Effect of aluminium on osteocalcin production in the rat.

In renal failure, aluminium is an important factor in the development of osteomalacia. The mechanism by which aluminium produces osteomalacia is not clear; it may be toxic to the osteoblast, and as a result of its effect on osteoblasts, impair mineralisation. Another possibility is that aluminium may directly impair mineralisation independent of osteoblast function. Osteocalcin is considered to be a specific marker of osteoblast activity and its production is stimulated by calcitriol. In the present study, calcitriol-stimulated production of osteocalcin was studied as a marker of osteoblast activity in aluminium toxicity. Four groups of rats were evaluated: (1) normals; (2) normal renal function plus aluminium; (3) renal failure; and (4) renal failure plus aluminium. Osteocalcin production was determined by measuring serum osteocalcin at baseline and after stimulation with calcitriol. In rats receiving aluminium, the baseline serum osteocalcin levels were not different from their respective controls. After stimulation with calcitriol, the increase in serum osteocalcin was less in the renal failure group receiving aluminium. However, when corrected for the number of osteoblasts, the increase in serum osteocalcin was not decreased. In summary, although aluminium administration decreased the number of osteoblasts in rats with renal failure, osteocalcin production by the remaining osteoblasts was not decreased.