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Nihon Rinsho Meneki Gakkai Kaishi. 2017;40(5):367-376. doi: 10.2177/jsci.40.367.

[Inflammation and osteoclasts].

[Article in Japanese]

Author information

1
Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University.

Abstract

  Osteoclasts are differentiated from precursors of the monocyte/macrophage lineage originated from bone marrow hematopoietic stem cells and are the sole bone-resorbing cells in the body. Osteoclast differentiation is thought to require M-CSF (macrophage colony-stimulating factor) and RANKL (receptor activator of nuclear factor kappa-B ligand) signaling. However, it has recently been proposed that under chronic inflammatory conditions, such as systemic autoimmune diseases (e.g., rheumatoid arthritis), an increase in inflammatory cytokine levels within joints induces pathological osteoclast differentiation, causing excessive bone resorption. In addition, the authors have reported that stimulating mouse bone marrow monocytes and human CD14+ monocytes with combination of TNFα and IL-6 can induce differentiation of osteoclast-like cells, which are cells with bone resorption activity. In the present article, we discuss the mechanism of osteoclast differentiation of RANKL-independent bone-resorbing cells, using both data from the aforementioned report as well as the latest findings. Understanding the mechanisms underlying RANKL-independent, cytokine-mediated osteoclast differentiation could facilitate the development of novel therapies for inflammatory joint diseases.

KEYWORDS:

RANKL-independent osteclast diffferentiation; inflammation; osteoclasts; rheumatoid arthritis

PMID:
29238019
DOI:
10.2177/jsci.40.367
[Indexed for MEDLINE]
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