Study highlights association between gum disease and alzheimer's plaque buildup

Scientists have found a link between periodontal (gum) disease and the formation of amyloid plaque, a hallmark of Alzheimer’s disease. The study, published in the Journal of Neuroinflammation, found that gum disease can lead to changes in brain cells called microglial cells, responsible for defending the brain from amyloid plaque, a type of protein that is associated with cell death.

The research provides important insight into how oral bacteria makes its way to the brain, and the role of neuroinflammation in Alzheimer’s disease, a brain disorder that slowly destroys memory and thinking skills. “We knew from one of our previous studies that inflammation associated with gum disease activates an inflammatory response in the brain,” said senior study author, Alpdogan Kantarci, from the Forsyth Institute in the US.

“In this study, we were asking the question, can oral bacteria cause a change in the brain cells?” Kantarci said in a statement. The microglial cells the researchers studied are a type of white blood cell responsible for digesting amyloid plaque. They found that when exposed to oral bacteria, the microglial cells became overstimulated and ate too much. “They basically became obese. They no longer could digest plaque formations,” Kantarci said.

The finding is significant for showing the impact of gum disease on systemic health. Gum disease causes lesions to develop between the gums and teeth. “The area of this lesion is the size of your palm. It’s an open wound that allows the bacteria in your mouth to enter your bloodstream and circulate to other parts of your body, Kantarci explained.

These bacteria can pass through the blood/brain barrier — a protective layer that lines the inner surfaces of the blood vessels inside the brain — and stimulate the microglial cells in the organ. Using mouse oral bacteria to cause gum disease in lab mice, the scientists were able to track periodontal disease progression in mice and confirm that the bacteria had travelled to the brain.

They then isolated the brain microglial cells and exposed them to the oral bacteria. This exposure stimulated the microglial cells, activated neuroinflammation, and changed how microglial cells dealt with amyloid plaques. “Recognising how oral bacteria causes neuroinflammation will help us to develop much more targeted strategies,” said Kantarci. “This study suggests that in order to prevent neuroinflammation and neurodegeneration, it will be critical to control the oral inflammation associated with periodontal disease,” Kantarci added.