The contribution of trabecular bone to the visibility of the lamina dura: An in vitro radiographic study

2002 ◽  
Vol 93 (1) ◽  
pp. 118-122 ◽  
Author(s):  
Marcelo G.P. Cavalcanti ◽  
Axel Ruprecht ◽  
William T. Johnson ◽  
Thomas E. Southard ◽  
Jane Jakobsen
Keyword(s):  
Trabecular Bone ◽  
Radiographic Study

Bone blood flow and In vitro proliferation of bone marrow and trabecular bone osteoblast-like cells in ovariectomized rats

1992 ◽  
Vol 50 (4) ◽  
pp. 336-341 ◽  
Author(s):  
Dominique Egrise ◽  
Dominique Martin ◽  
Pierre Neve ◽  
Anne Vienne ◽  
Michel Verhas ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Blood Flow ◽  
Trabecular Bone ◽  
Ovariectomized Rats ◽  
Bone Blood Flow ◽  
In Vitro Proliferation

scholarly journals Simvastatin-Loaded Nanomicelles Enhance the Osteogenic Effect of Simvastatin

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Xianling Feng ◽  
Xinxin Yue ◽  
Mao Niu
Keyword(s):  
Trabecular Bone ◽  
Drug Loading ◽  
Two Dimensions ◽  
Gelatin Sponge ◽  
Cell Cycle Distribution ◽  
Mineral Density ◽  
Mg63 Cells ◽  
Proliferation Activity

Objectives. The present study intended to further verify that simvastatin-loaded nanomicelles (SVNs) enhanced the role of simvastatin (SV) in promoting osteoblast differentiation in vitro and to evaluate the effect of SVNs on bone defect repair in vivo. Methods. SVNs were synthesized by dialysis. MG63 cells were subjected to intervention with 0.25 μmol/l of SVNs and SV. A 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay kit and flow cytometry were used to determine cell proliferation activity, cell cycle distribution, and apoptosis. The osteoblastic differentiation of MG 63 cells was evaluated by measuring alkaline phosphatase (ALP) activity, ALP staining, and the expression levels of the osterix (Osx) and osteocalcin (OC) proteins. In addition, 0.5 mg of SVNs or SV was applied to the skull defect area of rabbits. Micro-CT, hematoxylin and eosin (HE) staining, and Masson’s trichrome staining were used for qualitative and quantitative evaluation of new bone in three dimensions and two dimensions. Results. The SVNs had a mean diameter of 38.97 nm. The encapsulation and drug-loading efficiencies were 54.57 ± 3.15 % and 10.91 ± 0.63 % , respectively. In vitro, SVNs and SV can inhibit the proliferation activity and promote osteogenic differentiation of MG63 cells by arresting MG63 cells at the G0/G1 phase without increasing the apoptosis rate. In vivo quantitative results showed that the bone mineral density (BMD), bone volume (BV)/total volume (TV) ratio, and trabecular number (Tb.N) in the gelatin sponge with SVNs (SVNs-GS) group and gelatin sponge with SV (SV-GS) group were 362.1%, 292.0%; 181.3%, 158.0%; and 215.2%, 181.8% of those in the blank control (BC) group, respectively. Histological results identified the new bone tissue in each group as irregular fibrous bone, and the arrangement of trabecular bone was disordered. There were significantly more osteoblasts and new capillaries around the trabecular bone in the SVNs-GS group and SV-GS group than in both the BC and drug-free nanomicelle (DFNs) groups. Both in vitro and in vivo, SVNs exhibited greater osteogenic efficacy than SV. Conclusion. SVNs significantly improved the osteogenic efficacy of SV.

