CORTICOSTEROID-INDUCED OSTEOPOROSIS AND OSTEONECROSIS: ROLE OF OXIDATIVE STRESS

Reham Alattar, Abdel Alim Abdel Alim, Sabry Abdelmetal, Sayed Abdel Aziz

Abstract


Glucocorticoids (GC) play a significant role in body metabolism. In the last few years, advances and highlights have been made to understand the role of oxidative stress induced by corticosteroids in the pathogenesis of osteonecrosis (ON) and osteoporosis (OP) and the door for digging in GC mechanistic has been opened by the newly detection of high-affinity receptors for glucocorticoids and calcitriol in bones. The harmful free radicals produced by corticosteroid administration are strong emitters of many regulatory cytokines such as tumor necrosis factor (TNF), nuclear factor kappa β (NF-kB) and interleukins. For this, a great attention has been directed toward the possibility of using a novel free radical scavenger like natural antioxidant, e.g. ginseng, that can be helpful in the management of ON and OP. The use of antioxidants for the management of osteoporosis characterized by many improvements in the way of control the incidence rate of ON and OP. Many antioxidants have an anti-osteoporotic effect, with an overall redox state maintenance. Also, the lipid peroxides are alleviated and the intraosseous vascular integrity within the bone marrow are repaired. Moreover, the oxidative damage of DNA is contoured. The objective of this review is to highlight the role of oxidative stress in the pathogenesis of corticosteroid-induced osteonecrosis (ON) and osteoporosis (OP) and studying the possibility of using a novel free radical scavenger, a natural antioxidant, e.g. Ginseng, that can be helpful in the management of OP & ON.

Key words: osteoporosis; osteonecrosis; corticosteroids; oxidative stress; ginseng


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Rao, L., Will tomatoes prevent osteopo-rosis. Endocrinology Rounds, 2005; 5: 118–35.

Bouvard, B., et al., Ultrastructural char-acteristics of glucocorticoid-induced osteoporo-sis. Osteoporosis international, 2009; 20: 1089-–92.

Boyle, W.J., W.S. Simonet, and D.L. Lacey, Osteoclast differentiation and activation. Nature, 2003; 423: 337.

Jilka, R.L., et al., Increased bone for-mation by prevention of osteoblast apoptosis with parathyroid hormone. The Journal of clini-cal investigation, 1999; 104: 439–46.

Cole, T.J., et al., Targeted disruption of the glucocorticoid receptor gene blocks adren-ergic chromaffin cell development and severely retards lung maturation. Genes & development, 1995; 9: 1608–21.

Schmidt, S., et al., Glucocorticoid-induced apoptosis and glucocorticoid resistance: molecular mechanisms and clinical relevance. Cell death and differentiation, 2004; 11: S45.

O’brien, C.A., et al., Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength. Endocrinology, 2004; 145: 1835–41.

Moudgil, V., Steroid receptors in health and disease An Oakland University-Serono Symposia, USA Conference, September 20–23, 1987, Meadow Brook Hall, Rochester. MI 48309-9908, USA. FEBS letters, 1988; 226: 213–6.

Jondal, M., A. Pazirandeh, and S. Okret, A role for glucocorticoids in the thymus? TRENDS in Immunology, 2001; 22: 185–6.

Laudet, V. and H. Gronemeyer, The nu-clear receptor factsbook. 2002: Gulf Profes-sional Publishing.

Bai, X.-c., et al., Oxidative stress inhib-its osteoblastic differentiation of bone cells by ERK and NF-κB. Biochemical and biophysical research communications, 2004; 314: 197–7.

Briot, K., et al., 2014 update of recom-mendations on the prevention and treatment of glucocorticoid-induced osteoporosis. Joint Bone Spine, 2014; 81: 493–1.

Nishimura, J. and S. Ikuyama, Gluco-corticoid-induced osteoporosis: pathogenesis and management. Journal of bone and mineral metabolism, 2000; 18: 350–2.

Provvedini, D.M., et al., 1, 25-dihydroxyvitamin D3 receptors in human leu-kocytes. Science, 1983; 221: 1181–3.

Tsoukas, C.D., D.M. Provvedini, and S.C. Manolagas, 1, 25-dihydroxyvitamin D3: a novel immunoregulatory hormone. Science, 1984; 224: 1438–40.

