Normal and abnormal mineralization in mammals.
It is widely accepted that cells play a crucial role in the mineralization of dentin, cartilage and bone. The initial locus of calcification appears to be the matrix vesicle, a 200 nm submicroscopic extracellular, membrane-invested particle which is shed from the osteoblast, chondrocyte, or odontoblast and carries into the matrix calcifiable lipids and phosphatases. During Phase 1 of mineralization, the initiation phase, apatite appears within matrix vesicles, probably preceded by amorphous calcium phosphate. Initially, acidic phospholipids of matrix vesicles may attract calcium to form complexes with phosphate and protein. In vitro studies of cartilage slices and isolated matrix vesicles indicate the essentiality of vesicle phosphatases for mineral initiation. In pathological calcification is self-sustaining. Given physiological amounts of Ca2+ and PO43(-), calcification will spread by crystal proliferation into the extracellular matrix surrounding vesicles (Phase 2). During Phase 2 the rate of crystal proliferation is controlled by matrical factors: Collagen can orient and apparently promote apatite formation. Proteoglycans, pyrophosphate, gamma-carboxyglutamic acid-containing proteins and phosphoproteins in calcifying matrix bind Ca2+ by their anionic subgroups, and all have been shown to impede hydroxyapatite formation in vitro. The latter substances are visualized as regulating Phase 2 by inhibiting mineral growth. The calcification process involves an interaction of all of the above. When viewed as a 2-phase phenomenon, it is possible to integrate each of these factors into a comprehensive concept od biological mineralization.
D002113:Calcification, Physiologic; D002114:Calcinosis / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D009369:Neoplasms / Q000473:pathology