PHASIC CHANGES OF BONE MASS, BONE TURNOVER MARKERS, AND ESTROGEN LEVELS AT DIFFERENT TIME POINTS AFTER GLUCOCORTICOID INTERVENTION AND THEIR CORRELATION IN RATS_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

RENHui ¹ , SHENGengyang ¹ ,  JIANGXiaobing ² , LIANGDe ² , TANGJingjing ¹ , CUIJianchao ¹ , LINShunxin ¹ , ZHUANGHong ² , YANGZhidong ² , ZHANGShuncong ² , YAOZhensong ²

1. The First School of Clinic Medicine, Guangzhou University of Chinese Medicine, Guangzhou Guangdong, 510405, P. R. China;
2. Department of Spinal Surgery, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou Guangdong, 510405, P. R. China;

Corresponding author：

JIANGXiaobing, Email: spinedrjxb@sina.com

Keywords：

Glucocorticoid-induced osteoporosis; Bone mass; N-terminal propeptide of type I procollagen; C-terminal cross-linking telopeptide of type I collagen; Estrogen; Rat

DOI：

10.7507/1002-1892.20150066

Video：

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Objective To analyze the phasic changes of bone mass, bone turnover markers, and estrogen levels at different time points after glucocorticoid (GC) intervention in rat and their correlation. Methods Thirty-four female 3-month-old Sprague Dawley rats were randomly divided into the following 3 groups:baseline group (n=6), dexamethasone (DXM) group (n=14), and control group (n=14). Rats were injected with DXM at the dose of 0.75 mg/kg, twice a week for 12 weeks in DXM group, with salt solution lavage in control group, and no treatment was given in baseline group. The body mass, adrenal weight, and uterus weight were measured. Bone mineral density (BMD), bone mineral content (BMC), and bone area (BA) of lumbar vertebral and femurs were detected by dual energy X-ray absorptiometry. Meanwhile, the serum levels of N-terminal propeptide of type I procollagen (PINP), C-terminal cross-linking telopeptide of type I collagen (β-CTX), and estrogen levels were determined by ELISA before experiment in baseline group and at 4, 8, and 12 weeks after experiment in control and DXM groups. At last, the correlation was analyzed among body weight, BMD, PINP, β-CTX, estrogen levels, and GC intervention duration of DXM group. Results The body mass, adrenal weight, and uterus weight in DXM group were significantly lower than those in baseline group and control group at all the time points (P<0.05). The levels of PINP and β-CTX elevated slowly in DXM group, significant difference was found at 12 weeks (P<0.05), but no significant difference at the 4 and 8 weeks (P>0.05) when compared with those in baseline group and control group. The estrogen level in DXM group was significantly lower than that in baseline group and control group at all the time points (P<0.05). BMD, BMC, and BA of lumbar vertebral and femurs in DXM group were significantly lower than those in control group at all the time points after GC intervention (P<0.05). Loss of bone mass of L₂ and femoral trochanteric region in DXM group was the lowest of all ranges of interest (ROIs). BMC and BA of lumbar vertebrae and BA of femoral shaft in DXM group at 4 weeks were significantly lower than those in baseline group (P<0.05). But there was no significant difference in BMD, BMC, and BA of other lumbar vertebrae and femurs' ROIs between DXM group and baseline group at all the time points (P>0.05). After GC intervention, BMD of lumbar vertebrae and femurs had negative correlation with PINP and β-CTX (P<0.05) and positive correlation with estrogen level (P<0.05). Conclusion The bone mass decreases rapidly at the early stage after GC intervention and then maintains a low level with time, the levels of bone turnover markers show a progressive increase, and the estrogen levels show a decrease trend. In addition, body weight, the levels of bone turnover markers and estrogen are associated with the change of bone mass.

Citation： RENHui, SHENGengyang, JIANGXiaobing, LIANGDe, TANGJingjing, CUIJianchao, LINShunxin, ZHUANGHong, YANGZhidong, ZHANGShuncong, YAOZhensong. PHASIC CHANGES OF BONE MASS, BONE TURNOVER MARKERS, AND ESTROGEN LEVELS AT DIFFERENT TIME POINTS AFTER GLUCOCORTICOID INTERVENTION AND THEIR CORRELATION IN RATS. Chinese Journal of Reparative and Reconstructive Surgery, 2015, 29(3): 307-314. doi: 10.7507/1002-1892.20150066 Copy

