期刊
BIOMATERIALS
卷 84, 期 -, 页码 167-183出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2016.01.034
关键词
Guided bone regeneration; Membrane; In vivo; Gene expression; Western blot; Histomorphometry
资金
- BIOMATCELL VINN Excellence Center of Biomaterials and Cell Therapy
- Vastra Gotaland Region
- Swedish Research Council [K2015-52X-09495-28-4]
- LUA/ALF grant
- Stiftelsen Handlanden Hjalmar Svensson
- Vilhelm and Martina Lundgren Vetenskapsfond
- IngaBritt and Arne Lundberg Foundation
- Area of Advance Materials of Chalmers
- GU Biomaterials within the Strategic Research Area initiative
- Ministry of Higher Education, Libya
The working hypothesis of guided bone regeneration (GBR) is that the membrane physically excludes non-osteogenic tissues from interfering with bone healing. However, the underlying mechanisms are insufficiently explained. This study aimed to investigate the molecular and structural pattern of bone healing in trabecular bone defects, with and without naturally derived resorbable membrane. Defects were created in rat femurs and treated with the membrane or left empty (sham). After 3d, 6d and 28d, the defect sites and membranes were harvested and analyzed with histology, histomorphometry, quantitative-polymerase chain reaction (qPCR), Western blot (WB) and immunohistochemistry (IHC). Histomorphometry demonstrated that the presence of the membrane promoted bone formation in early and late periods. This was in parallel with upregulation of cell recruitment and coupled bone remodeling genes in the defect. Cells recruited into the membrane expressed signals for bone regeneration (BMP-2, FGF-2, TGF-beta 1 and VEGF). Whereas the native membrane contained FGF-2 but not BMP-2, an accumulation of FGF-2 and BMP-2 proteins and immunoreactive cells were demonstrated by WB and IHC in the in vivo implanted membrane. The results provide cellular and molecular evidence suggesting a novel role for the membrane during GBR, by acting as a bioactive compartment rather than a passive barrier. (C) 2016 The Authors. Published by Elsevier Ltd.
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