Calcification of soft tissue without any distrubances of calcium metabolism is called

Ref Robbins 9/e p65 Dystrophic Calcification Dystrophic calcification is encountered in areas of necrosis of any type. It is viually inevitable in the atheromas of advanced atherosclerosis, associated with intimal injury in the aoa and large aeries and characterized byaccumulation of lipids (Chapter 9). Although dystrophic calcification may be an incidental finding indicating insig- nificant past cell injury, it may also be a cause of organ dysfunction. For example, calcification can develop in aging or damaged hea valves, resulting in severely com- promised valve motion. Dystrophic calcification of the aoic valves is an impoant cause of aoic stenosis in elderly persons (Fig. 10-17, Chapter 10). The pathogenesis of dystrophic calcification involves initiation (or nucleation) and propagation, both of which may be either intracellular or extracellular; the ultimate end product is the formation of crystalline calcium phos- phate. Initiation in extracellular sites occurs in membrane- bound vesicles about 200 nm in diameter; in normal cailage and bone they are known as matrix vesicles, and in pathologic calcification they derive from degenerating cells. It is thought that calcium is initially concentrated in these vesicles by its affinity for membrane phospholipids, while phosphates accumulate as a result of the action of membrane-bound phosphatases. Initiation of intracellular calcification occurs in the mitochondria of dead or dyingcells that have lost their ability to regulate intracellular calcium. After initiation in either location, propagation of crystal formation occurs. This is dependent on the concen- tration of Ca2+ and PO4 - , the presence of mineral inhibitors, and the degree of collagenization, which enhances the rate of crystal growth.