Abstract

Ectopic calcification is defined as inappropriate biomineralization occurring in soft tissues. 1 Ectopic calcifications are typically composed of calcium phosphate salts, including hydroxyapatite, but can also consist of calcium oxalates and octacalcium phosphate as seen in kidney stones. 2 In uremic patients, a systemic mineral imbalance is associated with widespread ectopic calcification, referred to as metastatic calcification. 3 In the absence of a systemic mineral imbalance, ectopic calcification is typically termed dystrophic calcification. Often, these sites show evidence of tissue alteration and/or necrosis. Dystrophic mineralization is commonly observed in soft tissues as a result of injury, disease, and aging. Although most soft tissues can undergo calcification, skin, kidney, tendons, and cardiovascular tissues appear particularly prone to developing this pathology. 4 In addition, a number of prosthetic devices are prone to ectopic calcification, as discussed below. Recent insights into the mechanisms regulating ectopic calcification have come from studies of cardiovascular calcification, including that by Kim et al 5 in this issue of the Journal, and thus will be the major focus of this article. The reader is referred to other reviews for information about additional tissue-specific ectopic calcifications. 2,6,7

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