(1) マウス骨修復モデルで, ニコチン群は仮骨架橋形成が有意に不良だった。骨折部の仮骨量は少なく, 内軟骨性骨化が障害されていると考えられた。(2) マウス大腿骨の培養におけるpentosidineの測定でニコチン群で有意に高くニコチン添加で骨質が低下した。α7 nAchR KOでは, いずれも有意な上昇はみられなかった。(3) 骨形態計測では, α7 nAchR KOで骨密度は有意に高値を示した。破骨細胞数はKOで少なく, 骨形成や軟骨形成の検討では両者に差がなかったことからα7nAchRは生理的骨代謝において, 破骨細胞を活性化させる代謝経路に関与することが推測された。
(1) To examine the influence of nicotine on ossification, a mouse bone restoration model was adopted. As the result performed after having maintained high density of internal nicotine for a long duration, the callus bridging formation was significantly worse than control group in two weeks. Additionally, few callus formation implied that the enchondral ossification was impaired. (2) We cultured the mouse thighbone and measured intraosseous pentosidine, one of AGEs. The result was that, not in α7nAchR knockout mouse (KO), but in wild type mouse (WT), pentosidine level was significantly higher in nicotine group, which indicated nicotine affects bone quality. (3) As a result of bone morphometry for WT and KO, in KO the bone density was significantly higher and osteoclasts were fewer. There was no difference in the histological examination of osteogenesis and chondrogenesis between them, by which it was supposed that α7nAchR activated osteoclasts in physiological bone metabolism.