Experimental aluminum intoxication and parathormone: effects on the mineralization process.
In order to study the effect of aluminum intoxication on bone and bone cells in normal animals and its relationship with hyperparathyroidism, and so to obtain further data on a pathogenetic role of this condition in inducing osteomalacia in uremic patients, 31 rats divided in four groups were injected intraperitoneally for 11 weeks with: Al (75.6 mg); Al-PTH (Al = 75.6 mg + PTH = 200 USP during the last week); C (saline solution), and C-PTH (saline solution + PTH = 200 USP during the last week). Al injection induced a consistent increase in the element in serum and tibia. PTH administration further enhanced Al content in tibia. The trabecular bone surfaces of Al-administered rats were stained by aluminon; the endosteal borders of their compact bone were always negative. Rib histomorphometry showed absence of osteomalacia in Al group and increase in osteoid in Al-PTH group, with development of mild osteomalacia. In these groups osteoclasts were less numerous than in controls. Dynamic bone parameters showed no separation of double tetracycline labels in trabecular bone of both Al-administered groups. Cortical bone was only slightly affected by treatment. All these data indicate that Al alone, in the quantity administered, does not induce osteomalacia in normal rats and that PTH, although given for a few days, enhances Al content in bone and induces osteoid increment. The reduction of tetracycline labels in all Al-treated animals is due to reduction of calcification and formation rate, which might be an index of osteoblast inhibition. The decrease in the number of osteoclasts suggests that Al might inhibit their formation.