Inhibitory effect of titanium particles on osteoclast formation generated by treatment of mouse bone marrow cells with PGE<sub>2</sub>

Nakano, Masaki; Tsuboi, Takahiro; Kato, Masanori; Kurita, K.; Togari, Akifumi

doi:10.1034/j.1601-0825.2003.02904.x

Cited by 5 publications

(4 citation statements)

References 44 publications

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“…The results of the present study are in apparent contradiction with the work of Nakano et al [35]. In their study, Nakano found that Ti particles inhibited RANKL expression in bone marrow cells treated with PGE 2 .…”

Section: Article In Presscontrasting

confidence: 57%

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Pioletti

Kottelat

2004

Biomaterials

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Orthopedic implant failures are often associated with peri-implant osteolysis. Particles generated from the wear process have been suspected to play an important role in this situation. Indeed, the peri-implant osteolysis could be due to the presence of particles stimulating the osteoclastogenesis process. We hypothesize then that the presence of a low particle concentration positively influences osteoblasts to produce osteoclastogenesis factors. If true, this hypothesis would then support the idea that the particles could be at the origin of the process leading to implant loosening. To check the validity of this hypothesis, we quantified in vitro the production of different genes involved in the osteoclastogenesis process using primary isolated human osteoblasts treated or not with particles. Results showed that low concentrations of particles might have a stimulating effect on osteoblasts to produce osteoclastogenesis factors as demonstrated by the increase of RANKL and CSF-1 gene expression in the particle group. r

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Section: Article In Presscontrasting

confidence: 57%

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Pioletti

Kottelat

2004

Biomaterials

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“…Increasing osteoclastogenesis and the inhibition of bone formation is the primary cause of aseptic loosening and osteolysis [ 34 ]. Growing evidence suggests that Ti particle impairs the function of mature osteoblasts as well as inducing osteoclast differentiation [ 35 – 37 ], which is consistent with the current study. In addition, our results strongly indicate that QUE inhibits Ti-induced osteolysis in vivo as evident by decreased osteoclast numbers and increased bone area.…”

Section: Discussionsupporting

confidence: 92%

Inhibitory effect of quercetin on titanium particle induced endoplasmic reticulum stress related apoptosis and in vivo osteolysis

Zhang

Tian

et al. 2017

Bioscience Reports

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Wear particle induced periprosthetic osteolysis is the main cause of aseptic loosening of orthopedic implants. The aim of the present study is to determine the protective effect of quercetin (QUE) against titanium (Ti) particle induced endoplasmic reticulum stress (ERS) related apoptosis and osteolysis. In the present study, RAW264.7 cells were pretreated with different concentrations (40, 80, and 160 μmol/l) of QUE for 30 min and then treated with Ti particle (5 mg/ml) for 24 h. Cell viability and apoptosis were determined using MTT assay and Annexin V-FITC Apoptosis Detection Kit, respectively. Protein and mRNA expressions of ERS-related genes were examined by Western blot and real-time PCR, respectively. The release of inflammatory cytokines was detected by ELISA. Then, a mouse calvarial osteolysis model was established. Histological sections of calvaria were stained with Hematoxylin-Eosin (H&E) or tartrate-resistant acid phosphatase (TRAP). The results showed that Ti particle reduced cell viability and induced apoptosis in RAW264.7 macrophages. The cytotoxic effects of Ti particle were dramatically inhibited by QUE pretreatment. Interestingly, we found that QUE also significantly reduced Ti particle induced up-regulation of the expression levels of protein kinase RNA-like ER kinase (PERK), inositol-requiring enzyme-1 (IRE1), glucose-regulated protein (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-12, and caspase-3 and enhanced the down-regulation of Bcl-2. In addition, QUE decreased Ti particle-induced inflammatory cytokines release from RAW264.7 cells. Moreover, treatment with QUE markedly decreased osteoclast number. In a mouse calvarial osteolysis model, QUE inhibited Ti particle induced osteolysis in vivo by inhibiting osteoclast formation and expressions of ERS-related genes. In conclusion, QUE can protect RAW264.7 cells from Ti particle induced ERS-related apoptosis and suppress calvarial osteolysis in vivo.

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“…the beginning of osteoclast generation, researchers found that titanium particles enhanced osteoclast bone resorption ability (16,17). However, this finding contradicts the results of a study by nakano et al, who found that titanium particles had no effect on osteoclast bone resorption activity or on osteoclast survival (18). This contradiction may be due to the differences between the methods used in the two studies; that is, the culture media contained no cytokines while our media contained 1,25(OH) 2 d 3 and PGe 2 .…”

Section: Discussioncontrasting

confidence: 56%

Effect of titanium particles on osteoclast activity in vitro

et al. 2010

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Abstract. Titanium particles generated from orthopedic and dental implants are suspected to play an important role in peri-implant osteolysis. elucidation of the mechanisms involved in the effects of titanium particles on osteolysis may provide methods for preventing osteolysis. Therefore, in the present study, we investigated the effect of titanium particles on osteoclast activity in vitro. We evaluated bone resorption pits on dentin slices and osteoclast F-actin rings after treatment with titanium particles. The influence of titanium particles on the expression of TraP, cat K and ca ii mrna was also evaluated. We found that osteoclast bone resorption activity was enhanced at a lower concentration of titanium particles, but inhibited by a higher concentration of titanium particles. Titanium particles can be phagocytosed by osteoclasts, but the F-actin ring was not destroyed after phagocytosis. in addition, a lower concentration of titanium particles enhanced the mrna expression of TraP and cat K, while higher concentrations of titanium particles decreased their expression. By contrast, the mrna expression of ca ii was decreased at all concentrations of titanium particles. These results suggest that direct exposure to titanium particles at a low concentration enhances osteoclast activity, while exposure to a high concentration inhibits their activity. This understanding of the direct effect of titanium particles on osteoclast activity suggests that aseptic loosening is caused not only by the generation of osteoclasts, but also by enhanced osteoclast activity.

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Inhibitory effect of titanium particles on osteoclast formation generated by treatment of mouse bone marrow cells with PGE₂

Cited by 5 publications

References 44 publications

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Inhibitory effect of quercetin on titanium particle induced endoplasmic reticulum stress related apoptosis and in vivo osteolysis

Effect of titanium particles on osteoclast activity in vitro

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Inhibitory effect of titanium particles on osteoclast formation generated by treatment of mouse bone marrow cells with PGE2

Cited by 5 publications

References 44 publications

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Inhibitory effect of quercetin on titanium particle induced endoplasmic reticulum stress related apoptosis and in vivo osteolysis

Effect of titanium particles on osteoclast activity in vitro

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Inhibitory effect of titanium particles on osteoclast formation generated by treatment of mouse bone marrow cells with PGE₂