scholarly journals Comparative Evaluation of Bone Repair with Four Different Bone Substitutes in Critical Size Defects

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Gustavo Grossi-Oliveira ◽  
Leonardo P. Faverani ◽  
Bruno Coelho Mendes ◽  
Tárik Ocon Braga Polo ◽  
Gabriel Cury Batista Mendes ◽  
...  
Keyword(s):  
Bone Repair ◽  
Immunohistochemical Analysis ◽  
Bone Substitutes ◽  
Vascular Endothelial ◽  
Calvarial Bone ◽  
Critical Size Defects ◽  
Related Transcription Factor ◽  
Osteoconductive Property ◽  
Bovine Hydroxyapatite ◽  
Endothelial Growth Factor

This study evaluated the osteoconductive potential of four biomaterials used to fill bone defects. For this, 24 male Albino rabbits were submitted to the creation of a bilateral 8 mm calvarial bone defect. The animals were divided into four groups—bovine hydroxyapatite, Bio-Oss® (BIO); Lumina-Bone Porous® (LBP); Bonefill® (BFL); and an alloplastic material, Clonos® (CLN)—and were euthanized at 14 and 40 days. The samples were subjected to histological and histometric analysis for newly formed bone area. Immunohistochemical analysis for Runt-related transcription factor 2 (Runx2), vascular endothelial growth factor (VEGF), and osteocalcin (OC) was performed. After statistical analysis, the CLN group showed greater new bone formation (NB) in both periods analyzed (p<0.05). At 14 days, the NB showed greater values in BIO in relation to LBP and BFL groups; however, after 40 days, the LBP group surpassed the results of BIO (p<0.001). The immunostaining showed a decrease in Runx2 intensity in BIO after 40 days, while it increased for LBP (p<0.05). The CLN showed increased OC compared to the other groups in both periods analyzed (p<0.05). Therefore, CLN showed the best osteoconductive behavior in critical defects in rabbit calvaria, and BFL showed the lowest osteoconductive property.

Adenovirus-mediated expression of vascular endothelial growth factor-a potentiates bone morphogenetic protein9-induced osteogenic differentiation and bone formation

2016 ◽  
Vol 397 (8) ◽  
pp. 765-775 ◽  
Author(s):  
Chang-jun Pi ◽  
Kai-lu Liang ◽  
Zhen-yong Ke ◽  
Fu Chen ◽  
Yun Cheng ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Bone Formation ◽  
Osteogenic Differentiation ◽  
Bone Repair ◽  
Osteoporotic Fractures ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Akt Inhibitor ◽  
Endothelial Growth Factor

Abstract Mesenchymal stem cells (MSCs) are suitable seed cells for bone tissue engineering because they can self-renew and undergo differentiation into osteogenic, adipogenic, chondrogenic, or myogenic lineages. Vascular endothelial growth factor-a (VEGF-a), an angiogenic factor, is also involved in osteogenesis and bone repair. However, the effects of VEGF-a on osteogenic MSCs differentiation remain unknown. It was previously reported that bone morphogenetic protein9 (BMP9) is one of the most important osteogenic BMPs. Here, we investigated the effects of VEGF-a on BMP9-induced osteogenesis with mouse embryo fibroblasts (MEFs). We found that endogenous VEGF-a expression was undetectable in MSCs. Adenovirus-mediated expression of VEGF-a in MEFs potentiated BMP9-induced early and late osteogenic markers, including alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). In stem cell implantation assays, VEGF-a augmented BMP9-induced ectopic bone formation. VEGF-a in combination with BMP9 effectively increased the bone volume and osteogenic activity. However, the synergistic effect was efficiently abolished by the phosphoinositide 3-kinase (PI3K)/AKT inhibitor LY294002. These results demonstrated that BMP9 may crosstalk with VEGF-a through the PI3K/AKT signaling pathway to induce osteogenic differentiation in MEFs. Thus, our findings demonstrate the effects of VEGF-a on BMP9-induced bone formation and provide a new potential strategy for treating nonunion fractures, large segmental bony defects, and/or osteoporotic fractures.

Immunohistochemical analysis of vascular endothelial growth factor cellular expression in ovarian endometriomata

2004 ◽  
Vol 81 (6) ◽  
pp. 1528-1533 ◽  
Author(s):  
Gaia Goteri ◽  
Guendalina Lucarini ◽  
Alessandra Filosa ◽  
Alessandra Pierantoni ◽  
Nina Montik ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Immunohistochemical Analysis ◽  
Vascular Endothelial ◽  
Cellular Expression ◽  
Endothelial Growth Factor

Tissue-type plasminogen activator deficiency delays bone repair: roles of osteoblastic proliferation and vascular endothelial growth factor

2014 ◽  
Vol 307 (3) ◽  
pp. E278-E288 ◽  
Author(s):  
Naoyuki Kawao ◽  
Yukinori Tamura ◽  
Katsumi Okumoto ◽  
Masato Yano ◽  
Kiyotaka Okada ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Bone Repair ◽  
Tissue Type ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Vessel Formation ◽  
Type Plasminogen Activator ◽  
Bone Damage ◽  
Annexin 2 ◽  
Endothelial Growth Factor

Further development in research of bone regeneration is necessary to meet the clinical demand for bone reconstruction. Recently, we reported that plasminogen is crucial for bone repair through enhancement of vessel formation. However, the details of the role of tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) in the bone repair process still remain unknown. Herein, we examined the effects of plasminogen activators on bone repair after a femoral bone defect using tPA-deficient ( tPA−/−) and uPA-deficient ( uPA−/−) mice. Bone repair of the femur was delayed in tPA−/− mice, unlike that in wild-type ( tPA+/+) mice. Conversely, the bone repair was comparable between wild-type ( uPA+/+) and uPA−/− mice. The number of proliferative osteoblasts was decreased at the site of bone damage in tPA−/− mice. Moreover, the proliferation of primary calvarial osteoblasts was reduced in tPA−/− mice. Recombinant tPA facilitated the proliferation of mouse osteoblastic MC3T3-E1 cells. The proliferation enhanced by tPA was antagonized by the inhibition of endogenous annexin 2 by siRNA and by the inhibition of extracellular signal-regulated kinase (ERK)1/2 phosphorylation in MC3T3-E1 cells. Vessel formation as well as the levels of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α) were decreased at the damaged site in tPA−/− mice. Our results provide novel evidence that tPA is crucial for bone repair through the facilitation of osteoblast proliferation related to annexin 2 and ERK1/2 as well as enhancement of vessel formation related to VEGF and HIF-1α at the site of bone damage.

Sign in / Sign up

Export Citation Format

Share Document