Direct measurement of bone resorption and calcium conservation during vitamin D deficiency or hypervitaminosis D

When bone is remodeled during the growth of a given size bone to a larger size, some bone is resorbed and some is deposited. Much of the resorbed bone mineral, calcium, can be reutilized during bone formation. The net and absolute effects of normal growth, vitamin D deficiency, or vitamin D excess were compared on bone resorption, bone formation, and calcium reutilization. Growing chicks were prelabeled extensively with three isotopes:45 Ca, [3 H]tetracycline, and [3 H]proline. Data were obtained weekly during 3 weeks of control growth, vitamin D deficiency, or vitamin D overdosage while on a nonradioactive diet. Bone resorption as measured by increases in the marrow (inner) diameter of the midshaft of the femur and humerus and by the weekly losses of total [3 H]tetracycline and [3 H]collagen per whole bone was not significantly different among any of the groups studied. The data indicated that the high rate of cortical bone resorption in experimental chicks was not increased above that observed in experimental chicks was not increased above that observed in control chicks. Vitamin D deficiency had little effect on the total45 Ca in whole bones, whereas vitamin D-treated chicks lost 40% of their45 Ca. Thus, vitamin D overdosage resulted in a decrease of45 Ca reutilization, whereas vitamin D deficiency resulted in an apparent increase of45 Ca reutilization. Both vitamin D-deficient and vitamin D-treated chicks had a decreased accumulation of dietary calcium per whole bone. The insufficient mineral mass in vitamin D-deficient chicks resulted from the indirect inhibition of bone mineralization due to the low intestinal absorption of calcium rather than from a change in bone resorption. In vitamin D-treated chicks the apparent bone atrophy and net loss of45 Ca from bone resulted from inhibiting bone matrix formation and mineralization instead of increasing bone resorption. The constancy of bone resorption under these experimental conditions suggests that bone mineralization is the major regulator of bone mass.