Joerg H. Holstein, Julia Schmalenbach, Markus Herrmann, Ilona Ölkü, Patric Garcia, Tina Histing, Wolfgang Herrmann, Michael D. Menger, Tim Pohlemann, Lutz Claes
Med Sci Monit 2012; 18(12): BR469-474
Background: An elevated serum concentration of homocysteine (hyperhomocysteinemia) has been shown to disturb fracture healing. As the essential amino acid, methionine, is a precursor of homocysteine, we aimed to investigate whether excess methionine intake affects bone repair.
Material/Methods: We analyzed bone repair in 2 groups of mice. One group was fed a methionine-rich diet (n=13), and the second group received an equicaloric control diet without methionine supplementation (n=12). Using a closed femoral fracture model, bone repair was analyzed by histomorphometry and biomechanical testing at 4 weeks after fracture. Blood was sampled to measure serum concentrations of homocysteine, the bone formation marker osteocalcin, and the bone resorption marker collagen I C-terminal crosslaps
Results: Serum concentrations of homocysteine were significantly higher in the methionine group than in the control group, while serum markers of bone turnover did not differ significantly between the 2 groups. Histomorphometry revealed no significant differences in size and tissue composition of the callus between animals fed the methionine-enriched diet and those receiving the control diet. Accordingly, animals of the 2 groups showed a comparable bending stiffness of the healing bones.
Conclusions: We conclude that excess methionine intake causes hyperhomocysteinemia, but does not affect fracture healing in mice.
Keywords: Methionine - pharmacology, Metabolic Networks and Pathways - drug effects, Homocysteine - blood, Fracture Healing - drug effects, Femur - radiography, Diet, Dietary Supplements, Collagen Type I - blood, Biomechanical Phenomena - drug effects, Animals, Mice, Osteocalcin - blood, Peptides - blood