Li Yizhou, Wang Yuan, Guo Yongchang, Wang Quanjian, Ouyang Yongri, Cao Yuju, Jin Tianbo, Wang Jianzhong
Inner Mongolia Medical University, Hohhot, Inner Mongolia Zhengzhou TCM Traumatology Hospital, Zhengzhou, Henan National Engineering Research Center for Miniaturized Detection System, Xi'an, Shanxi The College of Life Sciences Northwest University Department of Orthopedics and Traumatology, The 2nd Affiliated Hospital of Inner Mongolia University, Hohhot, Inner Mongolia, China.
Medicine (Baltimore). 2016 Jun;95(25):e3981. doi: 10.1097/MD.0000000000003981.
Alcohol-induced osteonecrosis of the femoral head (ONFH) is an important pathogenesis of nontraumatic ONFH. However, the mechanisms of the pathogenesis are still unknown. Osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) have been implicated in multiple functions including blocking osteoclast maturation, controlling vascular calcifications, and promoting tumor growth and metastasis. The purpose of this article was to explore the association between OPG and RANKL gene variants and alcohol-induced ONFH. Six hundred seventy male subjects (335 patients and 335 normal individuals) were enrolled in our study. We selected 24 single-nucleotide polymorphisms (SNPs) to evaluate the association between genetic susceptibility variants and alcohol-induced ONFH using the chi-square test and gene model analysis. Overall, the OPG SNPs (rs1032128 and rs11573828) were associated with the strongest increased risk of alcohol-induced ONFH in the recessive model (rs1032128: odds ratio [OR] 1.49, 95% confidence interval [CI] 1.00-2.22, P = 0.04 for G/A; rs11573828: OR 3.32, 95% CI 1.07-10.30, P = 0.03 for T/C). The RANKL SNP rs2200287 was also an increased risk factor (OR 3.65, 95% CI 1.53-8.47, P = 0.003 for T/C) in the recessive model. The rs11573856, rs3134056, and rs1564861 SNPs were considered protective factors for alcohol-induced ONFH. We concluded that OPG and RANKL polymorphisms were associated with the occurrence of alcohol-induced ONFH.
酒精性股骨头坏死（ONFH）是非创伤性ONFH的一种重要发病机制。然而，其发病机制仍不清楚。骨保护素（OPG）和核因子κB受体活化因子配体（RANKL）参与多种功能，包括阻断破骨细胞成熟、控制血管钙化以及促进肿瘤生长和转移。本文旨在探讨OPG和RANKL基因变异与酒精性ONFH之间的关联。我们的研究纳入了670名男性受试者（335例患者和335名正常个体）。我们选择了24个单核苷酸多态性（SNP），采用卡方检验和基因模型分析来评估遗传易感性变异与酒精性ONFH之间的关联。总体而言，在隐性模型中，OPG的SNP（rs1032128和rs11573828）与酒精性ONFH风险增加最为相关（rs1032128：优势比[OR]1.49, 95%置信区间[CI]1.00 - 2.22, G/A的P = 0.04；rs11573828：OR 3.32, 95% CI 1.07 - 10.30, T/C的P = 0.03）。RANKL的SNP rs2200287在隐性模型中也是一个风险增加因素（OR 3.65, 95% CI 1.53 - 8.47, T/C的P = 0.003）。rs11573856、rs3134056和rs1564861的SNP被认为是酒精性ONFH的保护因素。我们得出结论，OPG和RANKL基因多态性与酒精性ONFH的发生有关。
