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目的:探究毒性弥漫性甲状腺肿(又称Graves病，GD)患者外周血调节性T细胞(Treg)/辅助性T细胞17(Th17)及相关细胞因子与骨密度的相关性。方法:随机抽取2018年3月至2019年3月河南大学淮河医院收治的80例初诊GD患者为GD组，另抽取30例同期健康体检者为对照组，检测并比较两组外周血Treg/Th17，血清炎性因子水平和骨密度指标。结果:与对照组相比，GD组患者第1～4腰椎与股骨颈的骨密度值降低，血清中转化生长因子-β(TGF-β)表达及骨保护蛋白(OPG)/细胞核因子-κB受体活化因子配体(RANKL)比值亦降低，外周血中Treg/Th17同样降低，而白细胞介素-17(IL-17)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、OPG、核因子κB受体激活因子(RANK)、RANKL表达水平增加。Pearson相关性分析显示，Treg/Th17与腰椎及股骨颈的骨密度变化以及TGF-β、OPG/RANKL呈正相关(n P<0.05)，与IL-6、IL-17、TNF-α呈负相关(n P<0.05)。n 结论:GD患者骨密度的降低可能与Treg/Th17平衡紊乱介导的OPG/RANK/RANKL系统对骨代谢的负性调控相关。“,”Objective:To investigate the correlation of peripheral blood the regulatory T cells (Treg)/T helper cell 17 (Th17), and related cytokines with bone mineral density (BMD) in patients with Graves disease (GD).Methods:Eighty newly diagnosed GD patients admitted to Huaihe Hospital of Henan University from March 2018 to March 2019 were randomly selected as the GD group, and another 30 healthy people in the same period were selected as the control group. Treg/Th17 in peripheral blood, the levels of serum inflammatory factors and BMD were detected and compared between the two groups.Results:Compared with the control group, the BMD of the 1st to 4th lumbar vertebrae and femoral neck of GD patients were significantly reduced, the expression of transforming growth factor-β (TGF-β) and osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL) in serum were also significantly reduced, Treg/Th17 in peripheral blood were also significantly decreased, while the expression of interleukin-17 (IL-17), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), OPG, receptor activator of nuclear factor kappa B (RANK), RANKL were significantly increased. Pearson correlation analysis showed that Treg/Th17 was positively correlated with the changes of BMD in lumbar spine and femoral neck, TGF-β, and OPG/RANKL (n P<0.05), and it was negatively correlated with IL-6, IL-17 and TNF-α(n P<0.05).n Conclusions:The decrease of BMD in GD patients may be related to the negative regulation of OPG/RANK/RANKL system on bone metabolism mediated by Treg/Th17 imbalance.