Medial calcific sclerosis a form of arteriosclerosis in which extensive calcium deposits are found in the tunica media of the artery with little obstruction of the lumen. Also called medial arteriosclerosis. and Mönckeberg's arteriosclerosis  

Typically, Monckeberg’s arteriosclerosis is not associated with symptoms unless complicated by atherosclerosis, calciphylaxis, or accompanied by some other disease However presence of Monckeberg’s arteriosclerosis is associated with poorer prognosi. This is probably due to vascular calcification causing increased arterial stiffness, increased pulse pressure and resulting in exaggerated damage to the heart and kidneys.

Often Monckeberg’s arteriosclerosis is discovered as an incidental finding in an X ray radiograph; in autopsy; or in association with investigation of some other disease, such as diabetes mellitus or chronic kidney disease. Typically calcification is observed in the arteries of the upper and lower limb although it has been seen in numerous other medium size arteries In the radial or ulnar arteries it can cause "pipestem" arteries, which present as a bounding pulse at the end of the calcific zone. It may also result in "pulselessness." Epidemiological studies have used the ratio of ankle to brachial blood pressure (ankle brachial pressure index, ABPI or ABI) as an indicator of arterial calcification with ABPI >1.3 to >1.5 being used as a diagnostic criterion depending on the study

Minor degrees of calcification of the cardiovascular system are common in elderly people and the prevalence of vascular calcification is increased by some diseases , 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 tumour necrosis factor (TNF)-related apoptosis-induceing ligand protein have been implicated in this process. It is unclear whether Monckeberg's arteriosclerosis 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 Monckeberg's arteriosclerosis 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 Monckeberg's arteriosclerosis. 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 Monckeberg's arteriosclerosis.

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