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ORIGINAL ARTICLE
Year : 2019  |  Volume : 62  |  Issue : 2  |  Page : 70-79

Different susceptibilities of osteoclasts and osteoblasts to glucocorticoid-induced oxidative stress and mitochondrial alterations


1 Institute of Biotechnology, National Taiwan University, Taipei; Department of Orthopedics, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan; Department of Orthopedics, National Defense Medical Center, Tri-Service General Hospital, Taipei, Taiwan
2 Department of Animal Science, National Pingtung University of Science and Technology, Pingtung, Taiwan
3 Department of Orthopedics, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan, Taiwan
4 Department of Animal Science and Technology, National Taiwan University, Taipei; Department of Animal Science and Biotechnology, Tunghai University, Taichung, Taiwan
5 Institute of Biotechnology, National Taiwan University; Department of Animal Science and Technology, National Taiwan University, Taipei, Taiwan

Correspondence Address:
Dr. Shinn-Chih Wu
No. 50, Lane 155, Section 3, Keelung Rd., Da'an District, Taipei 10672
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/CJP.CJP_7_19

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Glucocorticoid-induced bone loss is the most common form of secondary osteoporosis. This toxic effect has not been efficiently managed, possibly due to the incomplete understanding of the extraordinarily diverse cellular responses induced by glucocorticoid treatment. Previous literatures revealed that high dose of exogenous glucocorticoid triggers apoptosis in osteocytes and osteoblasts. This cell death is associated with glucocorticoid-induced oxidative stress. In this study, we aimed to investigate the mechanisms of glucocorticoid-induced apoptosis in osteoblasts and examine the responses of osteoclasts to the synthetic glucocorticoid, dexamethasone. We demonstrated the biphasic effects of exogenous glucocorticoid on osteoblastic mitochondrial functions and elevated intracellular oxidative stress in a dose- and time-dependent manner. On comparison, similar treatment did not induce mitochondrial dysfunctions and oxidative stress in osteoclasts. The production of reactive oxygen/nitrogen species was decreased in osteoclasts. The differences are not due to varying efficiency of cellular antioxidant system. The opposite effects on nitrogen oxide synthase might provide an explanation, as the expression levels of nos2 gene are suppressed in the osteoclast but elevated in the osteoblast. We further revealed that glucocorticoids have a substantial impact on the osteoblastic mitochondria. Basal respiration rate and ATP production were increased upon 24 h incubation of glucocorticoids. The increase in proton leak and nonmitochondrial respiration suggests a potential source of glucocorticoid-induced oxidative stress. Long-term incubation of glucocorticoids accumulates these detrimental changes and results in cytochrome C release and mitochondrial breakdown, consequently leading to apoptosis in osteoblasts. The mitochondrial alterations might be other sources of glucocorticoid-induced oxidative stress in osteoblasts.


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