Résumé
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 celular 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 inclusion criteria, 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 mRNA and protein levels, inhibit osteoblast apoptosis by against oxidative stress, so as to promote osteogenesis.