scholarly journals Cortical bone development under the growth plate is regulated by mechanical load transfer

2006 ◽  
Vol 208 (1) ◽  
pp. 73-79 ◽  
Author(s):  
E. Tanck ◽  
G. Hannink ◽  
R. Ruimerman ◽  
P. Buma ◽  
E. H. Burger ◽  
...  
Keyword(s):  
Cortical Bone ◽  
Growth Plate ◽  
Load Transfer ◽  
Mechanical Load ◽  
Bone Development

Isolation, Culture and Identification of Bovine Skeletal Stem Cells

2021 ◽  
Vol 11 (12) ◽  
pp. 2337-2345
Author(s):  
Junhui Lai ◽  
Qin Yang ◽  
Ruining Liang ◽  
Weijun Guan ◽  
Xiuxia Li
Keyword(s):  
Stem Cells ◽  
Cell Surface ◽  
Bone Formation ◽  
Growth Plate ◽  
Bone Development ◽  
Long Bone ◽  
Biological Characterization ◽  
Self Renewal ◽  
And Cartilage

The growth plate is essential in long bone formation and contains a wealth of skeletal stem cells (SSCs). Though the origin and the mechanism for SSCs generation remain uncertain, recent studies demonstrate the transition from cartilage to bone that in the lineage for bone development. SSCs possesses the ability to differentiate into bone and cartilage in vitro. In this research, we aimed to isolate and culture the skeletal stem cells from bovine cattle and then studied its biological characterization. The results showed that these bovine SSCs are positive for PDPN+CD73+CD164+CD90+CD44+ cell surface bio-markers, they are capable of self-renewal and differentiation. Our dates proved that SSCs exists in bovine’s long bone.

Altered Load Transfer in the Pelvis in the Presence of Periprosthetic Osteolysis

2014 ◽  
Vol 136 (11) ◽  
Author(s):  
Jacob T. Munro ◽  
Justin W. Fernandez ◽  
James S. Millar ◽  
Cameron G. Walker ◽  
Donald W. Howie ◽  
...  
Keyword(s):  
Cortical Bone ◽  
Load Transfer ◽  
Von Mises Stress ◽  
Patient Specific ◽  
Fe Model ◽  
Stress Concentrations ◽  
Periprosthetic Osteolysis ◽  
Total Hip ◽  
Long Term Follow Up ◽  
Von Mises

Periprosthetic osteolysis in the retroacetabular region with cancellous bone loss is a recognized phenomenon in the long-term follow-up of total hip replacement. The effects on load transfer in the presence of defects are less well known. A validated, patient-specific, 3D finite element (FE) model of the pelvis was used to assess changes in load transfer associated with periprosthetic osteolysis adjacent to a cementless total hip arthroplasty (THA) component. The presence of a cancellous defect significantly increased (p < 0.05) von Mises stress in the cortical bone of the pelvis during walking and a fall onto the side. At loads consistent with single leg stance, this was still less than the predicted yield stress for cortical bone. During higher loads associated with a fall onto the side, highest stress concentrations occurred in the superior and inferior pubic rami and in the anterior column of the acetabulum with larger cancellous defects.

Fatigue of Notched CMC Plates Under Variable Thermomechanical Loads

2000 ◽  
Author(s):  
Arvind Nagar ◽  
Ming Xie
Keyword(s):  
Load Transfer ◽  
Mechanical Load ◽  
Empirical Relation ◽  
Ceramic Matrix Composite ◽  
Peak Stress ◽  
Load Cycle ◽  
Fatigue Tests ◽  
Laminated Plates ◽  
Open Hole ◽  
Stress Ratios

Abstract The work is a part of a major study to develop design analysis methods for strength and life of CMC structural joints. This paper describes results of thermomechanical fatigue tests conducted on open hole ceramic matrix composite laminated plates. The open hole represent the zero load transfer in a joint. The thermomechanical spectrum loads included mechanical load cycle blocks of various stress levels and stress ratios. The thermal loads were varied simultaneously with mechanical loads for the duration of a representative generic flight. The spectrum peak stress versus life data was developed for the case when the peak temperature is 1500 F. An empirical relation to describe the fatigue life is presented. The results show that a CMC laminate with an open hole spend most of the life during initiation.

scholarly journals Predicting cortical bone adaptation to axial loading in the mouse tibia

