中文摘要：

背景：骨质疏松是表现为骨矿化密度低下以及骨微结构不良,从而易导致骨折发生的一种疾病,常并发口腔表征。甲状旁腺激素是在骨形成以及钙盐沉积过程中的重要调节因素,间歇性的甲状旁腺激素注射已经被广泛的证实可以促进骨质的形成。目的：探讨甲状旁腺激素增强骨密度以及调节骨形成代谢的可能细胞及分子机制。方法：由第一作者用计算机检索全国期刊全文数据库（CNKI）,Medline数据库,检索词分别为＂甲状旁腺激素,骨质疏松,成骨细胞,骨形成＂和＂Parathyroid hormone;osteoporosis;osteoblast;osteogenesis＂。从甲状旁腺激素对成骨细胞分化、增殖的作用,甲状旁腺激素对成骨细胞凋亡的作用,甲状旁腺激素与Wnt/β-catenin通路以及其他细胞因子的作用关系3个方面进行总结。按纳入和排除标准对文献进行筛选,共纳入41篇文章。结果与结论：甲状旁腺激素作用于甲状旁腺激素Ⅰ型受体,触发经典的G蛋白信号通路。甲状旁腺激素主要通过蛋白激酶信号A通路,调节其下游反应蛋白。间歇性使用甲状旁腺激素提高成骨细胞增殖能力,提高成骨细胞骨转录因子runx2和骨钙素（m RNA和蛋白水平）的表达,通过对抗氧化应激抑制成骨细胞凋亡,从而促进成骨。

英文摘要：

BACKGROUND： Osteoporosis is characterized by low bone mineral density and/or poor bone microarchitecture leading to an increased risk of fractures. Oral manifestations can be frequently discovered in osteoporosis patients. Osteoporosis therapies have mostly relied on antiresorptive drugs. Parathyroid hormone plays a significant role in osteogenesis and calcium deposition. Intermittent exposure to parathyroid hormone has been widely proved to lead to a net increase in bone formation. OBJECTIVE： To discuss the possibly cellular and molecular mechanism of parathyroid hormone in strengthening the bone mineral density and regulating bone formation. METHODS： An online search of CNKI and Medline databases was performed for relevant articles using keywords of ＂parathyroid hormone; osteoporosis; osteoblast; osteogenesis＂ in Chinese and English, respectively. Relevant articles were summarized from three aspects： effects of parathyroid hormone on differentiation and proliferation of osteoblasts, effects of parathyroid hormone on osteoblast apoptosis, and the relationship of parathyroid hormone with Wnt/beta-catenin pathway and other cytokines. According to inclusioncriteria, 41 articles were retained at last. RESULTS AND CONCLUSION：Parathyroid hormone exerts an effect on parathyroid hormone type Ⅰ receptor, triggering a classic G protein signaling pathway. Parathyroid hormone mainly works through protein kinase A signaling pathway, adjusting its downstream c-reactive protein. Intermittent use of parathyroid hormone can increase osteoblast proliferation, increase osteoblast runx2 and osteocalcin at m RNA and protein levels, inhibit osteoblast apoptosis by against oxidative stress, so as to promote osteogenesis.