Kai Dong1, Wen-Juan Zhou1, Zhong-Hao Liu1, Peng-Jie Hao2. 1. Department of Dental Implantology, Yantai Stomatological Hospital Affiliated to Binzhou Medical College, No. 142, North Great Str, Yantai, Shandong, 264008, People's Republic of China. 2. Department of Dental Implantology, Yantai Stomatological Hospital Affiliated to Binzhou Medical College, No. 142, North Great Str, Yantai, Shandong, 264008, People's Republic of China. haopengjie2006@163.com.
Abstract
BACKGROUND: Concentrated growth factor (CGF) is a third-generation platelet concentrate product; the major source of growth factors in CGF is its extract; however, there are few studies on the overall effects of the extract of CGF (CGF-e). The aim of this study was to investigate the effect and mechanism of CGF-e on MC3T3-E1 cells in vitro and to explore the effect of combination of CGF-e and bone collagen (Bio-Oss Collagen, Geistlich, Switzerland) for bone formation in cranial defect model of rats in vivo. METHODS: The cell proliferation, ALP activity, mineral deposition, osteogenic-related gene, and protein expression were evaluated in vitro; the newly formed bone was evaluated by histological and immunohistochemical analysis through critical-sized cranial defect rat model in vivo. RESULTS: The cell proliferation, ALP activity, mineral deposition, osteogenic-related gene, and protein expression of CGF-e group were significantly increased compared with the control group. In addition, there was significantly more newly formed bone in the CGF-e + bone collagen group, compared to the blank control group and bone collagen only group. CONCLUSIONS: CGF-e activated the PI3K/AKT signaling pathway to enhance osteogenic differentiation and mineralization of MC3T3-E1 cells and promoted the bone formation of rat cranial defect model.
BACKGROUND: Concentrated growth factor (CGF) is a third-generation platelet concentrate product; the major source of growth factors in CGF is its extract; however, there are few studies on the overall effects of the extract of CGF (CGF-e). The aim of this study was to investigate the effect and mechanism of CGF-e on MC3T3-E1 cells in vitro and to explore the effect of combination of CGF-e and bone collagen (Bio-Oss Collagen, Geistlich, Switzerland) for bone formation in cranial defect model of rats in vivo. METHODS: The cell proliferation, ALP activity, mineral deposition, osteogenic-related gene, and protein expression were evaluated in vitro; the newly formed bone was evaluated by histological and immunohistochemical analysis through critical-sized cranial defect rat model in vivo. RESULTS: The cell proliferation, ALP activity, mineral deposition, osteogenic-related gene, and protein expression of CGF-e group were significantly increased compared with the control group. In addition, there was significantly more newly formed bone in the CGF-e + bone collagen group, compared to the blank control group and bone collagen only group. CONCLUSIONS: CGF-e activated the PI3K/AKT signaling pathway to enhance osteogenic differentiation and mineralization of MC3T3-E1 cells and promoted the bone formation of rat cranial defect model.
Authors: Henning Schliephake; Alberto Sicilia; Bilal Al Nawas; Nikos Donos; Reinhard Gruber; Søren Jepsen; Iva Milinkovic; Andrea Mombelli; Jose Manuel Navarro; Marc Quirynen; Isabella Rocchietta; Morten Schiødt; Søren Schou; Alexandra Stähli; Andreas Stavropoulos Journal: Clin Oral Implants Res Date: 2018-10 Impact factor: 5.977