Applications of micro-CT and MR microscopy to study pre-clinical models of osteoporosis and osteoarthritis

Kapadia, Rasesh; Stroup, George B.; Badger, Alison M.; Koller, Bruno; Levin, Josh; Coatney, Robert W.; Dodds, Robert A.; Liang, Xiaguong; Lark, Michael W.; Gowen, Maxine

doi:10.3233/thc-1998-65-609

Cited by 102 publications

(43 citation statements)

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“…From literature review, significant bone loss occurs from 4 to 8 weeks following ovariectomy in rats, depending on bone site examined and the technology applied. [19][20][21] It is reported that a loss of trabecular connection can be seen at 2 weeks following ovariectomy. 22 In this study, osteoporosis was induced and then a significant effect on trabecular bone was observed as early as 3 weeks after OVX surgery.…”

Section: Discussionmentioning

confidence: 99%

Effect of osteoporosis on fixation of osseointegrated implants in rats

Hua

et al. 2016

J Biomed Mater Res

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The effect of osteoporosis on implant osseointegration has been widely investigated, whereas osteoporosis may also newly occur in patient with previously osseointegrated implant. This study was designed to investigate the effect of osteoporosis on implant fixation in rats after successful osseointegration had been obtained. Seventy female Sprague-Dawley rats were included, and each animal received two titanium implants in the distal metaphysis of femur bilaterally. Eight weeks later, ten rats were sacrificed to confirm the establishment of implant osseointegration. All left rats were randomly subjected to bilateral ovariectomy (OVX) or sham operation. Three, six, and twelve weeks later, implant osseointegration, peri-implant bone tissue, and biomechanical properties of implant were analyzed. Right femurs with implants were used for micro-CT and histological analysis, and left femurs with implants were used for biomechanical test. Micro-CT, histology, and biomechanical test confirmed the destructive effect of OVX on previously osseointegrated implant in rats; when compared to sham-operated rats, peri-implant bone volume, trabecular architecture, bone-to-implant contact ratio, as well as biomechanical parameters decreased progressively within 12 weeks. Results also indicated that the effect of OVX on undisturbed bone (proximal tibiae) was much stronger than that on peri-implant bone. Osteoporosis produced a progressive negative effect on previously osseointegrated implant in distal femora of rats during 12 weeks. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 105B: 2426-2432, 2017.

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Section: Discussionmentioning

confidence: 99%

Effect of osteoporosis on fixation of osseointegrated implants in rats

Hua

et al. 2016

J Biomed Mater Res

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“…In trabecular bone, basic structural metrics were measured using direct 3D morphometry. (35,36) The images were also rendered for 3D display and visualization.…”

Section: Bone Phenotyping Of Dkk1 +/− Animalsmentioning

confidence: 99%

Deletion of a Single Allele of the Dkk1 Gene Leads to an Increase in Bone Formation and Bone Mass

Morvan

Boulukos

Clément-Lacroix³

et al. 2006

Journal of Bone and Mineral Research

498

354

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Wnt/␤-catenin signaling has been proven to play a central role in bone biology. Unexpectedly, the Wnt antagonist Dkk2 is required for terminal osteoblast differentiation and mineralized matrix formation. We show that Dkk1, unlike Dkk2, negatively regulates osteoblast differentiation and bone formation. Introduction:The Wnt co-receptor LRP5 is a critical regulator of bone mass. Dickkopf (Dkk) proteins act as natural Wnt antagonists by bridging LRP5/6 and Kremen, inducing the internalization of the complex. Wnt antagonists are thus expected to negatively regulation bone formation. However, Dkk2 deficiency results in increased bone, questioning the precise role of Dkks in bone metabolism. Materials and Methods:In this study, we investigated specifically the role of Dkk1 in bone in vitro and in vivo. Using rat primary calvaria cells, we studied the effect of retroviral expression of Dkk1 on osteoblast differentiation. In addition, the effect of Dkk1 osteoblast was studied in MC3T3-E1 cells by means of recombinant protein. Finally, to address the role of Dkk1 in vivo, we analyzed the bone phenotype of Dkk1 +/− animals. Results: Retroviral expression of Dkk1 in rat primary calvaria cells resulted in a complete inhibition of osteoblast differentiation and formation of mineralized nodules, with a marked decrease in the expression of alkaline phosphatase. Dkk1 expression also increased adipocyte differentiation in these cell cultures. Recombinant murine Dkk1 (rmDkk1) inhibited spontaneous and induced osteoblast differentiation of MC3T3-E1 cells. To determine the role of Dkk1 in vivo and overcome the embryonic lethality of homozygous deletion, we studied the bone phenotype in heterozygous Dkk1-deficient mice. Structural, dynamic, and cellular analysis of bone remodeling in Dkk1 +/− mice showed an increase in all bone formation parameters, with no change in bone resorption, leading to a marked increase in bone mass. Importantly, the number of osteoblasts, mineral apposition, and bone formation rate were all increased several fold. Conclusions: We conclude that Dkk1 protein is a potent negative regulator of osteoblasts in vitro and in vivo. Given that a heterozygous decrease in Dkk1 expression is sufficient to induce a significant increase in bone mass, antagonizing Dkk1 should result in a potent anabolic effect.

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“…Its application in the medical [2][3][4] and dental [5][6][7][8][9] fields is nowadays widespread. Because two-dimensional histologic data provide only limited information on three-dimensional structures, the complex architecture of trabecular bone specimens was one of the first objects of interest to be visualized by ACT.…”

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confidence: 99%