J Rheum Dis.  2016 Jun;23(3):148-153. 10.4078/jrd.2016.23.3.148.

Pro-inflammatory Cytokines Modulating Osteoclast Differentiation and Function

• Seong S
• Kim JH
• Kim N

• KMID: 2326729
• DOI: http://doi.org/10.4078/jrd.2016.23.3.148

Abstract

In general, bone homeostasis is maintained through the balance between bone formation and resorption. Disruption in this balance results in bone-related diseases such as osteopetrosis, osteoporosis, and rheumatoid arthritis. Often, enhanced osteoclastogenesis is followed by accelerated bone resorption that is induced by pro-inflammatory cytokines in osteoporosis or rheumatoid arthritis, and leads to bone destruction. In this review study, factors involved in osteoclast differentiation and function are discussed, and how the prevention of such factors is effective in ameliorating bone loss in osteoporosis or rheumatoid arthritis.

Keyword

Bone and bones; Osteoclasts; Rheumatoid arthritis; Cytokines

MeSH Terms

Arthritis, Rheumatoid
Bone and Bones
Bone Resorption
Cytokines*
Homeostasis
Osteoclasts*
Osteogenesis
Osteopetrosis
Osteoporosis
Cytokines

Figure

• 

  Figure 1. Roles of proinflammatory cytokines in osteoclastogenesis. Pro-inflammatory cytokines are produced from various immune cells including T cells, B cells, macrophages, dendritic cells, FLS, etc. Proinflammatory cytokines induce osteoclastogenesis either dependent or independent of the RANKL-RANK signaling pathway. FLS: fibroblast-like synoviocytes, IL: interleukin, RANKL: receptor activator of nuclear factor kappa-B ligand, TNF-α: tumor necrosis factor alpha.

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