Experimental soft-tissue calcification was induced in the hind paw of rats injected intravenously with lead acetate and locally with egg white. This mineralization was inhibited by treatment with sodium salicylate given orally. Sodium salicylate did not influence the extravasation of lead in the treated paw, but decreased the lead-induced hypercalcemia and hyperphosphatemia. A parallelism was found between the blood levels of calcium, phosphorus, and lead. A secondary deposition of lead was evident in the heavily calcified paws.