative regulation of osteoclastogenesis and bone resorption by inflammatory factors and cytokines, downstream signaling pathways, and a newly described network of transcriptional repressors plays a key role in bone homeostasis by fine tuning bone remodeling and restraining excessive bone resorption in inflammatory settings. In this review we discuss negative regulators of osteoclastogenesis and mechanisms by which these factors suppress bone resorption.