Mechanism in inhibitory effects of vitamin K2 on osteoclastic bone resorption: In vivo study in osteopetrotic (op/op) mice

Abstract

Osteoclast deficiency in op/op mice was cured by a single injection of 5μg 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.