| First Author | Kawata T | Year | 1999 |
| Journal | J Nutr Sci Vitaminol (Tokyo) | Volume | 45 |
| Issue | 4 | Pages | 501-7 |
| PubMed ID | 10575640 | Mgi Jnum | J:59641 |
| Mgi Id | MGI:1352011 | Doi | 10.3177/jnsv.45.501 |
| Citation | Kawata T, et al. (1999) Mechanism in inhibitory effects of vitamin K2 on osteoclastic bone resorption: in vivo study in osteopetrotic (op/op) mice. J Nutr Sci Vitaminol (Tokyo) 45(4):501-7 |
| abstractText | Osteoclast deficiency in op/op mice was cured by a single injection of 5 micrograms recombinant human macrophage colony-stimulating factor (M-CSF). On d 5, the osteoclast number reached a maximum value. By d 15, the osteoclast number had decreased to about 70% of the maximum level. Moreover, by d 20, the osteoclast number had decreased to about 30% of its maximum level. On d 5, the osteoclast number of vitamin K2 12 h previously had decreased to about 30% of the M-CSF-only injected mice. Moreover, on d 5, the osteoclast number of the mice receiving a single injection of vitamin K2 24 h previously had decreased to about 15% that of mice injected only with M-CSF. These results indicate that vitamin K2 inhibits in vivo osteoclast formation. On d 20, the osteoclast number of the mice injected with a single dose of vitamin K2 12 or 24 h previously had decreased to 0% compared with those receiving only M-CSF. The present results suggest that the vitamin K2 'causes cell death' to mature osteoclasts and inhibits in vivo osteoclast formation. |
