• 대한의용생체공학회:학술대회논문집
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• 대한의용생체공학회 1996년도 추계학술대회
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• pp.337-346
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• 1996

Debonding of cement-femoral stem interface has been suggested as a initial focus of loosening mechanism in many previous studies of cemented total hip replacement. The purpose of this study was to investigate the effect of debonding of cement-femoral stem interface to the bone-cement interface by using three-dimensional non-liner finite element analysis. Three cases of partial debonded, full debonded, full bonded cement-bone interface were modelled with partial bonding of distal 70mm from the tip of femoral stem. Each situation was studied under loading stimulating one-leg stanced gait of 68kg patient. The results showed that under partial and full debonded cement-stem interface condition the peak von Mises stress(3.1 MPa) were observed at the cement of bone-cement interface just under the calcar of proximal medial of femur, and sudden high peak stresses(3.5MPa) were developed at the distal tip of femoral stem at the lateral bone-cement interface in all 3 cases of bonding. The stresses were transfered very little to the cement of upper lateral bone-cement interface in partial and full debonded cases. Thus, once partial or full debonded cement-femoral stem interface occured, 3 times higher stress concentration were developed on the cement of proximal medial bone-cement interface than full bonded interface, and these could cause loosening of cemented total hip replacement. Clinically, preservation of more rigid cement-femoral stem interface may be important factor to prevent loosening of femoral stem.

• 한방재활의학과학회지
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• 제29권2호
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• pp.135-147
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• 2019

Objectives This study was performed to evaluate the effect of Pyrola japonica extract (NJ) and its principal constituent, homoarbutin (HA) on osteoclast differentiation and gene expression and bone resorption. The osteoclastogenesis and gene expression were determined in receptor activator of nuclear factor kappa B ligand (RANKL)-stimulated RAW264.7 cell. Methods In order to evaluate the effect of HA extracted from NJ on bone resorption, osteoclasts were used to be differentiated and formed by stimulating RAW264.7 cells with RANKL. Tartarate-resistant acid phosphatase (TRAP) (+) polynuclear osteoclast formation ability was evaluated, and differentiation control genes including cathepsin K, matrix metalloproteinases-9 (MMP-9), and TRAP in osteoclast differentiation were analyzed by real-time polymerase chain reaction (PCR). Immunoblotting was performed to measure the effect of mitogen-activated protein kinase (MAPK) factors on bone resorption, and the effect of osteoclasts on osteoclast differentiation was measured. Results Both NJ and high concentration of HA blocked RANKL-stimulated differentiation from RAW264.7 cell to TRAP-positive multinucleated cells. NJ reduced RANKL-induced expression of TRAP, cathepsin K. Both NJ and high concentration of HA inhibited RANKL-mediated expression of MMP-9, nuclear factor of activated T-cells, cytoplasmic 1, and cellular Jun-fos. NJ suppressed RANKL-stimulated expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase, tumor necrosis factor-alpha, and levels of interleukins. Both NJ and HA decreased bone resorption in osteoclast-induced bone pit formation model. Conclusions These results suggest that NJ and HA blocked bone resorption by decreasing RANKL-mediated osteoclastogenesis through down-regulation of genes for osteoclast differentiation.

• International Journal of Oral Biology
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• 제34권2호
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• pp.81-86
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• 2009

Baicalin is a flavonoid purified from the medicinal plant Scutellaria baicalensis. It has been reported that baicalin exhibits antibacterial, anti-inflammatory and analgesic effects. The present study was undertaken to determine the underlying cellular mechanisms of baicalin action in preosteoclasts. The effects of this flavonoid on preosteoclasts were determined by measuring osteoclast generation and osteoclast activity in macrophage-colony stimulating factor (M-CSF)-dependent bone marrow cells (MDBMCs) and in co-cultures of MDBMCs and osteoblasts. Osteoclast generation was assayed by measuring the number of tartrateresistant acid phosphatase (TRAP) (+) multinucleated cells after culture. Osteoclast activity was assayed by measuring the area of the resorption pit after culture. We found that osteoclast generation was induced by M-CSF and receptor activator of NF-kB ligand (RANKL), and by the 1.25-dihydroxycholecalciferol in our cultures. Baicalin decreased both osteoclast generation and activity in MDBM cultures and co-cultures indicating that it may inhibit bone resorption.

