Background: Clinical studies have suggested, that vitamin K2 prevents bone loss and protect against fractures. Vitamin K2 is suggested to affect bone through the bone matrix protein osteocalcin (OC). OC is produced by the osteoblast in an undercarboxylated form (ucOC) that is carboxylated with vitamin K2 as a cofactor. Carboxylated OC promotes mineralisation of bone. The aim of the study was to investigate the effect of vitamin K2 on bone metabolism. Bone is affected by many factors, which may not be reflected or measurable in peripheral blood. We therefore wanted to investigate if bone formation markers in the bone marrow are affected by K2.
Methods: In this randomised placebo-controlled double blinded clinical trial, 142 postmenopausal women (60-80 years old) with osteopenia were treated with vitamin K2 (375 μg MK-7) or placebo for 1 year. Both groups also received vitamin D3 (38 μg/day) and calcium (800 mg/day). Bone marrow aspirates were obtained from 56 women at baseline and after three months of treatment. Bone marrow serum was analysed for OC, ucOC and procollagen 1, N-terminal propeptide (P1NP).
Results: Baseline levels of ucOC was 5.0 μg/l±4.4; OC was 18.8 μg/l±5.8; P1NP was 66.4 μg/l±25.3, without differences between groups. After three months, ucOC was reduced by 68% in the vitamin K2 treated group, compared with the placebo group (p<0.001). OC and P1NP did not change.
Conclusion: Three months of treatment with vitamin K2 reduces ucOC in bone marrow, but does not change total OC or PINP. This suggests that the effect of vitamin K2 on bone is not mediated by stimulation of bone formation, but through changes in the bone matrix.
Further analyses of bone markers and gene expression are needed to understand the exact underlying mechanisms.
Disclosure: The authors declared no competing interests. This work was supported by Axellus.