1.	Overman RA, Gourlay ML, Deal CL, et al. Fracture rate associated with quality metric-based anti-osteoporosis treatment in glucocorticoid-induced osteoporosis. Osteoporosis International, 2015.[Epub ahead of print].
2.	Briota K, Cortetb B, Roux C, et al. 2014 update of recommendations on the prevention and treatment of glucocorticoid-induced osteoporosis. Joint Bone Spine, 2014, 81(6):493-501.
3.	den Uyl D, Bultink IE, Lems WF. Advances in glucocorticoid-induced osteoporosis. Curr Rheumatol Rep, 2011, 13(3):233-240.
4.	田丽花, 梁敏, 张劼, 等. 糖皮质激素性骨质疏松大鼠模型建立的研究. 广西医科大学学报, 2013, 30(1):5-7.
5.	Pasqualetti S, Congiu T, Banfi G, et al. Alendronate rescued osteoporotic phenotype in a model of glucocorticoid-induced osteoporosis in adult zebrafish scale. Int J Exp Pathol, 2015.[Epub ahead of print].
6.	Hulley PA, Conradie MM, Langeveldt CR, et al. Glucocorticoid-induced osteoporosis in the rat is prevented by tyrosine phosphatase inhibitor, sodium orthovanadate. Bone, 2002, 31(1):220-229.
7.	Wimalawansa SJ, Simmons DJ. Prevention of corticosteroid induced bone loss with alendronate. Proc Soc Exp Biol Med, 1998, 217(2):162-167.
8.	Kim HK, Kim MG, Leem KH. Osteogenic activity of collagen peptide via ERK/MAPK pathway mediated boosting of collagen synthesis and its therapeutic efficacy in osteoporotic bone by back-scattered electron imaging and microarchitecture analysis. Molecules, 2013, 18(12):15474-15489.
9.	Ma B, Zhang Q, Wu D, et al. Strontium fructose 1, 6-diphosphate prevents bone loss in a rat model of postmenopausal osteoporosis via the OPG/RANKL/RANK pathway. Acta Pharmacol Sin, 2012, 33(4):479-89.
10.	周乐, 吴铁, 崔燎. 淫羊藿调节BMP-7预防糖皮质激素致大鼠骨损害的研究. 中国骨质疏松杂志, 2014, 20(3):234-237, 241.
11.	陈婷颖, 任伟. 成人生长激素缺乏症与骨质疏松. 现代医药卫生, 2014, 30(13):1965-1967.
12.	Lin S, Huang J, Zheng L, et al. Glucocorticoid-induced osteoporosis in growing rats. Calcif Tissue Int, 2014, 95(4):362-373.
13.	戴哲浩, 康意军, 吕国华, 等. 糖皮质激素对成年大鼠骨量的影响. 中国骨质疏松杂志, 2014, 20(4):366-371.
14.	柯务. 体重指数与男性骨质疏松关系的研究. 中国现代医生, 2013, 51(21):25-26.
15.	Hamidi MS, Corey PN, Cheung AM. Effects of vitamin E on bone turnover markers among US postmenopausal women. J Bone Miner Res, 2012, 27(6):1368-1380.
16.	Sbrocchi AM, Rauch F, Matzinger M, et al. Vertibral fractures despite normal spine bone mineral density in a boy with nephritic syndrome. Pediatr Nephrol, 2011, 26(1):139-142.
17.	Li M, Li Y, Deng W, et al. Chinese bone turnover marker study:reference ranges for C-terminal telopeptide of type I collagen and procollagen I N-terminal Peptide by age and gender. PLoS One, 2014, 9(8):e103841.
18.	欧萌萌, 黄建荣. 绝经后妇女骨质疏松症患者血清β-Crosslaps、PINP和N-MID检测的评价. 标记免疫分析与临床, 2011, 18(4):238-240.
19.	Farahmand P, Marin F, Hawkins F, et al. Early changes in biochemical markers of bone formation during teriparatide therapy correlate with improvements in vertebral strength in men with glucocorticoid-induced osteoporosis. Osteoporos Int, 2013, 24(12):2971-2981.
20.	刘晓红, 卢文, 钱浩, 等. 糖皮质激素对肾小球疾病患者骨密度和骨转换指标的影响. 实用医学杂志, 2014, 30(22):3583-3586.
21.	McManus MM, Grill RJ. Longitudinal evaluation of mouse hind limb bone loss after spinal cord injury using novel, in vivo, methodology. J Vis Exp, 2011, (58):e3246.