Manolagas, S.C., Steroids and osteopo-rosis: the quest for mechanisms. The Journal of clinical investigation, 2013; 123: 1919–21.

Yang, S.Y., et al., Antioxidant and Anti-Osteoporosis Activities of Chemical Constitu-ents of the Stems of Zanthoxylum piperitum. Molecules, 2018; 23: 457.

Ichiseki, T., et al., The initial phase of oxidative stress in a steroid-induced osteonecro-sis rabbit model. Advances in Bioscience and Biotechnology, 2012; 3: 978.

Okazaki, S., et al., Oxidative Stress In The Corticosteroid-induced Osteonecrosis Of The Femoral Head Rat Model.

Roux, C., Osteoporosis in inflammatory joint diseases. Osteoporosis International, 2011; 22: 421–33.

Halliwell, B. and J.M. Gutteridge, Free radicals in biology and

medicine. 2015: Oxford University Press, USA.

Valko, M., et al., Free radicals and anti-oxidants in normal physiological functions and human disease. The international journal of biochemistry & cell biology, 2007; 39: 44–84.

Orrenius, S., V. Gogvadze, and B. Zhivotovsky, Mitochondrial oxidative stress: implications for cell death. Annu. Rev. Pharma-col. Toxicol., 2007; 47: 143–83.

Farrugia, G. and R. Balzan, Oxidative stress and programmed cell death in yeast. Fron-tiers in oncology, 2012; 2: 64.

Matés, J.M., et al., Oxidative stress in apoptosis and cancer: an update. Archives of toxicology, 2012; 86: 1649–65.

Das, J., et al., Mangiferin exerts hepato-protective activity against D-galactosamine in-duced acute toxicity and oxidative/nitrosative stress via Nrf2–NFκB pathways. Toxicology and applied pharmacology, 2012; 260: 35–7.

Valko, M., H. Morris, and M. Cronin, Metals, toxicity and oxidative stress. Current medicinal chemistry, 2005; 12: 1161–1208.

Abdollahi, M., et al., Pesticides and oxi-dative stress: a review. Medical Science Moni-tor, 2004; 10: RA141–7.

Gruver-Yates, A.L. and J.A. Cidlowski, Tissue-specific actions of glucocorticoids on apoptosis: a double-edged sword. Cells, 2013; 2: 202–23.

Anderson, K., et al., Free radicals and reactive oxygen species in programmed cell death. Medical hypotheses, 1999; 52: 451–63.

Andreyev, A.Y., Y.E. Kushnareva, and A. Starkov, Mitochondrial metabolism of reac-tive oxygen species. Biochemistry (Moscow), 2005; 70: 200–14.

Pratt, W.B. and D.O. Toft, Steroid re-ceptor interactions with heat shock protein and immunophilin chaperones. Endocrine reviews, 1997; 18: 306–60.

Oakley, R.H., M. Sar, and J.A. Cidlowski, The human glucocorticoid receptor isoform expression, biochemical properties, and putative function. Journal of Biological Chemis-try, 1996; 271: 9550–9.

Finkel, T. and N.J. Holbrook, Oxidants, oxidative stress and the biology of ageing. Na-ture, 2000; 408: 239.

Li, G.-Y., et al., Edaravone, a novel free radical scavenger, prevents steroid-induced os-teonecrosis in rabbits. Rheumatology, 2012; 52: 438–47.

Ichiseki, T., et al., Oxidative stress and vascular permeability in steroid-induced oste-onecrosis model. Journal of Orthopaedic Sci-ence, 2004; 9: 509–15.

Mody, N., et al., Oxidative stress modu-lates osteoblastic differentiation of vascular and bone cells. Free Radical Biology and Medicine, 2001; 31: 509–19.

Key Jr, L., et al., Oxygen derived free radicals in osteoclasts: the specificity and loca-tion of the nitroblue tetrazolium reaction. Bone, 1990; 11: 115–9.

Steinbeck, M.J., et al., NADPH-oxidase expression and in situ production of superoxide by osteoclasts actively resorbing bone. The Journal of Cell Biology, 1994; 126: 765-772.

Suda, N., et al., Participation of oxida-tive stress in the process of osteoclast differen-tiation. Biochimica et Biophysica Acta (BBA)-General Subjects, 1993; 1157: 318–23.

