MR phase imaging to quantify bone volume fraction: Computer simulations and in vivo measurements

2000 ◽  
Vol 18 (3) ◽  
pp. 275-279 ◽  
Author(s):  
Sophie Allein ◽  
Evangelia Mihalopoulou ◽  
Rob Luypaert ◽  
Olivia Louis ◽  
George Panayiotakis ◽  
...  
2012 ◽  
Vol 83 (3) ◽  
pp. 402-409 ◽  
Author(s):  
Nan Ru ◽  
Sean Shih-Yao Liu ◽  
Li Zhuang ◽  
Song Li ◽  
Yuxing Bai

ABSTRACT Objective: To observe the real-time microarchitecture changes of the alveolar bone and root resorption during orthodontic treatment. Materials and Methods: A 10 g force was delivered to move the maxillary left first molars mesially in twenty 10-week-old rats for 14 days. The first molar and adjacent alveolar bone were scanned using in vivo microcomputed tomography at the following time points: days 0, 3, 7, and 14. Microarchitecture parameters, including bone volume fraction, structure model index, trabecular thickness, trabecular number, and trabecular separation of alveolar bone, were measured on the compression and tension side. The total root volume was measured, and the resorption crater volume at each time point was calculated. Univariate repeated measures analysis of variance with Bonferroni corrections were performed to compare the differences in each parameter between time points with significance level at P < .05. Results: From day 3 to day 7, bone volume fraction, structure model index, trabecular thickness, and trabecular separation decreased significantly on the compression side, but the same parameters increased significantly on the tension side from day 7 to day 14. Root resorption volume of the mesial root increased significantly on day 7 of orthodontic loading. Conclusions: Real-time root and bone resorption during orthodontic movement can be observed in 3 dimensions using in vivo micro-CT. Alveolar bone resorption and root resorption were observed mostly in the apical third on day 7 on the compression side; bone formation was observed on day 14 on the tension side during orthodontic tooth movement.


2016 ◽  
Vol 13 (114) ◽  
pp. 20150991 ◽  
Author(s):  
Patrik Christen ◽  
Friederike A. Schulte ◽  
Alexander Zwahlen ◽  
Bert van Rietbergen ◽  
Stephanie Boutroy ◽  
...  

A bone loading estimation algorithm was previously developed that provides in vivo loading conditions required for in vivo bone remodelling simulations. The algorithm derives a bone's loading history from its microstructure as assessed by high-resolution (HR) computed tomography (CT). This reverse engineering approach showed accurate and realistic results based on micro-CT and HR-peripheral quantitative CT images. However, its voxel size dependency, reproducibility and sensitivity still need to be investigated, which is the purpose of this study. Voxel size dependency was tested on cadaveric distal radii with micro-CT images scanned at 25 µm and downscaled to 50, 61, 75, 82, 100, 125 and 150 µm. Reproducibility was calculated with repeated in vitro as well as in vivo HR-pQCT measurements at 82 µm. Sensitivity was defined using HR-pQCT images from women with fracture versus non-fracture, and low versus high bone volume fraction, expecting similar and different loading histories, respectively. Our results indicate that the algorithm is voxel size independent within an average (maximum) error of 8.2% (32.9%) at 61 µm, but that the dependency increases considerably at voxel sizes bigger than 82 µm. In vitro and in vivo reproducibility are up to 4.5% and 10.2%, respectively, which is comparable to other in vitro studies and slightly higher than in other in vivo studies. Subjects with different bone volume fraction were clearly distinguished but not subjects with and without fracture. This is in agreement with bone adapting to customary loading but not to fall loads. We conclude that the in vivo bone loading estimation algorithm provides reproducible, sensitive and fairly voxel size independent results at up to 82 µm, but that smaller voxel sizes would be advantageous.


Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1329-1337 ◽  
Author(s):  
J. Peng ◽  
M. Bencsik ◽  
A. Louie ◽  
W. Lu ◽  
S. Millard ◽  
...  

