scholarly journals Bone Remodeling Model Integrating the Biological Function and Damage Influences for the Cortical-Trabecular Interface

2021 ◽  
Vol 9 ◽  
Author(s):  
Imed SOLTANI ◽  
◽  
Imane AIT OUMGHAR ◽  
Abdelwahed BARKAOUI ◽  
Tarek LAZGHAB ◽  
...  

Bone remodeling process has been widely investigated in literature from an experimental and theoretical viewpoint. Indeed, the biological process of bone remodeling allows a continuous renewal of the microstructure over time and thus, it contributes to decrease the bone damage by repairing it. This research work aims to study the biological function’s (fbio) effects on the bone remodeling process trough bone density evolution. Parameter fbio is one of the important parameters that controls bone volume variation. The biological bone remodeling process is modeled in terms of equations describing the activity of the Basic Multi-cellular Units (BMU). We use a mathematical model to simulate damage repair, based on Garcia Aznar’s model. The results of simulation show a good match with experimental and clinical data: bone porosity decreases over time and decreases also as the biological factors increase. In the same view, the apparent density (ρa) decreases with bone volume fraction increases. We note that the governance of the evolution of bone density leads to consider the evolution of bone volume during youthful and the maturation phase with their saturation zone for adult in terms of growth.

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 492-501 ◽  
Author(s):  
Catherine A. Brownstein ◽  
Junhui Zhang ◽  
Althea Stillman ◽  
Bruce Ellis ◽  
Nancy Troiano ◽  
...  

Inactivating mutations of PHEX cause X-linked hypophosphatemia and result in increased circulating fibroblast growth factor 23 (FGF23). FGF23 action is dependent upon Klotho, which converts FGF receptor 1 into an FGF23-specific receptor. Disruption of Klotho results in a complex bone phenotype and hyperphosphatemia, the converse phenotype of X-linked hypophosphatemia. We examined effects of disrupting both Klotho and PHEX by creating a double-knockout (Klotho/HYP) mouse. The combined disruption corrected the hypophosphatemia in HYP mice, indicating that Klotho is epistatic to PHEX. FGF23 levels remained elevated in all groups except wild-type, indicating that Klotho is necessary for FGF23-dependent phosphaturic activity. 1,25-Dihydroxyvitamin D levels, reduced in HYP mice, were comparably elevated in Klotho and Klotho/HYP mice, demonstrating that Klotho is necessary for FGF23’s effect on vitamin D metabolism. Serum PTH levels were reduced in both Klotho and Klotho/HYP mice. Moreover, the Klotho null phenotype persisted in Klotho/HYP, maintaining the runty phenotype and decreased life span of Klotho null mice. Notably, microcomputed tomography analysis demonstrated greater trabecular bone volume fraction in Klotho/HYP mice than that in all other groups (Klotho/HYP, 56.2 ± 6.3%; Klotho, 32.5 ± 10.3%; HYP, 8.6 ± 7.7%; and wild type, 21.4 ± 3.4%; P < 0.004). Histomorphometric analysis confirmed the markedly increased trabecular bone density in Klotho/HYP mice and the well-established increase in osteoid volume in HYP mice. These observations suggest that with addition of Klotho loss of function, the overabundant osteoid typically produced in HYP mice (but fails to mineralize) is produced and mineralized in the double knockout, resulting in markedly enhanced trabecular bone density.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jingyan Fu ◽  
Matthew Goldsmith ◽  
Sequoia D. Crooks ◽  
Sean F. Condon ◽  
Martin Morris ◽  
...  

AbstractAnimals in space exploration studies serve both as a model for human physiology and as a means to understand the physiological effects of microgravity. To quantify the microgravity-induced changes to bone health in animals, we systematically searched Medline, Embase, Web of Science, BIOSIS, and NASA Technical reports. We selected 40 papers focusing on the bone health of 95 rats, 61 mice, and 9 rhesus monkeys from 22 space missions. The percentage difference from ground control in rodents was –24.1% [Confidence interval: −43.4, −4.9] for trabecular bone volume fraction and –5.9% [−8.0, −3.8] for the cortical area. In primates, trabecular bone volume fraction was lower by –25.2% [−35.6, −14.7] in spaceflight animals compared to GC. Bone formation indices in rodent trabecular and cortical bone were significantly lower in microgravity. In contrast, osteoclast numbers were not affected in rats and were variably affected in mice. Thus, microgravity induces bone deficits in rodents and primates likely through the suppression of bone formation.


2013 ◽  
Vol 135 (12) ◽  
Author(s):  
Arnav Sanyal ◽  
Tony M. Keaveny

The biaxial failure behavior of the human trabecular bone, which has potential relevance both for fall and gait loading conditions, is not well understood, particularly for low-density bone, which can display considerable mechanical anisotropy. Addressing this issue, we investigated the biaxial normal strength behavior and the underlying failure mechanisms for human trabecular bone displaying a wide range of bone volume fraction (0.06–0.34) and elastic anisotropy. Micro-computed tomography (CT)-based nonlinear finite element analysis was used to simulate biaxial failure in 15 specimens (5 mm cubes), spanning the complete biaxial normal stress failure space in the axial-transverse plane. The specimens, treated as approximately transversely isotropic, were loaded in the principal material orientation. We found that the biaxial stress yield surface was well characterized by the superposition of two ellipses—one each for yield failure in the longitudinal and transverse loading directions—and the size, shape, and orientation of which depended on bone volume fraction and elastic anisotropy. However, when normalized by the uniaxial tensile and compressive strengths in the longitudinal and transverse directions, all of which depended on bone volume fraction, microarchitecture, and mechanical anisotropy, the resulting normalized biaxial strength behavior was well described by a single pair of (longitudinal and transverse) ellipses, with little interspecimen variation. Taken together, these results indicate that the role of bone volume fraction, microarchitecture, and mechanical anisotropy is mostly accounted for in determining the uniaxial strength behavior and the effect of these parameters on the axial-transverse biaxial normal strength behavior per se is minor.