Basu, S., et al., Association between ox-idative stress and bone mineral density. Bio-chemical and biophysical research communica-tions, 2001; 288: 275–9.

Lee, Y.-S., X. Chen, and J.J. Anderson, Physiological concentrations of genistein stimu-late the proliferation and protect against free radical-induced oxidative damage of MC3T3-E1 osteoblast-like cells. Nutrition Research, 2001; 21: 1287–98.

Baker, P.J., The role of immune re-sponses in bone loss during periodontal disease. Microbes and Infection, 2000; 2: 1181–92.

Abdollahi, M., et al., Role of oxidative stress in osteoporosis. Therapy, 2005; 2: 787–96.

Garnero, P., et al., Markers of bone turnover predict postmenopausal forearm bone loss over 4 years: the OFELY study. Journal of Bone and Mineral Research, 1999; 14: 1614–21.

Iotsova, V., et al., Osteopetrosis in mice lacking NF-κB1 and NF-κB2. Nature medicine, 1997; 3: 1285.

Deyama, Y., et al., Inactivation of NF-κB involved in osteoblast development through interleukin-6. Biochemical and biophysical re-search communications, 2001; 282: 1080–4.

Kurokouchi, K., et al., TNF‐α increases expression of IL‐6 and ICAM‐1 genes through activation of NF‐κB in osteoblast‐like ROS17/2.8 cells. Journal of Bone and Mineral Research, 1998; 13: 1290–9.

Polidori, M.C., et al., Profiles of antiox-idants in human plasma. Free Radical Biology and Medicine, 2001; 30: 456–62.

Meier, C., et al., Supplementation With Oral Vitamin D3 and Calcium During Winter Prevents Seasonal Bone Loss: A Randomized Controlled Open-Label Prospective Trial. Jour-nal of Bone and Mineral Research, 2004; 19: 1221–30.

Ricci, C., et al., Mitochondrial DNA damage triggers mitochondrial-superoxide gen-eration and apoptosis. American Journal of Physiology-Cell Physiology, 2008; 294: C413–22.

Mikami, T., et al., Prevention of steroid-induced osteonecrosis by intravenous admin-istration of vitamin E in a rabbit model. J Or-thop Sci, 2010; 15: 674–7.

Martindale, J.L. and N.J. Holbrook, Cel-lular response to oxidative stress: signaling for suicide and survival. J Cell Physiol, 2002; 192: 1-15.

Zhou, J.-Y., et al., Corticosterone exerts immunostimulatory effects on macrophages via en-doplasmic reticulum stress. BJS, 2010; 97: 281–93.

Colavitti, R., et al., Reactive oxygen species as downstream mediators of angiogenic signaling by vascular endothelial growth factor receptor-2/KDR. J Biol Chem, 2002; 277: 3101–8.

Kannan, K. and S.K. Jain, Oxidative stress and apoptosis. Pathophysiology, 2000; 7: 153–63.

Angeli, A., et al., High prevalence of asymptomatic vertebral fractures in post-menopausal women receiving chronic glucocor-ticoid therapy: a cross-sectional outpatient study. Bone, 2006; 39: 253–9.

Salvesen, G.S. and V.M. Dixit, Caspase activation: the induced-proximity model. Proc Natl Acad Sci U S A, 1999; 96: 10964–7.

Cao, Y., et al., Glucocorticoid receptor translational isoforms underlie maturational stage-specific glucocorticoid sensitivities of dendritic cells in mice and humans. Blood, 2013: blood-2012-05-432336.

Kerachian, M.A., et al., New insights in-to the pathogenesis of glucocorticoid-induced avascular necrosis: microarray analysis of gene expression in a rat model. Arthritis Research & Therapy, 2010; 12: R124.

Sinha, K., et al., Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis. Arch Toxi-col, 2013; 87: 1157–80.

Yamamoto, T., et al., Effects of pulse methylprednisolone on bone and marrow tis-sues. Corticosteroid‐induced osteonecrosis in rabbits. Arthritis & Rheumatism: Official Jour-nal of the American College of Rheumatology, 1997; 40: 2055–64.

Lu, B.-B. and K.-H. Li, Lipoic acid pre-vents steroid-induced osteonecrosis in rabbits. Rheumatology international, 2012; 32: 1679–83.




DOI: http://dx.doi.org/10.26873/SVR-765-2019

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