G protein-coupled receptors (GPCRs) coupled to activation of Gs, such as the PTH1 receptor (PTH1R), have long been known to regulate skeletal function and homeostasis. However, the role of GPCRs coupled to other G proteins such as Gi is not well established. We used the tet-off system to regulate the expression of an activated Gi-coupled GPCR (Ro1) in osteoblasts in vivo. Skeletal phenotypes were assessed in mice expressing Ro1 from conception, from late stages of embryogenesis, and after weaning. Long bones were assessed histologically and by microcomputed tomography. Expression of Ro1 from conception resulted in neonatal lethality that was associated with reduced bone mineralization. Expression of Ro1 starting at late embryogenesis resulted in a severe trabecular bone deficit at 12 wk of age (>51% reduction in trabecular bone volume fraction in the proximal tibia compared with sex-matched control littermates; n = 11; P < 0.01). Ro1 expression for 8 wk beginning at 4 wk of age resulted in a more than 20% reduction in trabecular bone volume fraction compared with sex-matched control littermates (n = 16; P < 0.01). Bone histomorphometry revealed that Ro1 expression is associated with reduced rates of bone formation and mineral apposition without a significant change in osteoblast or osteoclast surface. Our results indicate that signaling by a Gi-coupled GPCR in osteoblasts leads to osteopenia resulting from a reduction in trabecular bone formation. The severity of the phenotype is related to the timing and duration of Ro1 expression during growth and development. The skeletal phenotype in Ro1 mice bears some similarity to that produced by knockout of Gs-α expression in osteoblasts and thus may be due at least in part to Gi-mediated inhibition of adenylyl cyclase.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3518-3518
Author(s):  
Paola Neri ◽  
Pierfrancesco Tassone ◽  
Zhenxin Shen ◽  
Nipun Patel ◽  
Robert Fajardo ◽  
...  

Abstract Multiple Myeloma (MM) is associated with significant skeletal changes including ospeoporosis and bone lesions in more than 80% of patients. Bone resorption is caused by an enhanced osteoclast number and activation. However, molecular and cellular basis for these effects are not completely understood. Here we describe a model that allows us to evaluate in vivo, the relationship and interactions between MM cells and cellular elements of bone formation and resorption. In this model, the BM stroma and IL-6-dependent human MM cell line (INA-6) was injected in a human bone chip implanted into SCID mice. Bone chip in the control mice were injected with media alone. At different time points (days 1, 7 and 30) following injection, myelomatous and control bone chips were retrieved, fixed in paraformaldehyde and evaluated by micro-computed tomography (μCT) and histological examinations for effects of MM cells on bone compartment. The μCT is a non-invasive quantitative imaging method that can asses the degree and extent of bone disease as well as quantify changes in bone structure, that may reflect the effect of interaction between MM cells and bone elements. Additionally, we have measured the levels of human osteocalcin in murine serum to reflect the remodelling of human bone in mice. We have observed that only at day 30 after the MM cell injections, lesions in myelomatous bone is observed in mice; while no significant changes in the matched control bones are seen. By 3-D histomorphometric parameters, calculated from μCT (bone volume fraction= bone volume/total volume), the quantitative measurement confirmed that at day 30, a decreased bone volume fraction (314) was observed in bones with MM compared with normal bones (394), due to reduction of bone density in the trabecular bone. Moreover histological examination of the same bones revealed a significant increase in number of multinucleated TRAP-expressing osteoclasts in mice engrafted with MM versus control (52 versus 8 per field, p= 0.011). Also compared to serum from control mice, animals with bone containing myeloma cells had significantly elevated markers of bone remodelling. To confirm the validity of this model to study effect of MM cells on bone as well as to show its utility for evaluation of novel agents active in MM bone disease, we treated mice with Zoledronic acid at 0,6 mg/kg, weekly for 2 months. As evaluated by μCT, X-rays and TRAP staining Zoledronic acid was able to significantly inhibit the development of bone lesions in treated mice compared to untreated mice. Additionally, , we also observed that Zoledronic acid was also able to retard the MM tumor growth as measured by human IL-6sR released by INA-6 cells in mice sera corroborating its reported anti-MM activity. This model therefore provides a reproducible and predictable in vivo system to study biology of bone disease in MM and to identify and evaluate therapeutic targets and agents targeting MM bone disease.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1078.3-1078
Author(s):  
E. Soldati ◽  
L. Escoffier ◽  
S. Gabrie ◽  
J. P. Mattei ◽  
S. Camilleri ◽  
...  

