scholarly journals 3D Assessment of Cortical Bone Porosity and Tissue Mineral Density Using High-Resolution µCT: Effects of Resolution and Threshold Method

2013 ◽  
Vol 29 (1) ◽  
pp. 142-150 ◽  
Author(s):  
Paolo E Palacio-Mancheno ◽  
Adriana I Larriera ◽  
Stephen B Doty ◽  
Luis Cardoso ◽  
Susannah P Fritton
2015 ◽  
Vol 137 (1) ◽  
Author(s):  
Narges Kaynia ◽  
Elaine Soohoo ◽  
Tony M. Keaveny ◽  
Galateia J. Kazakia

This study investigated the effects of intraspecimen variations in tissue mineral density (TMD) on the apparent-level stiffness of human trabecular bone. High-resolution finite element (FE) models were created for each of 12 human trabecular bone specimens, using both microcomputed tomography (μCT) and “gold-standard” synchrotron radiation μCT (SRμCT) data. Our results confirm that incorporating TMD spatial variation reduces the calculated apparent stiffness compared to homogeneous TMD models. This effect exists for both μCT- and SRμCT-based FE models, but is exaggerated in μCT-based models. This study provides a direct comparison of μCT to SRμCT data and is thereby able to conclude that the influence of including TMD heterogeneity is overestimated in μCT-based models.


2021 ◽  
Vol 42 ◽  
pp. 220-231
Author(s):  
S von Kroge ◽  
◽  
EM Wölfel ◽  
LB Buravkova ◽  
DA Atiakshin ◽  
...  

Space missions provide the opportunity to investigate the influence of gravity on the dynamic remodelling processes in bone. Mice were examined following space flight and subsequent recovery to determine the effects on bone compartment-specific microstructure and composition. The resulting bone loss following microgravity recovered only in trabecular bone, while in cortical bone the tissue mineral density was restored after only one week on Earth. Detection of TRAP-positive bone surface cells in the trabecular compartment indicated increased resorption following space flight. In cortical bone, a persistent reduced viability of osteocytes suggested an impaired sensitivity to mechanical stresses. A compartment-dependent structural recovery from microgravity-induced bone loss was shown, with a direct osteocytic contribution to persistent low bone volume in the cortical region even after a recovery period. Trabecular recovery was not accompanied by changes in osteocyte characteristics. These post-space-flight findings will contribute to the understanding of compositional changes that compromise bone quality caused by unloading, immobilisation, or disuse.


Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 570
Author(s):  
Masayoshi Yamada ◽  
Chongxiao Chen ◽  
Toshie Sugiyama ◽  
Woo Kyun Kim

Changes in medullary and cortical bone structure with age remain unclear. Twenty Hy-Line W36 hens, 25 or 52 weeks of age, were euthanized, and both tibiae were collected when an egg was present in the magnum. Serial cross sections of the tibiae were stained with Alcian blue. The bones were scanned using micro-computed tomography. Trabecular width (Tb.Wi) was significantly higher (p < 0.05) in 25-week-old hens, whereas medullary bone tissue volume (TV) was significantly higher (p < 0.01) in 52-week-old hens. 25-week-old hens had significantly higher (p < 0.01) bone volume fraction (BVF = calcified tissue / TV). Moreover, the cortical bone parameters were significantly higher (TV and bone mineral content (BMC) at p < 0.05, and bone volume (BV) and BVF at p < 0.01) in younger hens. Open porosity and total porosity, which indicate less density, were significantly higher (p < 0.01) in older hens. Older hens showed significantly higher (p < 0.01) tibial diaphysis TV than younger hens. Younger hens had significantly higher (p < 0.01) BV, BVF and bone mineral density (BMD) of the tibial diaphysis. These findings reveal that reductions in medullary bone quality might be associated with age-related low estrogen levels and stimulation of osteoclastic bone resorption by parathyroid hormone. Cortical bone quality decreased with enlargement of the Haversian canals and loss of volume, with a longer egg-laying period leading to osteoporosis.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Basel M. Al-Barghouthi ◽  
Larry D. Mesner ◽  
Gina M. Calabrese ◽  
Daniel Brooks ◽  
Steven M. Tommasini ◽  
...  

