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Gingivitis Bacteria Triggers a Tailspin in Your Mouth

In small numbers a keystone pathogen can still cause destruction

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The vast majority of microbes that live in and on our bodies do not put our health at risk, but many can cause problems if their populations grow out of control. So the immune system keeps their numbers in check, culling resident bacteria here and there.

A few microbial species have found ways to sabotage the immune system and skew the balance of power in their favor. Take Porphyromonas gingivalis, a mouth-dwelling bacterium that has long been the prime suspect behind gum disease. Even in small numbers, P. gingivalis can stop white blood cells from producing certain chemicals that kill bacteria. Without these chemicals to restrict their growth, all the bacterial populations in the mouth—including those that had been contributing to a healthy ecosystem—grow explosively, causing tissue damage known as gingivitis.

In two recent studies, a team of University of Pennsylvania researchers led by dental microbiologist George Hajishengallis figured out the mechanism behind P. gingivalis’s subterfuge. Building on that knowledge, the scientists discovered that blocking a key chemical signal returned the microbial communities in the mouths of mice to normal.


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The standard care for gingivitis is a professional tooth cleaning and more flossing, which temporarily reduce bacterial numbers but do not restore white blood cells’ ability to kill. As such, dentists cannot do much to treat recurring inflammation. The team says the finding may lead to future treatment options.

Keystone pathogens may be the culprits behind other chronic inflammatory diseases, too, Hajishengallis says. But to pin down links, scientists need to better understand how keystone bacteria manipulate the checks and balances that allow humans to live in harmony with trillions of microbes.

Scientific American Magazine Vol 311 Issue 5This article was published with the title “Know the Jargon” in Scientific American Magazine Vol. 311 No. 5 (), p. 24
doi:10.1038/scientificamerican1114-24

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