Introduction

The generation of mineralised matrix within arterial conduits is common (see Figure 1). About 10%–20% of atherosclerotic vessels contain architecturally complete trabecular bone with fully formed marrow cavities with haematopoietic cells and vascular sinusoids. Although it is recognised that bone formation and arterial vessel calcification have common biochemical pathways, this so-called vascular calcification is a complex and incompletely understood phenomenon, which has proved difficult to prevent and treat.1 The process of extraskeletal ossification is not unlike embryonic ossification pathways which can be triggered by a variety of metabolic, inflammatory and genetic factors. For example, it is likely that proteins that normally restrict biomineralisation to skeletal bone are diminished (eg, fetuin A, matrix GIa, among others), and raise the prospect of identifying targets for therapeutic intervention. The two types of calcification—atherosclerotic (intimal calcification) and medial artery calcification—have different mechanisms, but both affect arterial stiffness and physiology, and increase the risk of adverse cardiovascular events.2