Effects of inflammatory and anti‐inflammatory cytokines on the bone

Abstract

Inflammatory diseases are linked to enhanced bone loss. The effect of inflammation on bone is mediated by proinflammatory cytokines, which regulate bone formation as well as bone resorption thereby altering bone homeostasis. In this article we summarize the key insights in cytokine regulation of bone. We describe the major pro- and anti-inflammatory mediators, which are involved in the regulation of bone and describe the mechanisms by which these cytokines alter bone balance. We describe the effects of tumor necrosis factor (TNF), interleukin (IL)- 1 family members, IL-6, IL-17 and interferons (IFN) on bone and discuss the mechanisms by which these individual cytokines affect the bone resorbing and the bone forming cells. Several proinflammatory cytokines (such as TNFa, IL-1 and IL-17) are major triggers for osteoclast activation explaining the enhanced bone loss during inflammation. Other such as IL-12, IL-18, IL-33 and IFN are strong suppressors of osteoclast differentiation and inhibit bone loss. Thus the cytokine composition of an inflammatory tissue is decisive whether inflammation triggers bone loss or not.