Calcification can lead to calcium deposits in the blood vessels and kidneys, and cause the blood vessels themselves to harden (medial artery calcification, or MAC), leading to an increased risk of heart attacks and strokes. Calcification of vascular tissue is a complication of diabetes, atherosclerosis, and kidney disease. It is also associated with ageing.
How Does Calcium Work in the Body?
There is always a large amount of calcium and phosphate in our bodies, because we "remodel" our entire skeleton every 10 years. But this constant construction needs to be controlled, and recent research shows that proteins play a vital role in promoting and slowing down calcification. Specifically, the matrix Gla protein (MGP), which inhibits calcification in soft tissues, and osteopontin (OPN), a protein that slows down calcification in hard tissues, such as teeth and bones. (If this seems counter-intuitive, imagine what would happen if bones never stopped growing.) Osteopontin also acts like a "glue" between old and new bone, to make sure the two bond completely.
But it seems that osteopontin also plays a part in pathological calcification (such as kidney stones or the unusual Eagle's Syndrome). In 2001 scientists were surprised to discover the proteins in kidney stones (1), and later research has shown that OPN is abundant at sites of calcification in human atherosclerotic plaques, diabetic arteries, and in native and prosthetic valves, but it is not present in normal arteries (2).
Why Does Pathological Calcification Occur?
There seems to be some connection between injury, or disease, and the onset of spontaneous calcification. As one Professor of Dentistry, Mark McKee of McGill University, put it "crystal growth is controlled by proteins expressed in diseased soft tissue to fight calcification. The same proteins were found in other body sites to shut down uninhibited crystal growth." (1). Another piece of research (3) stressed that OPN is strongly upregulated (increased) under conditions of injury.
Essentially, MGP is found in the blood vessels, and it acts as a "surveillance inhibitor", preventing any calcification from taking place. If this protein is lowered, and calcification does begin to take place, OPN is then expressed by the body to stop the process. If someone is deficient in both of these proteins, vascular calcification may occur under disease conditions.
There is also a simpler, ioatrogenic cause (i.e. resulting from medical treatment). Arterial calcification can be caused by blood-thinning drugs, such as Warfarin, which are given to people considered to be at risk from thrombosis. Unfortunately, Warfarin also inactivates MGP (the protein that prevents calcification). This has led to research into the potential role of Vitamin K in preventing calcification.
How Would I Know If I Had Calcified Blood Vessels?
If the blood vessels become hardened through calcification, they lose all flexibility and are unable to contract. One of the symptoms experienced is dizziness on standing. This is because when you stand up, your blood tries to pool in the veins in your legs (it rushes downwards with gravity) – but it is stopped by the contraction (squeezing) of the blood vessels, which pushes the blood upwards and back to the heart. If the veins can't contract, too much blood accumulates in the bottom half of the body, and not enough in the top, including the brain, leading to dizziness and even fainting.
However, note that dizziness is a symptom of low blood pressure generally – and the low pressure may be due to a number of causes, many of which need attention but are not sinister, such as dehydration. If dental X-rays or several symptoms suggest vascular calcification, this can be investigated by CT scan. Electron beam computer tomographic scanning (EBCT) can accurately determine coronary calcification.
Read more: Can Anything Cure Vascular Calcification?
References
- "The Bare Bones of Calcification", McGill Reporter, April 5, 2001; Volume 33 Number 14.
- "Smooth muscle cells deficient in osteopontin have enhanced susceptibility to calcification in vitro"; Mei Y. Speera, Yung-Ching Chienb, Mary Quana, Hsueh-Ying Yanga, Hojatollah Valib, Marc D. McKeeb and Cecilia M. Giachelli; Cardiovascular Research 2005 66(2):324-333; doi:10.1016/j.cardiores.2005.01.023
- Speer M.Y., Giachelli C.M. Regulation of cardiovascular calcification. Cardiovasc Pathol (2004) 13:63–70
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