Vitamin B12 and folic acid deficiency are associated with a higher serum concentration of homocysteine. A high serum homocysteine is a risk factor for fractures. Both vitamins play a role in the remethylation of homocysteine to methionine. The pathophysiology from a high serum homocysteine to fractures is not completely clear, but might involve bone mineral density, bone turnover, bone blood flow, DNA methylation, and/or physical function and fall risk. Genetic variation, especially polymorphisms of the gene encoding for methylenetetrahydrofolate reductase may play a role in homocysteine metabolism and fracture risk. It is uncertain whether supplementation with vitamin B12 and folate can decrease fracture incidence. One double blind clinical trial in post-stroke patients showed that these B vitamins could decrease hip fracture incidence, but the results of further clinical trials should be awaited before a definite conclusion can be drawn. © 2013 Springer Science+Business Media New York.