Figure 8.

Schematic illustrating four, non–mutually exclusive theories for vascular calcification: (1), cell death leading to release of apoptotic bodies and/or necrotic debris that may serve to nucleate apatite at sites of injury; (2), circulating nucleational complexes released from actively remodeling bone or matrix vesicular released locally; (3) loss of inhibition as a result of deficiency of constitutively expressed tissue-derived and circulating mineralization inhibitors leads to default apatite deposition; and (4) induction of bone formation resulting from altered differentiation of vascular smooth muscle or stem cells. (Reproduced and modified with permission from Speer MY, et al. Cardiovasc Pathol 2004;13: 63–70.)