Deficiencies of folate and vitamin B12 do not affect fracture healing in mice.

PURPOSE: Recently, hyperhomocysteinemia has been shown to be associated with impaired fracture healing in mice. The main causes for hyperhomocysteinemia are deficiencies of folate and vitamin B12. However, there is no information on whether deficiencies of these B vitamins are affecting bone repair, too.

METHODS: We used two groups of mice to investigate the impact of folate and vitamin B12 deficiency on fracture healing: mice of the first group were fed a folate- and vitamin B12-deficient diet (n=14), while mice of the second group received an equicaloric control diet (n=13). Four weeks after stabilizing a closed femur fracture, bone repair was analyzed by histomorphometry and biomechanical testing. In addition, serum concentrations of homocysteine, folate, vitamin B12, the bone formation marker osteocalcin (OC), and the bone resorption marker collagen I C-terminal crosslaps (CTX) were measured.

RESULTS: Serum analyses revealed significantly decreased concentrations of folate and vitamin B12 in animals fed the folate- and vitamin B12-deficient diet when compared to controls. This was associated with a moderate hyperhomocysteinemia in folate- and vitamin B12-deficient mice, while no hyperhomocysteinemia was found in controls. Three-point bending tests showed no significant differences in callus stiffness between bones of folate- and vitamin B12-deficient animals and those of control animals. In accordance, the histomorphometric analysis demonstrated a comparable size and tissue composition of the callus, and also serum markers of bone turnover did not differ significantly between the two groups.

CONCLUSIONS: We conclude that folate and vitamin B12 deficiency does not affect bone repair in mice.