Vitamin K-2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis

We attempted to investigate whether vitamin K-2 (menatetrenone) treatment e ffectively prevents the incidence of new fractures in osteoporosis. A total of 241 osteoporotic patients were enrolled in a 24-month randomized open l abel study. The control group (without treatment; n = 121) and the vitamin K-2-treated group (n = 120), which received 45 mg/day orally vitamin K-2, w ere followed for lumbar bone mineral density (LBMD; measured by dual-energy X-ray absorptiometry [DXA]) and occurrence of new clinical fractures. Seru m level of Glu-osteocalcin (Glu-OC) and menaquinone-4 levels were measured at the end of the follow-up period. Serum level of OC and urinary excretion of deoxypyridinoline (DPD) were measured before and after the treatment. T he background data of these two groups were identical. The incidence of cli nical fractures during the 2 years of treatment in the control was higher t han the vitamin K-2-treated group (chi(2) = 10.935; p = 0.0273). The percen tages of change from the initial value of LBMD at 6, 12, and 24 months afte r the initiation of the study were -1.8 +/- 0.6%, -2.4 +/- 0.7%, and -3.3 /- 0.8% for the control group, and 1.4 +/- 0.7%, -0.1 +/- 0.6%, and -0.5 +/ - 1.0% for the vitamin K-2-treated group, respectively. The changes in LBMD at each time point were significantly different between the control and th e treated group (p = 0.0010 for 6 months, p = 0.0153 for 12 months, and p = 0.0339 for 24 months). The serum levels of Glu-OC at the end of the observ ation period in the control and the treated group were 3.0 +/- 0.3 ng/ml an d 1.6 +/- 0.1 ng/ml, respectively (p < 0.0001), while the serum level of OC measured by the conventional radioimmunoassay (RIA) showed a significant r ise (42.4 +/- 6.9% from the basal value) in the treated group at 24 months (18.2 +/- 6.1% for the controls;p = 0.0081). There was no significant chang e in urinary DPD excretion in the treated group. These findings suggest tha t vitamin K-2 treatment effectively prevents the occurrence of new fracture s, although the vitamin K-2-treated group failed to increase in LBMD. Furth ermore, vitamin K-2 treatment enhances gamma-carboxylation of the OC molecu le.