High-Resolution Three-Dimensional-pQCT Images Can Be an Adequate Basis for In-Vivo μFE Analysis of Bone

2000 ◽  
Vol 123 (2) ◽  
pp. 176-183 ◽  
Author(s):  
W. Pistoia ◽  
B. van Rietbergen ◽  
A. Laib ◽  
P. Ru¨egsegger
Keyword(s):  
High Resolution ◽  
Trabecular Bone ◽  
Elastic Properties ◽  
Bone Structure ◽  
Reference Model ◽  
Von Mises Stress ◽  
Micro Ct ◽  
Von Mises

Micro-finite element (μFE) models based on high-resolution images have enabled the calculation of elastic properties of trabecular bone in vitro. Recently, techniques have been developed to image trabecular bone structure in vivo, albeit at a lesser resolution. The present work studies the usefulness of such in-vivo images for μFE analyses, by comparing their μFE results to those of models based on high-resolution micro-CT (μCT) images. Fifteen specimens obtained from human femoral heads were imaged first with a 3D-pQCT scanner at 165 μm resolution and a second time with a μCT scanner at 56 μm resolution. A third set of images with a resolution of 165 μm was created by downscaling the μCT measurements. The μFE models were created directly from these images. Orthotropic elastic properties and the average tissue von Mises stress of the specimens were calculated from six FE-analyses per specimen. The results of the 165 μm models were compared to those of the 56 μm model, which was taken as the reference model. The results calculated from the pQCT-based models, correlated excellent with those calculated from the reference model for both moduli R2>0.95 and for the average tissue von Mises stress R2>0.83. Results calculated from the downscaled micro-CT models correlated even better with those of the reference models (R2>0.99 for the moduli and R2>0.96 for the average von Mises stress). In the case of the 3D-pQCT based models, however, the slopes of the regression lines were less than one and had to be corrected. The prediction of the Poisson’s ratios was less accurate (R2>0.45 and R2>0.67) for the models based on 3D-pQCT and downscaled μCT images respectively). The fact that the results from the downscaled and original μCT images were nearly identical indicates that the need for a correction in the case of the 3D-pQCT measurements was not due to the voxel size of the images but due to a higher noise level and a lower contrast in these images, in combination with the application of a filtering procedure at 165 micron images. In summary: the results of μFE models based on in-vivo images of the 3D-pQCT can closely resemble those obtained from μFE models based on higher resolution μCT system.

Clopidogrel (plavix), a P2Y12 receptor antagonist, inhibits bone cell function in vitro and decreases trabecular bone in vivo

Bone ◽  
2012 ◽  
Vol 50 ◽  
pp. S45
Author(s):  
S. Syberg ◽  
A. Brandao-Burch ◽  
J.J. Patel ◽  
M.O. Hajjawi ◽  
T.R. Arnett ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Trabecular Bone ◽  
Cell Function ◽  
Bone Cell ◽  
P2y12 Receptor ◽  
P2y12 Receptor Antagonist

scholarly journals Clopidogrel (Plavix), a P2Y12receptor antagonist, inhibits bone cell function in vitro and decreases trabecular bone in vivo

2012 ◽  
Vol 27 (11) ◽  
pp. 2373-2386 ◽  
Author(s):  
Susanne Syberg ◽  
Andrea Brandao-Burch ◽  
Jessal J Patel ◽  
Mark Hajjawi ◽  
Timothy R Arnett ◽  
...  
Keyword(s):  
Trabecular Bone ◽  
Cell Function ◽  
Bone Cell

Knockdown Of Matrix Metalloproteinase 13 (MMP13) In 5TGM1 Multiple Myeloma Cells Inhibits Development Of Lytic Bone Lesions In Vivo

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 879-879
Author(s):  
Jing Fu ◽  
Shirong Li ◽  
Huihui Ma ◽  
G. David Roodman ◽  
Markus Y. Mapara ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Growth ◽  
Trabecular Bone ◽  
Research Funding ◽  
Bone Lesions ◽  
Mineral Density ◽  
Lytic Bone Lesions

