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Hydroxychloroquine affects bone resorption both in vitro and in vivo
Tim Both1, M Carola Zillikens2, Marijke Schreuders-Koedam2
1Division of Clinical Immunology, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Journal of Cellular Physiology
|May 31, 2017
Summary
Hydroxychloroquine (HCQ) was found to inhibit osteoclast function, reducing bone resorption. This suggests HCQ may protect bone mineral density (BMD) and benefit skeletal health in patients at risk of osteoporosis.
Area of Science:
- Immunology
- Rheumatology
- Bone Biology
Background:
- Patients with primary Sjögren syndrome (pSS) exhibit higher bone mineral density (BMD) than controls.
- Hydroxychloroquine (HCQ), used by 69% of these patients, may positively influence BMD.
Purpose of the Study:
- To investigate the effect of HCQ on osteoclast function and bone resorption.
Main Methods:
- Osteoclasts were cultured and treated with varying HCQ doses.
- Assessed osteoclast differentiation, activity, intracellular pH, and cholesterol trafficking.
- Measured serum bone resorption marker β-CTx in rheumatoid arthritis patients.
Main Results:
- HCQ inhibited osteoclast formation and bone resorption in vitro.
- HCQ treatment decreased intracellular pH and enhanced cholesterol uptake in osteoclasts.
- Serum β-CTx levels significantly decreased after 6 months of HCQ treatment in vivo.
Conclusions:
- HCQ suppresses osteoclast-mediated bone resorption.
- HCQ's effects on intracellular pH and cholesterol uptake suggest lysosomal membrane permeabilization.
- HCQ may prevent BMD loss and benefit skeletal health in at-risk populations.
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