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  • Title: Local renin-angiotensin system is associated with bone mineral density of glucocorticoid-induced osteoporosis patients.
    Author: Shuai B, Yang YP, Shen L, Zhu R, Xu XJ, Ma C, Lv L, Zhao J, Rong JH.
    Journal: Osteoporos Int; 2015 Mar; 26(3):1063-71. PubMed ID: 25516362.
    Abstract:
    UNLABELLED: The local renin-angiotensin system (RAS) is closely related to bone metabolism. However, it is unknown whether the local RAS is related to bone mineral density (BMD) in glucocorticoid-induced osteoporosis (GIOP). Here, we revealed that the two main characteristics of GIOP might inhibit bone formation and enhance bone resorption. INTRODUCTION: The aim of this study is to assess the expression of the main RAS components in the trabecular bone of lumbar vertebrae in GIOP and analyze the relationship between the major RAS components and BMD. METHODS: We collected 96 inpatient cases of lumbar disc herniation from patients who underwent dual-energy X-ray absorptiometry examinations followed by surgical treatment in our hospital. Patients were divided into the GIOP group (n = 48) and control group (n = 48). The circulating and local expression levels of the main RAS components were examined. The correlation between the main RAS components and BMD was then analyzed. RESULTS: The mRNA expression of local bone angiotensin type 1 and 2 receptors (AT1R and AT2R, respectively) and RANKL was higher in the GIOP group compared with the control group (p < 0.001), but there was no difference in the circulating protein levels between groups (p > 0.05). Multiple logistic regression analysis revealed that AT1R and AT2R expression and the RANKL/OPG ratio in local bone were negatively associated with BMD (p < 0.001, odds ratio (OR) 1.236, 95 % confidence interval (CI) 1.207-1.333; p < 0.001, OR 1.971, 95% CI 1.809-2.233; and p < 0.001, OR 1.676, 95% CI 1.546-1.845, respectively). CONCLUSION: This study provides evidence that the role of local RAS is related to BMD in GIOP patients, and suggests that local RAS might influence RANKL/OPG signaling to modulate bone metabolism.
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