J Rheum Dis.  2016 Jun;23(3):141-147. 10.4078/jrd.2016.23.3.141.

Osteoclasts: Crucial in Rheumatoid Arthritis

• Jeong WJ
• Kim HJ

• KMID: 2326728
• DOI: http://doi.org/10.4078/jrd.2016.23.3.141

Abstract

Osteoclasts are a major component of bone metabolism in physiologic condition and in rheumatoid arthritis (RA). RA is a chronic, autoimmune, inflammatory disease primarily affecting the joints. Joint inflammation leads to cartilage and bone destruction by osteoclast activation. This osteoclast activation leads to typical RA symptoms and is the therapeutic target. Several kinds of drugs are used for preventing bone loss by osteoclasts in RA patients. However, the bone destructive action of osteoclasts is not the only mechanism in RA pathogenesis. Recent research suggests that the osteoclasts regulate hematopoietic stem cell niches and invoke immune responses in bone. Osteoclasts are derived from bone marrow hematopoietic stem cells, and maintain the hematopoietic stem cell niches contract with osteoblasts. Osteoclasts secret several cytokines to regulate inflammation and T cell differentiation, and present antigen to T cells via major histocompatibility complex class I and class II molecules. Osteoclast concepts in both origins and functions are under major reconsideration and research. In this review, we will discuss these new insights.

Keyword

Osteoclasts; Osteoclastogenesis; Rheumatoid arthritis; RANK ligand; Immunity

MeSH Terms

Arthritis, Rheumatoid*
Bone Marrow
Cartilage
Cell Differentiation
Cytokines
Hematopoietic Stem Cells
Humans
Inflammation
Joints
Major Histocompatibility Complex
Metabolism
Osteoblasts
Osteoclasts*
RANK Ligand
T-Lymphocytes
Cytokines
RANK Ligand

Figure

• 

  Figure 1. Cross talk between the immune system and osteoclasts in osteoclastogenesis. Osteoclasts are derived from monocyte precursor cells. RANKL from B cell and IL-17 from Th17 cell induces osteoclastogenesis. IL-10 from Treg, IFN-γ from Th1, and IL-4 from Th2 inhibits osteoclastogenesis. I: major histocompatibility complex (MHC) class I, II: MHC class II, IFN: interferon, IL: interleukin, OPG: osteoprotegerin, RANKL: receptor activator of nuclear factor-kappa B ligand, Th1/2/17: T helper cells type 1/2/17, TGF: transforming growth factor, TNF: tumor necrosis factor, Treg: regulatory T cell.

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