Inflammation ushers in calcification: a cycle of damage and protection?

The layman’s term “hardening of the arteries” is synonymous with vascular disease and describes the ubiquitous calcification of the intima and media of the vessel wall that occurs in atherosclerosis and aging. Vascular calcification measured and quantified by electron beam computer tomography is a powerful predictor of myocardial infarction, vascular complications such as amputation, and all-cause mortality.1 Despite this fact, calcification has remained a neglected pathology, particularly in the field of atherosclerosis. This neglect is due in part to the controversy surrounding whether calcification is a bystander marker of disease load or acts to induce plaque rupture and thus increase the cardiovascular event rate; it is also due to the long-held belief that vascular calcification is an end-stage dystrophic process and therefore not amenable to manipulation. However, huge progress has been made over the last 10 years in elucidating the cell biological mechanisms underlying vascular calcification.