Abnormalities in fracture healing induced by vitamin B6-deficiency in rats.

Vitamin K1 is the intermediate carrier of reducing equivalents in mineralization. In fracture-healing in the rat metatarsal the primary source of these reducing equivalents appears to be NADPH, generated from glucose 6-phosphate dehydrogenase (G6PD) activity. Because recent evidence indicated that stimulation of G6PD activity can be induced by putrescine, derived from pyridoxal phosphate-dependent ornithine decarboxylase activity, the effect of pyridoxine (vitamin B6) deficiency has been studied in this system. Vitamin B6-deficiency caused marked diminution in the G6PD activity in the periosteal region of bone-formation and in the developing callus, with significant delay in the maturation of the callus and union. It also caused changes in the bone suggestive of imbalance in the coupling between osteoblasts and osteoclasts. These results suggest that the vitamin B6-status may be important in fracture-healing.