The mechanism of non-steroidal anti-inflammatory drugs on osteoclast differentiation and activation.

非类固醇抗炎药(NSAIDs)对骨重建有调节作用。非甾体抗炎药对骨重建的疗效存在争议。在临床上，非类固醇抗炎药由于其抑制炎症因子的作用而促进骨修复；相反，非类固醇抗炎药在动物模型中延缓骨折愈合。本研究旨在阐明非甾体抗炎药对破骨细胞分化和骨吸收活性的作用机制。环氧合酶(COX)-1和-2在破骨细胞分化早期(第3天)出现转录本。COX-2在成熟破骨细胞上增加，内毒素刺激炎性成熟破骨细胞。COX-2转录本水平对细胞外信号调节激酶的出现有影响。这些结果表明，COX-1和COX-2参与了破骨细胞的分化和骨吸收活性的调节。

Non-steroidal anti-inflammatory drugs(NSAIDs) have regulatory effect on bone remodeling. The efficacy of NSAIDs on bone remodeling is controversial. In clinics, NSAIDs progress bone repair as their inhibitory effect of inflammatory factors ; in contrast, NSAIDs delay bone fracture healing in animal models. The aim of this study was to elucidate the mechanism of NSAIDs on osteoclast differentiation and bone resorptive activity.Cyclloxygenase(COX)-1 and-2 transcripts were appeared in early stage of osteoclast differentiation(day3). COX-2 increased on mature osteoclasts and lipopolysaccharide stimulated inflammatory mature osteoclasts. Level of COX-2 transcript has efficacy on extracellular signal-regulated kinase appearance. These results showed that COX-1 and-2 involved in osteoclasts have regulatory effect on osteoclasts differentiation and bone resorptive activity.