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

Abstract

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, Ca, 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 Ca reutilization. Growing chicks were prelabeled extensively with 3 isotopes: 45Ca, [3H]tetracycline and [3H]proline. Data were obtained weekly during 3 wk 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 [3H]tetracycline and [3H]collagen per whole bone was not significantly different among any groups. The high rate of cortical bone resorption in experimental chicks was not increased above the observed in control chicks. Vitamin D deficiency had little effect on the total 45Ca in whole bones; vitamin D-treated chicks lost 40% of their 45Ca. Vitamin D overdosage resulted in a decrease of 45Ca reutilization; vitamin D deficiency resulted in an apparent increase of 45Ca reutilization. Vitamin D-deficient and vitamin D-treated chicks had a decreased accumulation of dietary Ca 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 Ca rather than from a change in bone resorption. In vitamin D-treated chicks the apparent bone atrophy and net loss of 45Ca from bone resulted from inhibiting bone matrix formation and mineralization instead of increasing bone resorption. Constancy of bone resorption under these conditions suggests that bone mineralization is the major regulator of bone mass.