vitamin-k-semiquinone-radical and Osteopetrosis

This article provides an in-depth summary of standard and recently developed biochemical assays that are useful for the evaluation of the patient with metabolic bone disease. In addition, each of the common metabolic bone diseases is discussed in the context of the associated chemical abnormalities.

Topics: Alkaline Phosphatase; Bone Diseases, Metabolic; Calcitonin; Calcium; Calcium-Binding Proteins; Chronic Kidney Disease-Mineral and Bone Disorder; Cyclic AMP; Female; Humans; Menopause; Osteitis Deformans; Osteitis Fibrosa Cystica; Osteocalcin; Osteogenesis Imperfecta; Osteomalacia; Osteopetrosis; Osteoporosis; Parathyroid Hormone; Phosphorus; Serum Albumin; Vitamin D; Vitamin K

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.

Topics: Animals; Bone Resorption; Cell Count; Cell Death; Female; Humans; Kinetics; Macrophage Colony-Stimulating Factor; Male; Mice; Mice, Mutant Strains; Osteoclasts; Osteopetrosis; Recombinant Proteins; Vitamin K