• 한국식품위생안전성학회지
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• 제14권1호
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• pp.45-54
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• 1999

The purpose of this study was to examine the increased bone loss caused by ovariectomy through monitoring the concentrations of the collagen and the pyridinoline crosslinks of collagen. The ovariectomized rats treated for 8 weeks, were divided at random into two or three groups of 10. Ovariectomies were carried out from the saline-treated group (Ovx), the estrogentreated group (Ovx+ES) and chondroitin sulfate-treated group (Ovx+CS). Sham operations were performed on the sham-operated group (Sham). Ovx+ES and Ovx+CS groups showed the remarkably increased collagen and pyridinoline amount in the bone and cartilage compared to Ovx group. And as the result of the measurement of SOD, Catalase and GPx which are antioxidant enzyme, SOD and Catalase activities in Ovx group were much higher than in Sham group. But they were significantly decreased in Ovx+CS group. Based on these results, it is supposed that estrogen and condroitin sulfate can enhance collagen synthesis and affect the pyridinoline formation in collagen fibrils through stimulating lysyl oxidase activity. And it is also thought that chondroitin sulfate can inhibit aging by reducing antioxidant enzyme.

• Molecules and Cells
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• 제37권8호
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• pp.598-604
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• 2014

Fatty acids, important components of a normal diet, have been reported to play a role in bone metabolism. Osteoclasts are bone-resorbing cells that are responsible for many bone-destructive diseases such as osteoporosis. In this study, we investigated the impact of a medium-chain fatty acid, capric acid, on the osteoclast differentiation, function, and survival induced by receptor activator of NF-${\kappa}B$ ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). Capric acid inhibited RANKL-mediated osteoclastogenesis in bone marrow-derived macrophages and suppressed RANKL-induced $I{\kappa}B{\alpha}$ phosphorylation, p65 nuclear translocation, and NF-${\kappa}B$ transcriptional activity. Capric acid further blocked the RANKL-stimulated activation of ERK without affecting JNK or p38. The induction of NFATc1 in response to RANKL was also attenuated by capric acid. In addition, capric acid abrogated M-CSF and RANKL-mediated cytoskeleton reorganization, which is crucial for the efficient bone resorption of osteoclasts. Capric acid also increased apoptosis in mature osteoclasts through the induction of Bim expression and the suppression of ERK activation by M-CSF. Together, our results reveal that capric acid has inhibitory effects on osteoclast development. We therefore suggest that capric acid may have potential therapeutic implications for the treatment of bone resorption-associated disorders.

• International Journal of Oral Biology
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• 제42권4호
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• pp.203-211
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• 2017

The aim of this study was to evaluate the role of demineralized and particulate autogenous tooth, and interleukin-6 in bone regeneration. A demineralized and particulate autogenous tooth was prepared and human osteoblast-like cells (MG63) and human osteosarcoma cells were inoculated into the culture. The rate of cell adhesion, proliferation and mineralization were examined, and the appearance of cellular attachment was observed. An 8 mm critical size defect was created in the cranium of rabbits. Nine rabbits were divided into three groups including: An experimental group A (3 rabbits), in which a demineralised and particulate autogenous tooth was grafted; an experimental group B (3 rabbits), in which a demineralized, particulate autogenous tooth was grafted in addition to interleukin-6 (20 ng/mL); and a control group. The rabbits were sacrificed at 1, 2, 4 and 6 weeks for histopathological examination with H-E and Masson's Trichrome, and immunohistochemistry with osteocalcin. The cell-based assay showed a higher rate of cell adhesion, mineralization and cellular attachment in the experimental group A compared with the control group. The animal study revealed an increased number of osteoclasts, newly formed and mature bones in the experimental group A compared with the control group. Eventually, a higher number of osteoclasts were observed in the experimental group B. However, the emergence of newly formed and mature bone was lower than in the experimental group A. The current results suggest that treatment with demineralized and particulate autogenous tooth and interleukin-6 is not effective in stimulating bone regeneration during the bone grafting procedure.

• 한국임상수의학회지
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• 제19권1호
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• pp.66-72
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• 2002