Background:In psoriatic arthritis (PA), a systemic inflammatory phenomenon, mainly mediated by TNFα, is characterized by a bone loss due to osteoclastic stimulation. Anti-TNFα treatment should inhibit this phenomenon having a role on systemic bone loss. Ultra-high field MRI (UHF MRI) may be a tool of choice for the quantification of bone microarchitecture (BM) in vivo.Objectives:The purpose of the present study was to quantify BM using UHF MRI in a PA patient and to follow up changes related to anti-TNFα treatment.Methods:An 18 years-old untreated PA patient with knee arthritis and 7 gender-matched healthy controls [21.6±0.8 years] were scanned using a gradient echo sequence at UHF MRI (TR/TE = 15/4.36ms). After a year of Adalimumab treatment, the patient underwent a second UHF MRI. BM analysis was performed on sagittal planes in regions corresponding to tendon insertion: proximal and distal patellar, and posterior tibial. A PET-FNa imaging was also performed before and after treatment. BM was characterized using the bone volume fraction (BVF), the trabecular thickness (TbTh) and the spacing (TbSp) and number of trabeculae (TbN). Student T-test was used for the statistical analysis and a p-value < 0.01 was considered as significative.Results:PET-FNa recorded before the treatment illustrated hypermetabolic areas which resumed after the treatment while the patient was in remission. The BM parameters are shown in figure 1. The BM parameters quantified before the treatment were very different as compared to controls. BVF was significatively lower (-33±23%), TbSp and TbN were significatively distinct (-27±3% and +27±9%) for all ROIs but proximal patellar, while TbTh was in the normal range (-2±2%). After 1 year of treatment, BM parameters were significantly improved. BVF was no longer different than controls (-8±6%). Similarly, TbSp and TbN were in the normal range (+13±12% and -15±10%) for all ROIs but posterior tibial. TbTh (-5±3%) was only significantly decreased for the distal patella.Table 1. Data are presented as mean ± SD. “P.” refers as patient. BVF: Bone volume fraction, TbTh: Trabecular Thickness, TbSp: Trabecular Space, TbN: Trabecular number. * indicates a statistically significant difference (p < 0.01) with the Healthy reference values.Conclusion:Our results illustrated knee microstructure alterations in a PA patient and a normalization after a year of treatment. The abnormalities initially observed were not only localized in the hypermetabolic regions identified by PET-FNa, suggesting that the bone loss was global and not related to inflammatory sites.Using UHF MRI, we highlighted and quantified in vivo BM anomalies in a patient with an inflammatory rheumatism together with the reversibility after one year of treatment.Acknowledgements:All the authors declare no conflict of interest.ES has received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Skodowska-Curie grant agreement No713750. Also, it has been carried out with the financial support of the Regional Council of Provence- Alpes-Côte d’Azur and with the financial support of the A*MIDEX (n° ANR- 11-IDEX-0001-02), funded by the “Investissements d’Avenir” project funded by the French Government, managed by the French National Research Agency (ANR). edgements to declare.Disclosure of Interests:None declared


Author(s):  
Ariane C. Scheuren ◽  
Paul Vallaster ◽  
Gisela A. Kuhn ◽  
Graeme R. Paul ◽  
Angad Malhotra ◽  
...  

AbstractIt is well established that cyclic, but not static, mechanical loading has anabolic effects on bone. However, the function describing the relationship between the loading frequency and the amount of bone adaptation remains unclear. Using a combined experimental and computational approach, this study aimed to investigate whether bone mechano-regulation is controlled by mechanical signals in the local in vivo environment and dependent on loading frequency. Specifically, by combining in vivo micro-computed tomography (micro-CT) imaging with micro-finite element (micro-FE) analysis, we monitored the changes in microstructural as well as the mechanical in vivo environment (strain energy density (SED) and SED gradient) of mouse caudal vertebrae over 4 weeks of either cyclic loading at varying frequencies of 2Hz, 5Hz, or 10Hz, respectively or static loading. Higher values of SED and SED gradient on the local tissue level led to an increased probability of bone formation and a decreased probability of bone resorption. In all loading groups, the SED gradient was superior in the determination of local bone formation and resorption events as compared to SED. Cyclic loading induced positive net remodeling rates when compared to sham and static loading, mainly due to an increase in mineralizing surface and a decrease in eroded surface. Consequently, bone volume fraction increased over time in 2Hz, 5Hz and 10Hz (+15%, +21% and +24%, p<0.0001), while static loading led to a decrease in bone volume fraction (−9%, p≤0.001). Furthermore, regression analysis revealed a logarithmic relationship between loading frequency and the net change in bone volume fraction over the four week observation period (R2=0.74). In conclusion, these results suggest that bone adaptation is regulated by mechanical signals in the local in vivo environment and furthermore, that mechano-regulation is logarithmically dependent on loading frequency with frequencies below a certain threshold having catabolic effects, and those above anabolic effects. This study thereby provides valuable insights towards a better understanding of the mechanical signals influencing bone formation and resorption in the local in vivo environment.


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.


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