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Effects of inflammatory and anti‐inflammatory cytokines on the bone
Author(s) -
Schett Georg
Publication year - 2011
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2011.02545.x
Subject(s) - proinflammatory cytokine , bone resorption , osteoclast , inflammation , cytokine , bone remodeling , tumor necrosis factor alpha , immunology , bone cell , medicine , endocrinology , receptor
Eur J Clin Invest 2011; 41 (12): 1361–1366 Abstract Background 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. Materials and methods 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. Results 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. Conclusions 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.