Minor degrees of calcification of the cardiovascular system are common in elderly people, and the prevalence of vascular calcification is increased by some diseases (see Epidemiology section). Vascular calcification results from the deposition of calcium phosphate crystals (hydroxyapatite) as a consequence of disordered calcium phosphate regulation in the blood vessel. Hydroxyapatite is secreted in vesicles that bleb out from vascular smooth muscle cells or pericytes in the arterial wall. The mechanism of vascular calcification is not fully understood, but probably involves a phenotypic change in the vascular smooth muscle cells in the wall with activation of bone-forming programs. Numerous regulators of calcification such as osteopontin, osteoprotegerin, matrix gla protein and fetuin-A, receptor activator of NF-kappa-B, receptor activator of NF-kappa-B ligand and tumor necrosis factor (TNF)-related apoptosis-inducing ligand protein have been implicated in this process. It is unclear whether<unk>  is a distinct entity or forms part of a spectrum of vascular calcification that includes atherosclerosis and calcification in the inner layer of the artery wall (tunica intima), calcification of the internal elastic lamina, calcification of cardiac valves and widespread soft tissue calcification. The existence of<unk>  has been disputed and it has been proposed that it is a part of a continuum of atherosclerotic disease: the majority of atherosclerotic plaques contain some calcium deposits and calcification of the internal elastic lamina is common in pathological specimens labelled as<unk> . However studies in animals suggest that a predominantly medial pattern of vascular calcification reflects different underlying mechanisms of disease, and despite involvement of the internal elastic lamina, evidence of inflammation is rare in<unk> .
Monckeberg's arteriosclerosis
Charcot–Bouchard aneurysm
Arterial tortuosity syndrome
Diabetic angiopathy
Takayasu's arteritis
Rasmussen's aneurysm
Chorangiosis
Arteriolosclerosis