2015 ◽  
Vol 12 (110) ◽  
pp. 20150590 ◽  
Author(s):  
A. F. Pereira ◽  
B. Javaheri ◽  
A. A. Pitsillides ◽  
S. J. Shefelbine
Keyword(s):  
Cortical Bone ◽  
Computational Models ◽  
Mechanical Load ◽  
Fluid Velocity ◽  
Structural Response ◽  
Axial Loading ◽  
Mechanical Stimulus ◽  
Bone Adaptation ◽  
Mouse Tibia ◽  
Efficient Loading

The development of predictive mathematical models can contribute to a deeper understanding of the specific stages of bone mechanobiology and the process by which bone adapts to mechanical forces. The objective of this work was to predict, with spatial accuracy, cortical bone adaptation to mechanical load, in order to better understand the mechanical cues that might be driving adaptation. The axial tibial loading model was used to trigger cortical bone adaptation in C57BL/6 mice and provide relevant biological and biomechanical information. A method for mapping cortical thickness in the mouse tibia diaphysis was developed, allowing for a thorough spatial description of where bone adaptation occurs. Poroelastic finite-element (FE) models were used to determine the structural response of the tibia upon axial loading and interstitial fluid velocity as the mechanical stimulus. FE models were coupled with mechanobiological governing equations, which accounted for non-static loads and assumed that bone responds instantly to local mechanical cues in an on–off manner. The presented formulation was able to simulate the areas of adaptation and accurately reproduce the distributions of cortical thickening observed in the experimental data with a statistically significant positive correlation (Kendall's τ rank coefficient τ = 0.51, p < 0.001). This work demonstrates that computational models can spatially predict cortical bone mechanoadaptation to a time variant stimulus. Such models could be used in the design of more efficient loading protocols and drug therapies that target the relevant physiological mechanisms.

Involvement of matrix metalloproteinases in the growth plate response to physiological mechanical load

2010 ◽  
Vol 108 (1) ◽  
pp. 172-180 ◽  
Author(s):  
Adi Reich ◽  
Stav Simsa Maziel ◽  
Ziv Ashkenazi ◽  
Efrat Monsonego Ornan
Keyword(s):  
Growth Plate ◽  
Mechanical Loading ◽  
Mechanical Load ◽  
Tissue Growth ◽  
Matrix Assembly ◽  
Growth Plates ◽  
Load Release ◽  
Catch Up

Enzymes from the matrix metalloproteinase (MMP) family play a crucial role in growth-plate vascularization and ossification via proteolytic cleavage and remodeling of the extracellular matrix. Their regulation in the growth plate is crucial for normal matrix assembly. Endochondral ossification, which takes place at the growth plates, is influenced by mechanical loading. Using an in vivo avian model for mechanical loading, we have found increased blood penetration into the growth plates of loaded chicks. The purpose of this work was to study the involvement of MMP-2, -3, -9, -13, and -16 in the growth plate's response to loading and in the catch-up growth resulting from load release. We found that mechanical loading, as well as release from load, upregulated MMP-2, -9, and -13 expressions. In contrast, MMP-3, associated with cartilage injuries, and its associated protein connective tissue growth factor (CTGF), were downregulated by the load. However, after release from load, MMP-3 was upregulated and CTGF levels were elevated and caught up with the control. MMP-3 and CTGF were also downregulated after 60 min of mechanical stretching in vitro. These results demonstrate the central role of MMPs in the growth plate's response to mechanical loading, as well as in the catch-up growth followed load release.

scholarly journals Predicting cortical bone adaptation to axial loading in the mouse tibia

2015 ◽  
Author(s):  
Andre F Pereira ◽  
Behzad Javaheri ◽  
Andrew Pitsillides ◽  
Sandra Shefelbine
Keyword(s):  
Cortical Bone ◽  
Computational Models ◽  
Mechanical Load ◽  
Fluid Velocity ◽  
Structural Response ◽  
Axial Loading ◽  
Mechanical Stimulus ◽  
Bone Adaptation ◽  
Mouse Tibia ◽  
Efficient Loading

