Fig. 2.26 ). Although hemosiderin accumulation is usually pathologic, small amounts of this pigment are normal in the mononuclear phagocytes of the bone marrow, spleen, and liver, where aging red cells are normally degraded. Excessive deposition of hemosiderin, called hemosiderosis, and more extensive accumulations of iron seen in hereditary hemochromatosis are described in Chapter 16.
Pathologic calcification, a common process in a wide variety of disease states, is the result of an abnormal deposition of calcium salts, together with smaller amounts of iron, magnesium, and other minerals. It can occur in two ways.
• Dystrophic calcification. In this form, calcium metabolism is normal but it deposits in injured or dead tissue, such as areas of necrosis of any type. It is virtually ubiquitous in the arterial lesions of advanced atherosclerosis (Chapter 10). Although dystrophic calcification may be an incidental finding indicating insignificant past cell injury, it also may be a cause of organ dysfunction. For example, calcification can develop in aging or damaged heart valves, resulting in severely compromised valve motion. Dystrophic calcification of the aortic valves is an important cause of aortic stenosis in elderly persons (Chapter 11).
Dystrophic calcification is initiated by the extracellular deposition of crystalline calcium phosphate in membrane-bound vesicles, which may be derived from injured cells, or the intracellular deposition of calcium in the mitochondria of dying cells. It is thought that the extracellular calcium is concentrated in vesicles by its affinity for membrane phospholipids, whereas phosphates accumulate as a result of the action of membrane-bound phosphatases. The crystals are then propagated, forming larger deposits.
• Metastatic calcification. This form is associated with hypercalcemia and can occur in normal tissues. The major causes of hypercalcemia are (1) increased secretion of parathyroid hormone, due to either primary parathyroid tumors or production of parathyroid hormone–related protein by other malignant tumors; (2) destruction of bone due to the effects of accelerated turnover (e.g., Paget disease), immobilization, or tumors (increased bone catabolism associated with multiple myeloma, leukemia, or diffuse skeletal metastases); (3) vitamin D–related disorders including vitamin D intoxication and sarcoidosis (in which macrophages activate a vitamin D precursor); and (4) renal failure, in which phosphate retention leads to secondary hyperparathyroidism.
MORPHOLOGYRegardlessofthesite,calciumsaltsareseenongrossexaminationasfinewhitegranulesorclumps,oftenfeltasgrittydeposits.Dystrophiccalcificationiscommoninareasofcaseousnecrosisintuberculosis.Sometimesatuberculouslymphnodeisessentiallyconvertedtoradiopaquestone.Onhistologicexamination,calcificationappearsasintracellularand/orextracellularbasophilicdeposits.Withtime,heterotopicbonemayforminfociofcalcification.
Fig. 2.26 Hemosideringranulesinlivercells.(A)Hematoxylin-eosin–stainedsectionshowinggolden-brown,finelygranularpigment.(B)IrondepositsshownbyaspecialstainingprocesscalledthePrussianbluereaction.
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