Calcification in atherosclerosis: Bone biology and chronic inflammation at the arterial crossroads

TLDR

Dystrophic or ectopic mineral deposition occurs in many pathologic conditions, including atherosclerosis, and calcium deposits serve as a radiographic surrogate marker that predicts higher risk of myocardial infarction and death, underscoring the need to understand plaque composition and stability. The authors summarize current models of intimal arterial plaque calcification and identify key questions for future research. They propose that plaque calcification results from the convergence of bone biology and vascular inflammatory pathobiology.

Abstract

Dystrophic or ectopic mineral deposition occurs in many pathologic conditions, including atherosclerosis. Calcium mineral deposits that frequently accompany atherosclerosis are readily quantifiable radiographically, serve as a surrogate marker for the disease, and predict a higher risk of myocardial infarction and death. Accelerating research interest has been propelled by a clear need to understand how plaque structure, composition, and stability lead to devastating cardiovascular events. In atherosclerotic plaque, accumulating evidence is consistent with the notion that calcification involves the participation of arterial osteoblasts and osteoclasts. Here we summarize current models of intimal arterial plaque calcification and highlight intriguing questions that require further investigation. Because atherosclerosis is a chronic vascular inflammation, we propose that arterial plaque calcification is best conceptualized as a convergence of bone biology with vascular inflammatory pathobiology.