Abstract Background Multiple myeloma (MM) cells secrete osteoclastogenic factors that activate osteoclasts (OCL) and contribute to development of pure lytic bone lesions in MM patients. We have recently shown that i) MMP13 is highly expressed by MM cells and ii) exogenous MMP13 increases OCL fusion and bone resorption (Feng et al, 2009). Further, MMP13 mediates these effects by upregulating dendritic cell-specific transmembrane protein (DC-STAMP), which is critical for OCL fusion and activation (Fu et al, 2012). Here, we investigated the role of MMP13 in MM-related bone disease (MMBD) in vivo and the underlying osteoclastogenic mechanisms. Methods and Results The role of MMP13 in MMBD was examined in vivo by the intratibial 5TGM1-GFP mouse MMBD model. Mouse MM cell line 5TGM1-GFP cells were transduced by pLKO.1-puro empty vector (EV) or sh-MMP13 (MMP13-KD) lentivirus followed by puromycin selection for 2 weeks. MMP13 knockdown in 5TGM1-MMP13-KD cells were confirmed by quantitative RT-PCR. 1×105 5TGM1-GFP-EV and 5TGM1-GFP-MMP13-KD cells were bilaterally intratibially injected into Recombination Activating Gene 2 (Rag2) knockout mice (n=9). After 4 weeks of tumor growth, tibiae were separated for micro quantitative computed tomography (micro-QCT) followed by immunohistochemistry (IHC) analysis. Following 5TGM1-GFP-EV injection, micro-QCT analysis of the tibiae and adjacent femurs indicated severe bone erosions, especially within trabecular bone. By contrast MMP13 KD inhibited the development of MM-induced bone lesions. Bone histomorphologic analysis showed that compared to 5TGM1-GFP-EV, MMP13-KD significantly reduced the MM induced trabecular bone loss with increased relative bone volume (0.069 ± 0.018 vs 0.0499 ± 0.016%; P=0.001), connective density (54.94 ± 33.03 vs 27.33 ± 18.97mm3; P=0.002), trabecular bone numbers (3.26 ± 0.29 vs 3.06 ± 0.33mm-1; P=0.032) and bone mineral density (159.1 ± 20.7 vs 134.2 ± 18.6mg/cm3; P=6E-04); as well as decreased triangulation bone surface to volume ratio (66.12 ± 6.67 vs 73.28 ± 10.07; P=0.017) and triangulation structure model index (3.05 ± 0.36 vs 3.42 ± 0.35 mm-1; P=0.002). In accordance with our finding that MMP13 induced OCL fusion, IHC results confirmed the presence of smaller TRAP+OCLs adjacent to the tumor in mice injected with 5TGM1-GFP-MMP13-KD cells compared with 5TGM1-GFP-EV cells. Although MMP13 knockdown showed no effects on 5TGM1-GFP cell growth in vitro, in vivo tumor progression represented by fluorescence imaging and sera immunoglobin 2G level (0.96 ± 0.12 vs 1.10 ± 0.11 mg/ml) was significantly inhibited (P=0.009 and 0.03 respectively), indicating MMP13 depletion in MM cells impaired OCL activation which, in turn, failed to support MM cell growth in bone marrow microenvironment as effectively in EV control group. In vitro studies demonstrated that MMP13 directly induced ERK1/2 phosphorylation in pre-osteoclasts. Consistent with a critical role for ERK1/2 phosphorylation in regulating OCL formation, U0126 (ERK1/2 inhibitor) blocked MMP13-induced ERK1/2 phosphorylation, ERK1/2-dependent DC-STAMP upregulation and MMP13-induced OCL fusion (P<0.01). Conclusion Our results demonstrate that silencing MMP13 expression in MM cells inhibits MM cell-induced OCL fusion and development of lytic bone lesions in vivo, indicating that MMP13 is essential for MM-induced bone diseases. Further, MMP13 upregulates DC-STAMP expression and OCL fusion via the activation of ERK1/2 signaling. Our data suggest that targeting MMP13 may represent a novel therapeutic approach for the treatment of MMBD. Disclosures: Roodman: Amgen: Membership on an entity’s Board of Directors or advisory committees; Lilly: Research Funding. Lentzsch:Celgene: Research Funding.

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