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Review
. 2013 Oct;46(10):479-83.
doi: 10.5483/bmbrep.2013.46.10.141.

The role of interleukin-17 in bone metabolism and inflammatory skeletal diseases

Affiliations
Review

The role of interleukin-17 in bone metabolism and inflammatory skeletal diseases

Youngkyun Lee. BMB Rep. 2013 Oct.

Abstract

The balance between osteoblast-dependent bone formation and osteoclast-dependent bone resorption maintains bone homeostasis. In inflammatory conditions, this balance shifts toward bone resorption, causing osteolytic bone lesions observed in rheumatoid arthritis and periodontitis. A recently discovered family of cytokine IL-17 is widely reported to mediate diverse inflammatory processes. During the last decade, novel roles for IL-17 in skeletal homeostasis have been discovered indicating the potential importance of this cytokine in bone metabolism. This review will summarize and discuss the involvement of IL-17 during bone homeostasis in both physiologic and pathologic conditions. A better understanding of the role of IL-17 in skeletal systems warrants an advance in bone biology, as well as development of therapeutic strategies against bone-lytic diseases, such as rheumatoid arthritis and periodontitis.

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Figures

Fig. 1.
Fig. 1.. The role of IL-17 in bone remodeling. IL-17, produced by Th17 cells, stimulate the production of MCSF and RANKL in osteoblasts and mesenchymal stem cells. These factors enhance the formation of bone-resorbing osteoclasts from monocyte/macrophage precursors. IL-17 not only accelerates the osteogenic differentiation of mesenchymal stem cells but also hampers adipogenic differentiation. Th17 cells are also RANKL-expressing T cells that support osteoclastogenesis.

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