scholarly journals Time kinetics of bone defect healing in response to BMP-2 and GDF-5 characterised by in vivo biomechanics

2011 ◽  
Vol 21 ◽  
pp. 177-192 ◽  
Author(s):  
D Wulsten ◽  
◽  
V Glatt ◽  
A Ellinghaus ◽  
K Schmidt-Ble ◽  
...  
Keyword(s):  
Bone Defect ◽  
Defect Healing ◽  
Bone Defect Healing ◽  
Kinetics Of

scholarly journals Augmentation of bone defect healing using a new biocomposite scaffold: An in vivo study in sheep

2010 ◽  
Vol 6 (9) ◽  
pp. 3755-3762 ◽  
Author(s):  
U. van der Pol ◽  
L. Mathieu ◽  
S. Zeiter ◽  
P.-E. Bourban ◽  
P.-Y. Zambelli ◽  
...  
Keyword(s):  
Bone Defect ◽  
In Vivo Study ◽  
Defect Healing ◽  
Bone Defect Healing

scholarly journals In vivo tracking of segmental bone defect healing reveals that callus patterning is related to early mechanical stimuli

2012 ◽  
Vol 24 ◽  
pp. 358-371 ◽  
Author(s):  
M Mehta ◽  
◽  
S Checa ◽  
J Lienau ◽  
D Hutmacher ◽  
...  
Keyword(s):  
Bone Defect ◽  
Mechanical Stimuli ◽  
Segmental Bone Defect ◽  
Defect Healing ◽  
Bone Defect Healing ◽  
Segmental Bone

scholarly journals Bone morphogenetic protein 2-induced cellular chemotaxis drives tissue patterning during critical-sized bone defect healing: an in silico study

2021 ◽  
Author(s):  
Edoardo Borgiani ◽  
Georg N. Duda ◽  
Bettina M. Willie ◽  
Sara Checa
Keyword(s):  
Bone Tissue ◽  
Bone Defect ◽  
Computer Model ◽  
In Silico ◽  
Bone Defects ◽  
Bone Morphogenetic Protein 2 ◽  
Defect Healing ◽  
Tissue Patterning ◽  
Bone Defect Healing

AbstractCritical-sized bone defects are critical healing conditions that, if left untreated, often lead to non-unions. To reduce the risk, critical-sized bone defects are often treated with recombinant human BMP-2. Although enhanced bone tissue formation is observed when BMP-2 is administered locally to the defect, spatial and temporal distribution of callus tissue often differs from that found during regular bone healing or in defects treated differently. How this altered tissue patterning due to BMP-2 treatment is linked to mechano-biological principles at the cellular scale remains largely unknown. In this study, the mechano-biological regulation of BMP-2-treated critical-sized bone defect healing was investigated using a multiphysics multiscale in silico approach. Finite element and agent-based modeling techniques were combined to simulate healing within a critical-sized bone defect (5 mm) in a rat femur. Computer model predictions were compared to in vivo microCT data outcome of bone tissue patterning at 2, 4, and 6 weeks postoperation. In vivo, BMP-2 treatment led to complete healing through periosteal bone bridging already after 2 weeks postoperation. Computer model simulations showed that the BMP-2 specific tissue patterning can be explained by the migration of mesenchymal stromal cells to regions with a specific concentration of BMP-2 (chemotaxis). This study shows how computational modeling can help us to further understand the mechanisms behind treatment effects on compromised healing conditions as well as to optimize future treatment strategies.

scholarly journals In vitro and in vivo assessment of nanostructured porous biphasic calcium phosphate ceramics for promoting osteogenesis in an osteoporotic environment

RSC Advances ◽  
2018 ◽  
Vol 8 (26) ◽  
pp. 14646-14653 ◽  
Author(s):  
Kun Zhang ◽  
Jieyu Zhang ◽  
Kelei Chen ◽  
Xuefeng Hu ◽  
Yunbing Wang ◽  
...  
Keyword(s):  
Calcium Phosphate ◽  
Bone Defect ◽  
Biphasic Calcium Phosphate ◽  
Calcium Phosphate Ceramics ◽  
Defect Healing ◽  
Bone Defect Healing ◽  
In Vivo Assessment ◽  
Porous Biphasic Calcium Phosphate

Nanostructured porous biphasic calcium phosphate ceramics are able to significantly promote bone defect healing in an osteoporotic environment.

scholarly journals Cellular hypoxia promotes osteogenic differentiation of mesenchymal stem cells and bone defect healing via STAT3 signaling

2019 ◽  
Vol 24 (1) ◽  
Author(s):  
Xin Yu ◽  
Qilong Wan ◽  
Xiaoling Ye ◽  
Yuet Cheng ◽  
Janak L. Pathak ◽  
...  
Keyword(s):  
Osteogenic Differentiation ◽  
Bone Defect ◽  
Precursor Cells ◽  
Defect Healing ◽  
Stat3 Signaling ◽  
Bone Defect Healing ◽  
Cellular Hypoxia

Abstract Background Hypoxia in the vicinity of bone defects triggers the osteogenic differentiation of precursor cells and promotes healing. The activation of STAT3 signaling in mesenchymal stem cells (MSCs) has similarly been reported to mediate bone regeneration. However, the interaction between hypoxia and STAT3 signaling in the osteogenic differentiation of precursor cells during bone defect healing is still unknown. Methods In this study, we assessed the impact of different durations of CoCl2-induced cellular hypoxia on the osteogenic differentiation of MSCs. Role of STAT3 signaling on hypoxia induced osteogenic differentiation was analyzed both in vitro and in vivo. The interaction between cellular hypoxia and STAT3 signaling in vivo was investigated in a mouse femoral bone defect model. Results The peak osteogenic differentiation and expression of vascular endothelial growth factor (VEGF) occurred after 3 days of hypoxia. Inhibiting STAT3 reversed this effect. Hypoxia enhanced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and STAT3 phosphorylation in MSCs. Histology and μ-CT results showed that CoCl2 treatment enhanced bone defect healing. Inhibiting STAT3 reduced this effect. Immunohistochemistry results showed that CoCl2 treatment enhanced Hif-1α, ALP and pSTAT3 expression in cells present in the bone defect area and that inhibiting STAT3 reduced this effect. Conclusions The in vitro study revealed that the duration of hypoxia is crucial for osteogenic differentiation of precursor cells. The results from both the in vitro and in vivo studies show the role of STAT3 signaling in hypoxia-induced osteogenic differentiation of precursor cells and bone defect healing.

Sign in / Sign up

Export Citation Format

Share Document