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Brush Your Teeth To Reduce The Risk Of Heart Disease

Date:
September 11, 2008
Source:
Society for General Microbiology
Summary:
Heart disease is the leading cause of death worldwide. However, many people with cardiovascular disease have none of the common risk factors such as smoking, obesity and high cholesterol. Now, researchers have discovered a new link between gum disease and heart disease that may help find ways to save lives.
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Heart disease is the leading cause of death worldwide. However, many people with cardiovascular disease have none of the common risk factors such as smoking, obesity and high cholesterol. Now, researchers have discovered a new link between gum disease and heart disease that may help find ways to save lives, scientists heard September 9, 2008 at the Society for General Microbiology's Autumn meeting being held at Trinity College, Dublin.

In recent years chronic infections have been associated with a disease that causes "furring" of the arteries, called atherosclerosis, which is the main cause of heart attacks. Gum disease is one of the most common infections of humans and there are now over 50 studies linking gum disease with heart disease and stroke.

"A number of theories have been put forward to explain the link between oral infection and heart disease," said Professor Greg Seymour from the University of Otago Dunedin, New Zealand. "One of these is that certain proteins from bacteria initiate atherosclerosis and help it progress. We wanted to see if this is the case, so we looked at the role of heat shock proteins."

Heat shock proteins are produced by bacteria as well as animals and plants. They are produced after cells are exposed to different kinds of stress conditions, such as inflammation, toxins, starvation and oxygen and water deprivation. Because of this, heat shock proteins are also referred to as stress proteins. They can work as chaperone molecules, stabilising other proteins, helping to fold them and transport them across cell membranes. Some also bind to foreign antigens and present them to immune cells.

Because heat shock proteins are produced by humans as well as bacteria, the immune system may not be able to differentiate between those from the body and those from invading pathogens. This can lead the immune system to launch an attack on its own proteins. "When this happens, white blood cells can build up in the tissues of the arteries, causing atherosclerosis," said Professor Seymour.

"We found white blood cells called T cells in the lesions of arteries in patients affected by atherosclerosis. These T cells were able to bind to host heat shock proteins as well as those from bacteria that cause gum disease. This suggests that the similarity between the proteins could be the link between oral infection and atherosclerosis," said Professor Seymour.

This molecular mimicry means that when the immune system reacts to oral infection, it also attacks host proteins, causing arterial disease. These findings could fundamentally change health policy, highlighting the importance of adult oral health to overall health and wellbeing: control of gum disease should be essential in reducing the risk of heart disease.

"This is a significant step towards a more complete understanding of heart disease and improving treatment and preventive therapies," said Professor Seymour. "An understanding of all the possible risk factors could help lower the risk of developing heart disease and lead to a significant change in disease burden."


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Society for General Microbiology. "Brush Your Teeth To Reduce The Risk Of Heart Disease." ScienceDaily. ScienceDaily, 11 September 2008. <www.sciencedaily.com/releases/2008/09/080908203017.htm>.
Society for General Microbiology. (2008, September 11). Brush Your Teeth To Reduce The Risk Of Heart Disease. ScienceDaily. Retrieved July 1, 2015 from www.sciencedaily.com/releases/2008/09/080908203017.htm
Society for General Microbiology. "Brush Your Teeth To Reduce The Risk Of Heart Disease." ScienceDaily. www.sciencedaily.com/releases/2008/09/080908203017.htm (accessed July 1, 2015).

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