Abstract

Pernicious anemia has recently been recognized as one of the risk factors for osteoporosis and bone fractures, but the underlying pathophysiologic mechanism is still unknown. To determine whether vitamin B 12 has any direct effect on osteoblasts, we studied the effects of vitamin B 12 on the proliferation and alkaline phosphatase activity in human bone marrow stromal osteoprogenitor cells (hBMSC) and UMR106 osteoblastic cells. Vitamin B 12 at concentrations as low as 10 −12 mol/L significantly stimulated [ 3H]-thymidine incorporation in both types of cells, but concentrations higher than 10 −12 mol/L did not produce a greater effect. Vitamin B 12 in the concentration range from 10 −12 to 10 −8 mol/L concentration-dependently increased alkaline phosphatase activity in both hBMSC and UMR106 cells. Based on these results, we suggest that a suppressed activity of osteoblasts may contribute to osteoporosis and fractures in patients with vitamin B 12 deficiency.

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