Korean safflower seed has been known to have healing effects on both bone fracture and osteoporosis. On the base of such a notice, this experiment was carried out to explore the effects of safflower seed on bone formation and bone repair. The toxicity test and the effect of Korean safflower seed were evaluated with 60 rats, 3-month old. Forty Sprague-Dawley rats composed of 20 male and 20 female were underwent unilateral tibial defect and then fastened with unilateral fixators. The operated rats were divided into two groups depending on the composition of diet, such as positive control group fed normal diet(C-OP group) and safflower seed group fed 30% of safflower seed diet and 70% of normal diet(S-OP group). Another 20 rats without operation were maintained, each 10 rats were fed either normal diet or 30% of safflower seed diet and 70% of normal diet, and observed the toxicity of safflower seed by measuring weight and urine parameters. Postoperative radiography were taken once in 2 weeks to evaluate callus formation for operated groups and blood collection via heart puncture were carried out once in 3 weeks for 3 groups. The concentration of Ca and Pi in serum were measured using both auto Kit and $^{31}$ P Nuclear Magnetic Resonance(NMR). At present study, no toxic effect was observed from both weight increment and urine index after feeding the safflower seed diet. The comparison of the radiography between C-OP and S-OP group were showed that the safflower seed diet appeared to stimulate the formation of callus in the rat. The ratio of Ca/P in serum was low in S-OP group compared to C-OP group with the auto Kit, but there were no significant differences between two groups (p < 0.05). In addition, the variations of Pi values in NMR examination were also confirmed based on the result of auto Kit. In conclusion, this study implied that safflower seed might influence to bone formation and shorten the periods of remedy by stimulating the calcification of bone

• BMB Reports
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• 제52권11호
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• pp.659-664
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• 2019

Vav1 is a Rho/Rac guanine nucleotide exchange factor primarily expressed in hematopoietic cells. In this study, we investigated the potential role of Vav1 in osteoclast (OC) differentiation by comparing the ability of bone marrow mononuclear cells (BMMCs) obtained from Vav1-deficient ($Vav1^{-/-}$) and wild-type (WT) mice to differentiate into mature OCs upon stimulation with macrophage colony stimulating factor and receptor activator of nuclear kappa B ligand in vitro. Our results suggested that Vav1 deficiency promoted the differentiation of BMMCs into OCs, as indicated by the increased expression of tartrate-resistant acid phosphatase, cathepsin K, and calcitonin receptor. Therefore, Vav1 may play a negative role in OC differentiation. This hypothesis was supported by the observation of more OCs in the femurs of $Vav1^{-/-}$ mice than in WT mice. Furthermore, the bone status of $Vav1^{-/-}$ mice was analyzed in situ and the femurs of $Vav1^{-/-}$ mice appeared abnormal, with poor bone density and fewer number of trabeculae. In addition, Vav1-deficient OCs showed stronger adhesion to vitronectin, an ${\alpha}_v{\beta}_3$ integrin ligand important in bone resorption. Thus, Vav1 may inhibit OC differentiation and protect against bone resorption.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제44권6호
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• pp.259-268
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• 2018

Objectives: The purpose of this study was to evaluate the synergic effect of recombinant human bone morphogenetic protein-2 (rhBMP-2) and low-level laser therapy (LLLT) on bisphosphonate-treated osteoblasts. Materials and Methods: Human fetal osteoblast cells (hFOB 1.19) were cultured with $100{\mu}M$ alendronate. Low-level Ga-Al-As laser alone or with 100 ng/mL rhBMP-2 was then applied. Cell viability was measured with MTT assay. The expression levels of receptor activator of nuclear factor kappa-B ligand (RANKL), macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG) were analyzed for osteoblastic activity inducing osteoclastic activity. Collagen type and transforming growth factor beta-1 were also evaluated for bone matrix formation. Results: The results showed that rhBMP-2 and LLLT had a synergic effect on alendronate-treated osteoblasts for enhancing osteoblastic activity and bone matrix formation. Between rhBMP-2 and LLLT, rhBMP-2 exhibited a greater effect, but did not show a significant difference. Conclusion: rhBMP-2 and LLLT have synergic effects on bisphosphonate-treated osteoblasts through enhancement of osteoblastic activity and bone formation activity.

• 대한의생명과학회지
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• 제23권3호
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• pp.194-200
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• 2017

Bone-resorbing osteoclasts play a major role in maintaining bone homeostasis with bone-forming osteoblasts. Although it has been reported that A2B adenosine receptor (A2BAR) regulates osteoclast differentiation, its effects on apoptosis or proliferation of osteoclasts have been less-defined. Here, we demonstrate that A2BAR stimulation regulates macrophage-colony stimulating factor (M-CSF)-mediated osteoclast proliferation. Stimulation with a specific agonist of A2BAR, BAY 60-6583, significantly reduced M-CSF-mediated osteoclast proliferation in a time- and dose-dependent manner. In addition, A2BAR stimulation induced both apoptosis of the cells and cell arrest in the G1 phase with a decrease of cell number in the G2/M phase. Stimulation with BAY 60-6583 inhibited the activation of Akt by M-CSF, whereas M-CSF-induced ERK1/2 activation was not affected. These results suggest that the inhibition of M-CSF-mediated Akt activation by A2BAR stimulation increases apoptotic response of osteoclasts and induces cell cycle arrest in the G1 phase, thus contributing to the down-regulation of osteoclast proliferation.