Journal
RHEUMATOLOGY
Volume 52, Issue 2, Pages 226-234Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/kes259
Keywords
osteoclast; bone erosion; rheumatoid arthritis; cellular dynamics; chemokine; RANKL; cathepsin; imaging
Categories
Funding
- Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST Program) from the Ministry of Education, Science, Sports and Culture of Japan [22689030, 22113007]
- Ministry of Health, Labor and Welfare of Japan [H21-010]
- International Human Frontier Science Program [RGY0077/2011]
- Takeda Science Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Astellas Foundation for Research on Metabolic Disorders
- Kanae Foundation for the Promotion of Medical Science
- Pfizer Health Research Foundation
- Grants-in-Aid for Scientific Research [22689030, 12J10335, 22113007] Funding Source: KAKEN
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RA is a chronic autoimmune disease characterized by joint synovial inflammation and progressive cartilage/bone destruction. Although various kinds of RA drug have been developed worldwide, there are currently no established methods for preventing RA-associated bone destruction, the most severe outcome of this disease. One of the major pathogenic factors in arthritic bone destruction is the enhanced activity of osteoclasts at inflammatory sites. Osteoclasts are bone-resorbing giant polykaryons that differentiate from mononuclear macrophage/monocyte-lineage haematopoietic precursors. Upon stimulation by cytokines, such as M-CSF and RANK ligand, osteoclast precursor monocytes migrate and attach onto the bone surface (migration). They then fuse with each other to form giant cells (differentiation) and mediate bone resorption (function). In this review, we summarize the current understanding regarding the mechanisms underlying these three dynamic steps of osteoclastic activity and discuss novel lines of osteoclast-targeted therapies that will impact future treatment of RA.
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