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  • Review Article
  • Published:

Adipokines in bone disease

Key Points

  • Factors derived from adipose tissue contribute to inflammation as well as to alterations to cartilage and bone

  • Expression of adipokines is elevated in rheumatic diseases, both systemically and locally at sites of bone damage

  • Adipokines not only have a proinflammatory effect in chronic inflammatory arthritis, but also affect bone remodelling in degenerative joint diseases such as osteoarthritis

  • Adipokines are potential biomarkers of disease owing to their association with progression of bone erosions and osteophyte formation

  • Targeting adipokine dysregulation presents future therapeutic options to modulate not only the immune response, but also cartilage and bone remodelling

Abstract

Adipose tissue secretes highly bioactive factors, the adipokines. Systemic levels of adipokines are often altered in the presence of inflammation. In turn, adipokines affect different tissues and cells systemically as well as locally, contributing to immunomodulatory and bone remodelling mechanisms. The role of adipokines has been evaluated in chronic inflammatory diseases, such as rheumatoid arthritis, as well as in primarily degenerative joint diseases, such as osteoarthritis, particularly with regard to their levels of expression and their effects on joint tissues including synovial membrane, cartilage and bone. Distinct adipokines have been found to modulate matrix remodelling as well as inflammatory responses. In this Review, we summarize current knowledge relating to adipokines in rheumatic diseases, with a particular focus on the effects of adipokines on bone remodelling.

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Figure 1: Adipokines and adipocytes.
Figure 2: The main effects of adipokines on bone remodelling in osteoarthritis.

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All authors researched data for the article, made substantial contributions to discussions of content, wrote the article and reviewed and/or edited the manuscript before submission.

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Neumann, E., Junker, S., Schett, G. et al. Adipokines in bone disease. Nat Rev Rheumatol 12, 296–302 (2016). https://doi.org/10.1038/nrrheum.2016.49

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