绝经后骨质疏松的骨免疫学机制
The mechanism of osteoimmunology in postmenopausal osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2023.07.019
中文关键词:  骨免疫学  免疫细胞  细胞因子  趋化因子  绝经后骨质疏松
英文关键词:osteoimmunology  immune cells  cytokines  chemokines  postmenopausal osteoporosis
基金项目:国家自然科学基金面上项目(81460171,81760164)
作者单位
何姣姣1 陈以发2 陈玉林1 张敏1 杨雅1* 1.南昌大学第二附属医院内分泌代谢科江西 南昌 330006 2.赣州市人民医院内分泌代谢科江西 赣州 341000 
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中文摘要:
      绝经后骨质疏松是雌激素缺乏引起骨形成与骨吸收解耦联,导致骨吸收大于骨形成,进而引起骨量减少,一般表现为骨密度的降低及骨微结构的破坏,最终骨脆性增加易于骨折。随着我国经济社会的发展,人口老龄化日益增加,绝经后骨质疏松的患病率也日趋上升,给患者家庭及社会医疗带来了极大的挑战。绝经后骨质疏松被认为是一种慢性低度炎症的全身性疾病。雌激素缺乏使得B细胞及T细胞被激活,激活的淋巴细胞分泌TNF-α、IL-17、IL-6及RANKL等促骨吸收因子促进破骨细胞骨吸收。目前认为雌激素缺乏导致的骨丢失与趋化因子、免疫细胞及其分泌的细胞因子密切相关,即绝经后骨质疏松的骨免疫学机制。
英文摘要:
      Postmenopausal osteoporosis is due to decoupling of bone formation and bone resorption caused by estrogen deficiency, which leads to bone resorption over bone formation, decrease of bone mass, decrease of bone mineral density, destruction of bone microstructure, and increase of bone fragility. With the economic and social development of our country, the aging population is increasing day by day. The prevalence of postmenopausal osteoporosis is also increasing, which brings great challenge to patients' families and social health care. Postmenopausal osteoporosis is considered to be a systemic disease of chronic low-grade inflammation. Estrogen deficiency activates B cells and T cells, and activates lymphocytes to secrete bone resorption factors, such as TNF-α, IL-17, IL-6, and RANKL, to promote bone resorption. It is believed that the bone loss caused by estrogen deficiency is closely related to chemokines, immune cells, and their secreted cytokines, which is the mechanism of osteoimmunology in postmenopausal osteoporosis.
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