2005 ◽  
Vol 874 ◽  
Author(s):  
Richard Weinkamer ◽  
Markus A. Hartmann ◽  
Yves Brechet ◽  
Peter Fratzl

AbstractUsing a stochastic lattice model we have studied the architectural changes of trabecular bone occurring while the structure is remodeled. Our model considers the mechanical feedback loop, which control the remodeling process. A fast algorithm was employed to solve approximately the mechanical problem. A general feature of the model is that a networklike structure emerges, which further coarsens while the bone volume fraction remains unchanged. Decreasing the mechanical response of the system by either lowering the external load or the internal mechano-sensitivity leads not only to a reduction of the bone volume fraction, but results in topological changes of the trabecular bone architecture, where the loss of horizontal trabeculae is the most obvious effect.


2021 ◽  
Vol 8 (6) ◽  
pp. 201401
Author(s):  
A. A. Felder ◽  
S. Monzem ◽  
R. De Souza ◽  
B. Javaheri ◽  
D. Mills ◽  
...  

Changes in trabecular micro-architecture are key to our understanding of osteoporosis. Previous work focusing on structure model index (SMI) measurements have concluded that disease progression entails a shift from plates to rods in trabecular bone, but SMI is heavily biased by bone volume fraction. As an alternative to SMI, we proposed the ellipsoid factor (EF) as a continuous measure of local trabecular shape between plate-like and rod-like extremes. We investigated the relationship between EF distributions, SMI and bone volume fraction of the trabecular geometry in a murine model of disuse osteoporosis as well as from human vertebrae of differing bone volume fraction. We observed a moderate shift in EF median (at later disease stages in mouse tibia) and EF mode (in the vertebral samples with low bone volume fraction) towards a more rod-like geometry, but not in EF maximum and minimum. These results support the notion that the plate to rod transition does not coincide with the onset of bone loss and is considerably more moderate, when it does occur, than SMI suggests. A variety of local shapes not straightforward to categorize as rod or plate exist in all our trabecular bone samples.


2010 ◽  
Vol 2010 ◽  
pp. 1-6
Author(s):  
Zelieann R. Craig ◽  
Samuel L. Marion ◽  
Janet L. Funk ◽  
Mary L. Bouxsein ◽  
Patricia B. Hoyer

Previous work showed that retaining residual ovarian tissue protects young mice from accelerated bone loss following ovarian failure. The present study was designed to determine whether this protection is also present in aged animals. Aged (9–12 months) C57BL/6Hsd female mice were divided into: CON (vehicle), VCD (160 mg/kg; 15d), or OVX (ovariectomized). Lumbar BMD was monitored by DXA andμCT used to assess vertebral microarchitecture. BMD was not different between VCD and CON at any time point but was lower (P<.05) than baseline, starting 1 month after ovarian failure in VCD and OVX mice. FollowingμCT analysis there were no differences between CON and VCD, but OVX mice had lower bone volume fraction, trabecular thickness, and a trend for decreased connectivity density. These findings provide evidence that retention of residual ovarian tissue may protect aged follicle-depleted mice from accelerated bone loss to a lesser extent than that observed in young mice.


Bone ◽  
2009 ◽  
Vol 44 ◽  
pp. S375
Author(s):  
E. Perilli⁎ ◽  
A.M. Briggs ◽  
J.D. Wark ◽  
S. Kantor ◽  
I.H. Parkinson ◽  
...  

Bone ◽  
2006 ◽  
Vol 39 (6) ◽  
pp. 1218-1225 ◽  
Author(s):  
Grant Bevill ◽  
Senthil K. Eswaran ◽  
Atul Gupta ◽  
Panayiotis Papadopoulos ◽  
Tony M. Keaveny

2020 ◽  
Vol 143 (2) ◽  
Author(s):  
Matthew B. L. Bennison ◽  
A. Keith Pilkey ◽  
W. Brent Lievers

Abstract Cancellous bone is an anisotropic structure with architectural and mechanical properties that vary due to both skeletal site and disease state. This anisotropy means that, in order to accurately and consistently measure the mechanical properties of cancellous bone, experiments should be performed along the primary mechanical axis (PMA), that is, the orientation in which the mechanical properties are at their maximum value. Unfortunately, some degree of misalignment will always be present, and the magnitude of the resulting error is expected to be architecture dependent. The goal of this work is to quantify the dependence of the misalignment error, expressed in terms of change in apparent elastic modulus (ΔE), on both the bone volume fraction (BV/TV) and the degree of anisotropy (DA). Finite element method (FEM) models of bovine cancellous bone from five different skeletal sites were created at 5 deg and 20 deg from the PMA determined for each region. An additional set of models was created using image dilation/erosion steps in order to control for BV/TV and better isolate the effect of DA. Misalignment error was found to increase with increasing DA and decreasing BV/TV. At 5 deg misaligned from the PMA, error is relatively low (&lt;5%) in all cases but increases to 8–24% error at 20 deg. These results suggest that great care is needed to avoid introducing misalignment error into experimental studies, particularly when studying regions with high anisotropy and/or low bone volume fraction, such as vertebral or osteoporotic bone.


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