Monckeberg's arteriosclerosis
| Mönckeberg's sclerosis | |
|---|---|
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| Microphotography of arterial wall with calcified (violet colour) atherosclerotic plaque (haematoxylin & eosin stain) | |
| Classification and external resources | |
| Specialty | cardiology |
| ICD-10 | I70.2 |
| ICD-9-CM | 440.20 |
| MeSH | D050380 |
Mönckeberg's arteriosclerosis, or Mönckeberg's sclerosis, also called medial calcific sclerosis or Mönckeberg medial sclerosis, is a form of arteriosclerosis or vessel hardening, where calcium deposits are found in the muscular middle layer of the walls of arteries (the tunica media). It is an example of dystrophic calcification. This condition occurs as an age-related degenerative process. However, it can occur in pseudoxanthoma elasticum and idiopathic arterial calcification of infancy as a pathological condition, as well. Its clinical significance and cause are not well understood and its relationship to atherosclerosis and other forms of vascular calcification are the subject of disagreement. Mönckeberg's arteriosclerosis is named after Johann Georg Mönckeberg, who first described it in 1903.
Typically, Mönckeberg’s arteriosclerosis is not associated with symptoms unless complicated by atherosclerosis, calciphylaxis, or accompanied by some other disease. However presence of Mönckeberg’s arteriosclerosis is associated with poorer prognosis. This is probably due to vascular calcification causing increased arterial stiffness, increased pulse pressure and resulting in exaggerated damage to the heart and kidneys.
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 tumour necrosis factor (TNF)-related apoptosis-induceing ligand protein have been implicated in this process.
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