期刊
BIOMATERIALS
卷 35, 期 22, 页码 5721-5730出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2014.04.006
关键词
Enoxacin; Prosthetic loosening; Osteolysis; Osteoclasts; JNK signaling
资金
- Science and Technology Commission of Shanghai Municipality [11DJ1400303]
- National Natural Science Foundation for the Youth of China [81201364]
- scientific research grant for youth of Shanghai [ZZjdyx 2097]
- 985 project-stem cell and regenerative medicine centre
- Shanghai Municipal Education Commission [13YZ031]
The aim of this study was to assess the effect of enoxacin on osteoclastogenesis and titanium particle-induced osteolysis. Wear particles liberated from the surface of prostheses are associated with aseptic prosthetic loosening. It is well established that wear particles induce inflammation, and that extensive osteoclastogenesis plays a critical role in peri-implant osteolysis and subsequent prosthetic loosening. Therefore, inhibiting extensive osteoclast formation and bone resorption could be a potential therapeutic target to prevent prosthetic loosening. In this study, we demonstrated that enoxacin, a fluoroquinolone antibiotic, exerts potent inhibitory effects on titanium particle-induced osteolysis in a mouse calvarial model. Interestingly, the number of mature osteoclasts decreased after treatment with enoxacin in vivo, suggesting that osteoclast formation might be inhibited by enoxacin. We then performed in vitro studies to confirm our hypothesis and revealed the mechanism of action of enoxacin. Enoxacin inhibited osteoclast formation by specifically abrogating RANKL-induced JNK signaling. Collectively, these results suggest that enoxacin, an antibiotic with few side effects that is widely used in clinics, had significant potential for the treatment of particle-induced pen-implant osteolysis and other diseases caused by excessive osteoclast formation and function. (C) 2014 Elsevier Ltd. All rights reserved.
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