Effect of oral malodorous compound on the osteoclast differentiation and alveolar bone loss.

本研究的目的是阐明硫化氢诱导破骨细胞在原代培养的破骨前体细胞和RAW264细胞中分化的信号转导机制。在缺乏RANKL的情况下，口腔空气中以生理浓度的硫化氢诱导小鼠骨髓源性破骨细胞前体细胞分化。此外，硫化氢激活了破骨细胞前体细胞中的ERK1/2磷酸化。低浓度NaHS诱导RAW 264细胞PKC磷酸化。当使用PKC抑制剂（GF109203x）预处理时，nahs诱导的RAW264细胞中PKC、c-Raf和ERK1/2的激活减弱。这些结果表明，生理浓度的硫化氢通过PKC、cRaf、ERK1/2通路刺激破骨细胞分化。

The objective of this study was to elucidate the signal transduction mechanisms of hydrogen sulfide-induced osteoclast differentiation in primary cultued osteoclast precursor cells and RAW264 cells. Hydrogen sulfide at physiologic concentrations in mouth air induced the differentiation of mouse bone marrow-derived osteoclast precursor cells in the absence of RANKL. Moreover, hydrogen sulfide activated ERK1/2 phosphorylation in the osteoclast precursor cells. A low concentrations of NaHS induced PKC phosphorylation in RAW 264 cells. When pretreatment with PKC inhibitor(GF109203x), NaHS-induced the activation of PKC, c-Raf and ERK1/2 in RAW264 cells were diminished. These results suggested that hydrogen sulfide at physiologic concentrations stimulate the osteoclast differentiation through the PKC, cRaf, ERK1/2 pathway.