Is RANKL a potential molecular target in osteoarthritis?
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2024
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Muratovic, D.
Atkins, G.J.
Findlay, D.M.
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Journal article
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Osteoarthritis and Cartilage, 2024; 32(5):493-500
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Dzenita Muratovic, Gerald J. Atkins, David M. Findlay
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Abstract
OBJECTIVE: Osteoarthritis (OA) is a disease of joints, in which the bone under the articular cartilage undergoes increased remodelling activity. The question is whether a better understanding of the causes and mechanisms of bone remodelling can predict disease-modifying treatments. DESIGN: This review summarizes the current understanding of the aetiology of OA, with an emphasis on events in the subchondral bone, and the cells and cytokines involved, to seek an answer to this question. RESULTS: Subchondral bone remodelling across OA changes the microstructure of the subchondral bone, which alters the load-bearing properties of the joint and seems to have an important role in the initiation and progression of OA. Bone remodelling is tightly controlled by numerous cytokines, of which RANKL and OPG are central factors in almost all known bone conditions. In terms of finding therapeutic options for OA, an important question is whether controlling the rate of subchondral bone remodelling would be beneficial. The role of RANKL in the pathogenesis and progression of OA and the effect of its neutralisation remain to be clarified. CONCLUSIONS: This review further makes the case for subchondral bone remodelling as important in OA and for additional study of RANKL in OA, both its pathophysiological role and its potential as an OA disease target.
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© 2024 University of Adelaide. Published by Elsevier Ltd on behalf of Osteoarthritis Research Society International. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).