RESUMO
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.
RESUMO
The present study investigated the detailed in vitro osteogenic differentiation process and in vivo bone regenerative property of human amniotic epithelial cells (hAECs). The in vitro osteogenic differentiation process of hAECs was evaluated by biochemical staining, real-time polymerase chain reaction, and immunofluorescence. Next, ß-tricalcium phosphate (ß-TCP) scaffolds alone or loaded with hAECs were implanted into the alveolar defects of rats. Micro-computed tomography evaluation and histologic studies were conducted. Our results validated the in vitro osteogenic capacity of hAECs by upregulation of Runx2, osterix, alkaline phosphatase, collagen I, and osteopontin, with positive biochemical staining for osteoblasts. An epithelial-mesenchymal transformation process might be involved in the osteogenic differentiation of hAECs by increased expression of transforming growth factor-ß1. Our data also demonstrated that in vivo implantation of hAECs loaded on ß-TCP scaffolds, not only improved bone regeneration by direct participation, but also reduced the early host immune response to the scaffolds. The presented data indicate that hAECs possess proper osteogenic differentiation potential and a modulatory influence on the early tissue remodeling process, making these cells a potential source of progenitor cells for clinical restoration of the alveolar defect.