AbstractGenome-wide association studies (GWASs) for osteoporotic traits have identified over 1000 associations; however, their impact has been limited by the difficulties of causal gene identification and a strict focus on bone mineral density (BMD). Here, we use Diversity Outbred (DO) mice to directly address these limitations by performing a systems genetics analysis of 55 complex skeletal phenotypes. We apply a network approach to cortical bone RNA-seq data to discover 66 genes likely to be causal for human BMD GWAS associations, including the genes SERTAD4 and GLT8D2. We also perform GWAS in the DO for a wide-range of bone traits and identify Qsox1 as a gene influencing cortical bone accrual and bone strength. In this work, we advance our understanding of the genetics of osteoporosis and highlight the ability of the mouse to inform human genetics.


Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  

Intermittent PTH treatment increases cancellous bone mass in osteoporosis patients; however, it reveals diverse effects on cortical bone mass. Underlying molecular mechanisms for anabolic PTH actions are largely unknown. Because PTH regulates expression of osteopontin (OPN) in osteoblasts, OPN could be one of the targets of PTH in bone. Therefore, we examined the role of OPN in the PTH actions in bone. Intermittent PTH treatment neither altered whole long-bone bone mineral density nor changed cortical bone mass in wild-type 129 mice, although it enhanced cancellous bone volume as reported previously. In contrast, OPN deficiency induced PTH enhancement of whole-bone bone mineral density as well as cortical bone mass. Strikingly, although PTH suppressed periosteal bone formation rate (BFR) and mineral apposition rate (MAR) in cortical bone in wild type, OPN deficiency induced PTH activation of periosteal BFR and MAR. In cancellous bone, OPN deficiency further enhanced PTH increase in BFR and MAR. Analysis on the cellular bases for these phenomena indicated that OPN deficiency augmented PTH enhancement in the increase in mineralized nodule formation in vitro. OPN deficiency did not alter the levels of PTH enhancement of the excretion of deoxypyridinoline in urine, the osteoclast number in vivo, and tartrate-resistant acid phosphatase-positive cell development in vitro. These observations indicated that OPN deficiency specifically induces PTH activation of periosteal bone formation in the cortical bone envelope.


2003 ◽  
Vol 95 (2) ◽  
pp. 631-634 ◽  
Author(s):  
Jill E. Shea ◽  
Scott C. Miller ◽  
David C. Poole ◽  
John P. Mattson

Recent evidence suggests that patients suffering from chronic obstructive pulmonary disease are also at an increased risk of developing osteoporosis. The pathophysiological mechanism(s) linking these progressive diseases is unknown. The goal of this investigation was to determine whether there were alterations in bone mineral density and content, cortical bone structure and strength, and indexes of bone formation and resorption in the elastase-induced emphysematous hamster. At 3 wk after induction of emphysema, the femoral bone mineral content was 8% less ( P = 0.026) and the femoral fracture strength was 6% less ( P = 0.032) in the emphysematous hamster than in controls. The cortical area was 8.4% less ( P = 0.013) and the periosteal mineral appositional rate was 27% less ( P = 0.05) than in controls. Additionally, the endocortical eroded surface in the emphysematous group was about twice that in the control group ( P = 0.003). Differences in some indexes of bone formation and resorption, paralleled by differences in bone structure and strength, were observed 3 wk after induction of emphysema. These differences in skeletal metabolism and strength may help explain some of the skeletal changes associated with chronic obstructive pulmonary disease in humans.


2019 ◽  
Vol 96 ◽  
pp. 421-435 ◽  
Author(s):  
Ronald Seidel ◽  
Andreas Roschger ◽  
Ling Li ◽  
Joseph J. Bizzarro ◽  
Qiuting Zhang ◽  
...  

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