Abstract
Calcification in necrosis has long been known. Of the tissue components, the cells are most vulnerable. Nevertheless, little attention has been paid to the role of cell death in calcification. This review attempts to update the mechanism of calcification with an emphasis on the role of apoptosis in calcification. A brief review on the basic sciences relevant to calcification is followed by a discussion of abnormal Ca2+ and P(i) homeostasis in cell injury and apoptosis. Concomitant increases in Ca2+ and P(i) in blebs (and matrix vesicles) formed by apoptotic and/or necrotic cells are apparently the primary mechanism of calcification. In addition, membranous cellular degradation products (CDP) resulting from cell disintegration in toto frequently serve as the nidus of calcification. Published data on physiological calcification are compared with findings in various dystrophic calcinoses. This led to the conclusion that apoptosis most likely underlies the mechanism of both physiological and pathological calcifications. It is concluded that calcification is an important function of apoptosis. The mechanism of calcification by CDP and morphology of the resultant calcific deposits are complex.
Original language | English (US) |
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Pages (from-to) | 1137-1178 |
Number of pages | 42 |
Journal | Scanning Microscopy |
Volume | 9 |
Issue number | 4 |
State | Published - 1995 |
Keywords
- Ca and P(i) metabolism
- Cell death
- Cellular degradation products
- blebbing
- calcium phosphate crystals
- cell aging
- matrix vesicles
- neoplastic calcinosis
- nephrocalcinosis
- phospholipids
- psammoma bodies
- stones
- vascular calcinosis
ASJC Scopus subject areas
- Instrumentation