Fabiola Atzeni, Piercarlo Sarzi-Puttini, Maorizio Bevilacqua
Journal: Rheumatic diseases clinics of North America 2006;32(2):413-26, viii
PMID: 16716887
Extracellular matrix mineralization or calcification occurs in many pathologic conditions, including atherosclerosis, medial wall calcification, diffuse idiopathic skeletal hyperostosis, and chondrocalcinosis. Vascular wall calcification is the most common and involves two mechanisms: passive calcification resulting from breakdown of the protection system and active calcification resulting from transdifferentiation of mesenchymal cells in the vascular wall to bone. Although reports are conflicting, several matrix proteins are identified as protective factors against dystrophic calcification in nonosseous tissues. Serum matrix Gla protein may be a marker of osteometabolic syndromes that cause hyperostosis and plays a role in Milwaukee shoulder syndrome.
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