Pathologic calcification involves the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other minerals. It is known as dystrophic calcification when it occurs in dead or dying tissue and as meta- static calcification when it occurs in normal tissue.
Dystrophic calcification represents the macroscopic deposition of calcium salts in injured tissue. It is often visible to the naked eye as deposits that range from gritty, sandlike grains to firm, hard rock material. The pathogenesis of dystrophic calcification involves the intracellular or extracellular formation of crystalline calcium phosphate. The components of the calcium deposits are derived from the bodies of dead or dying cells as well as from the circulation and interstitial fluid.
Dystrophic calcification is commonly seen in atheromatous lesions of advanced atherosclerosis, areas of injury in the aorta and large blood vessels, and damaged heart valves. Although the presence of calcification may only indicate the presence of previous cell injury, as in healed tuberculosis lesions, it is also a frequent cause of organ dysfunction. For example, calcification of the aortic valve is a frequent cause of aortic stenosis in older adults (Fig. 5.4).
In contrast to dystrophic calcification, which occurs in injured tissues, metastatic calcification occurs in normal tissues as the result of increased serum calcium levels (hypercalcemia). Almost any condition that increases the serum calcium level can lead to calcification in inappropriate sites such as the lung, renal tubules, and blood vessels. The major causes of hypercalcemia are hyperparathyroidism, either primary or secondary to phosphate retention in renal failure; increased mobilization of calcium from bone as in Paget disease, cancer with metastatic bone lesions, or immobilization; and vitamin D intoxication.