The development of predictive mathematical models can contribute to a deeper understanding of the specific stages of bone mechanobiology and the process by which bone adapts to mechanical forces. The objective of this work was to predict, with spatial accuracy, cortical bone adaptation to mechanical load, in order to better understand the mechanical cues that might be driving adaptation. The axial tibial loading model was used to trigger cortical bone adaptation in C57BL/6 mice and provide relevant biological and biomechanical information. A method for mapping cortical thickness in the mouse tibia diaphysis was developed, allowing for a thorough spatial description of where bone adaptation occurs. Poroelastic finite-element (FE) models were used to determine the structural response of the tibia upon axial loading and interstitial fluid velocity as the mechanical stimulus. FE models were coupled with mechanobiological governing equations, which accounted for non-static loads and assumed that bone responds instantly to local mechanical cues in an on-off manner. The presented formulation was able to simulate the areas of adaptation and accurately reproduce the distributions of cortical thickening observed in the experimental data with a statistically significant positive correlation (Kendall's tau rank coefficient \(\tau = 0.51\), \(p<0.001\)). This work demonstrates that computational models can spatially predict cortical bone mechanoadaptation to time variant stimulus. Such models could be used in the design of more efficient loading protocols and drugs therapies that target the relevant physiological mechanisms.

scholarly journals Cartilage Ablation of Sirt1 Causes Inhibition of Growth Plate Chondrogenesis by Hyperactivation of mTORC1 Signaling

Endocrinology ◽  
2019 ◽  
Vol 160 (12) ◽  
pp. 3001-3017 ◽  
Author(s):  
Xinxin Jin ◽  
Xiaomin Kang ◽  
Liting Zhao ◽  
Mao Xu ◽  
Tianping Xie ◽  
...  
Keyword(s):  
Growth Plate ◽  
Growth Retardation ◽  
Bone Growth ◽  
Bone Development ◽  
Conditional Knockout ◽  
Negative Regulator ◽  
Sirtuin 1 ◽  
Growth Plate Chondrocytes ◽  
Mtorc1 Signaling

Abstract A growing body of evidence implies a pivotal role of sirtuin-1 (Sirt1) in chondrocyte function and homeostasis; however, its underlying mechanisms mediating chondrogenesis, which is an essential process for physiological skeletal growth, are still poorly understood. In the current study, we generated TamCartSirt1−/− [Sirt1 conditional knockout (cKO)] mice to explore the role of Sirt1 during postnatal endochondral ossification. Compared with control mice, cKO mice exhibited growth retardation associated with inhibited chondrocyte proliferation and hypertrophy, as well as activated apoptosis. These effects were regulated by hyperactivation of mammalian target of rapamycin complex 1 (mTORC1) signaling, and thereby inhibition of autophagy and induction of endoplasmic reticulum stress in growth plate chondrocytes. IP injection of the mTORC1 inhibitor rapamycin to mice with Sirt1 deletion partially neutralized such inhibitory effects of Sirt1 ablation on longitudinal bone growth, indicating the causative link between SIRT1 and mTORC1 signaling in the growth plate. Mechanistically, SIRT1 interacted with tuberous sclerosis complex 2 (TSC2), a key upstream negative regulator of mTORC1 signaling, and loss of Sirt1 inhibited TSC2 expression, resulting in hyperactivated mTORC1 signaling in chondrocytes. In conclusion, our findings suggest that loss of Sirt1 may trigger mTORC1 signaling in growth plate chondrocytes and contributes to growth retardation, thus indicating that SIRT1 is an important regulator during chondrogenesis and providing new insights into the clinical potential of SIRT1 in bone development.

scholarly journals Osteosclerosis in F344/DuCrj rats

1988 ◽  
Vol 22 (2) ◽  
pp. 141-143 ◽  
Author(s):  
K. Yamasaki ◽  
C. Itakura
Keyword(s):  
Cortical Bone ◽  
Growth Plate ◽  
Lamellar Bone ◽  
Marrow Cavity ◽  
Aging Change ◽  
Bone Trabeculae ◽  
Regressive Changes

Osteosclerosis was observed in the tibia and sternum in F344/DuCrj rats of both sexes at 6, 18 and 30 months of age. The lesion first seen was a proliferation of osteogenic tissues on the marrow surface of the cortical bone and bone trabeculae, resulting in replacement of the marrow cavity by lamellar bone. Most of the affected rats had associated degenerative osteoarthrosis and regressive changes of the growth plate. Osteosclerosis was considered to be an aging change, lesions were observed at 6 months and increased in frequency with age.

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