1. Overman RA, Gourlay ML, Deal CL, et al. Fracture rate associated with quality metric-based anti-osteoporosis treatment in glucocorticoid-induced osteoporosis. Osteoporosis International, 2015.[Epub ahead of print].
2. Briota K, Cortetb B, Roux C, et al. 2014 update of recommendations on the prevention and treatment of glucocorticoid-induced osteoporosis. Joint Bone Spine, 2014, 81(6):493-501.
3. den Uyl D, Bultink IE, Lems WF. Advances in glucocorticoid-induced osteoporosis. Curr Rheumatol Rep, 2011, 13(3):233-240.
4. 田丽花, 梁敏, 张劼, 等. 糖皮质激素性骨质疏松大鼠模型建立的研究. 广西医科大学学报, 2013, 30(1):5-7.
5. Pasqualetti S, Congiu T, Banfi G, et al. Alendronate rescued osteoporotic phenotype in a model of glucocorticoid-induced osteoporosis in adult zebrafish scale. Int J Exp Pathol, 2015.[Epub ahead of print].
6. Hulley PA, Conradie MM, Langeveldt CR, et al. Glucocorticoid-induced osteoporosis in the rat is prevented by tyrosine phosphatase inhibitor, sodium orthovanadate. Bone, 2002, 31(1):220-229.
7. Wimalawansa SJ, Simmons DJ. Prevention of corticosteroid induced bone loss with alendronate. Proc Soc Exp Biol Med, 1998, 217(2):162-167.
8. Kim HK, Kim MG, Leem KH. Osteogenic activity of collagen peptide via ERK/MAPK pathway mediated boosting of collagen synthesis and its therapeutic efficacy in osteoporotic bone by back-scattered electron imaging and microarchitecture analysis. Molecules, 2013, 18(12):15474-15489.
9. Ma B, Zhang Q, Wu D, et al. Strontium fructose 1, 6-diphosphate prevents bone loss in a rat model of postmenopausal osteoporosis via the OPG/RANKL/RANK pathway. Acta Pharmacol Sin, 2012, 33(4):479-89.
10. 周乐, 吴铁, 崔燎. 淫羊藿调节BMP-7预防糖皮质激素致大鼠骨损害的研究. 中国骨质疏松杂志, 2014, 20(3):234-237, 241.
11. 陈婷颖, 任伟. 成人生长激素缺乏症与骨质疏松. 现代医药卫生, 2014, 30(13):1965-1967.
12. Lin S, Huang J, Zheng L, et al. Glucocorticoid-induced osteoporosis in growing rats. Calcif Tissue Int, 2014, 95(4):362-373.
13. 戴哲浩, 康意军, 吕国华, 等. 糖皮质激素对成年大鼠骨量的影响. 中国骨质疏松杂志, 2014, 20(4):366-371.
14. 柯务. 体重指数与男性骨质疏松关系的研究. 中国现代医生, 2013, 51(21):25-26.
15. Hamidi MS, Corey PN, Cheung AM. Effects of vitamin E on bone turnover markers among US postmenopausal women. J Bone Miner Res, 2012, 27(6):1368-1380.
16. Sbrocchi AM, Rauch F, Matzinger M, et al. Vertibral fractures despite normal spine bone mineral density in a boy with nephritic syndrome. Pediatr Nephrol, 2011, 26(1):139-142.
17. Li M, Li Y, Deng W, et al. Chinese bone turnover marker study:reference ranges for C-terminal telopeptide of type I collagen and procollagen I N-terminal Peptide by age and gender. PLoS One, 2014, 9(8):e103841.
18. 欧萌萌, 黄建荣. 绝经后妇女骨质疏松症患者血清β-Crosslaps、PINP和N-MID检测的评价. 标记免疫分析与临床, 2011, 18(4):238-240.
19. Farahmand P, Marin F, Hawkins F, et al. Early changes in biochemical markers of bone formation during teriparatide therapy correlate with improvements in vertebral strength in men with glucocorticoid-induced osteoporosis. Osteoporos Int, 2013, 24(12):2971-2981.
20. 刘晓红, 卢文, 钱浩, 等. 糖皮质激素对肾小球疾病患者骨密度和骨转换指标的影响. 实用医学杂志, 2014, 30(22):3583-3586.
21. McManus MM, Grill RJ. Longitudinal evaluation of mouse hind limb bone loss after spinal cord injury using novel, in vivo, methodology. J Vis Exp, 2011, (58):e3246.

Chinese Journal of Reparative and Reconstructive Surgery

PHASIC CHANGES OF BONE MASS, BONE TURNOVER MARKERS, AND ESTROGEN LEVELS AT DIFFERENT TIME POINTS AFTER GLUCOCORTICOID INTERVENTION AND THEIR CORRELATION IN RATS

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