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(Circulation Research. 2005;96:1219.)
© 2005 American Heart Association, Inc.

Editorials

Proinflammatory Vascular Calcification

Kristina Boström

From the Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, Calif.

Correspondence to Dr Kristina Boström, Division of Cardiology, David Geffen School of Medicine at UCLA, Box 951679, Rm 47-123 CHS, Los Angeles, CA 90095-1679. E-mail kbostrom@mednet.ucla.edu

See related article, pages 1248–1256

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Vascular calcification occurs as part of atherosclerosis. It is caused by the deposition of basic calcium phosphate (BCP) crystals in what appears to be a highly regulated process resembling bone formation.^1–4 Vascular calcification occurs in several forms,^1–4 including small crystal deposits in the neointima and large calcified areas in more advanced atherosclerotic plaques, which frequently take on the appearance of ectopic bone. Media sclerosis (Möncke-berg disease) is a form of calcification associated with the elastic lamellae and is distinct from atherosclerotic calcification.^1,3,4 It is common in diabetes mellitus and renal failure and is often seen in combination with atherosclerosis. Studies on the mechanism of vascular calcification have in most cases focused on similarities to bone formation^1–3; however, there are likely to be unique characteristics in the regulation of each type of calcification.⁴ Furthermore, the potential relationship between the different types of calcification is poorly understood.

The role of vascular calcification in atherosclerosis remains under discussion.^1,4 Even though it is accepted as a marker for the atherosclerotic plaque burden in coronaries and has been associated with an increased risk for cardiovascular morbidity and mortality,^1–5 its activity in the disease process has been questioned. On the one hand, it may limit plaque growth and represent a response to injury similar to fibrosis with no active contribution to the progression of atherosclerosis^1,4; on the other hand, it may actively impact the surrounding tissue and plaque stability.³

Evidence from studies on degenerative arthritis, a field that also involves deposition of BCP crystals, . . . [Full Text of this Article]

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