Skeletal Growth in Pyridoxine Deficient Mice. ∗

Summary and Conclusions

In pyridoxine deficient young mice, growth of cartilage and formation of bone were inhibited and finally ceased. Upon refeeding the complete diet, recovery was noticeable after 3 days and was still in progress after 14 days. The growth processes were quickly restored with mitoses present in the germinal layer of the cartilage as well as in the osteoblasts.

The effects of pyridoxine deficiency on cartilage resemble those seen in pantothenic acid deficient mice, 1 whereas the disturbance of ossification was not unlike that observed in riboflavin deficiency. 2 The specificity of the skeletal changes may thus be questioned.

In young rats fed a pyridoxine deficient diet, 3 the changes in the growth zones were comparable to those of underfed young guinea pigs, 4 kept on a quantitatively restricted but adequately balanced diet. To some extent this is true for the cartilage of mice also. However, the cartilage cells as well as the osteoblasts responded more unfavorably to the pyridoxine deficiency than to general underfeeding, and the formation of bone was more reduced than in any of our previous experiments. This difference might indicate a specific effect of the pyridoxine deficiency, but it may be a manifestation of the more marked sensitivity of the mouse to the deficiency as compared to that of the rat. 5 , 6

Feeding a high protein diet accentuated the effects of pyridoxine deficiency inasmuch as growth of cartilage and bone was more inhibited than in pyridoxine deficient mice receiving a diet with regular casein content. These findings are in agreement with previous observations on the greater requirements for pyridoxine in animals fed high protein diets.