There’s a better reason than bad breath to to get your gum disease under control. For one, research has shown that gum disease is a probable risk factor for Alzheimer’s disease.
Gum disease is a low-grade systemic disease. If you have it, you release a particular type of pro-inflammatory cell that systematically circulates and elevates C-reactive protein (CRP) throughout the body. CRP is a protein found in blood whose levels rise in response to inflammation.
Chronic gum disease means CRP is not only circulating, it’s signaling to your body you have an infection to fight. Invading pathogens from gum disease signal “All hands on deck!” to your immune system.
Now, some potentially game-changing research suggests that in some people this siren call to the immune system may contribute to Alzheimer’s disease. This is especially so if the immune system signals that the brain is under attack from invading pathogens.
One source of those harmful microbes? Diseased periodontal tissue. Your gums.
And, in fact, many of the harmful bacteria found in the blood and cerebrospinal fluid of Alzheimer’s patients can be traced back to gum disease. These microbes invade the brain via circulation or peripheral nerve pathways.
Both periodontitis – severe gum disease – and Alzheimer’s have plaques in common. The hallmark of Alzheimer’s is the buildup of amyloid plaques in particular. They’re made up of a small protein chain called beta-amyloid, with a mixture of other proteins and pieces of nerve cells. This accumulates in the brains of those with Alzheimer’s.
But the new research throws into question the earlier research showing that beta-amyloid chains are the result of abnormal processing of the amyloid precursor protein over time.
This NIH-funded study, published in Science Translational Medicine, suggests that beta-amyloids’ role may be akin to a natural antibiotic. But for some who have an abnormality in normal immune system activity, it may result in Alzheimer’s.
The study used genetically modified mice and worms and cultured human brain cells with excess beta-amyloid versus controls with no beta-amyloid. Researchers noted exposure to either bacteria or candida fungus in all groups resulted in
- Those with excess beta-amyloid surviving longer than the controls and having less bacteria in their brains.
- Those lacking beta-amyloid dying more often from infection.
- Those with beta-amyloid living longer.
These results point to the possibility that beta-amyloid may be the body’s response to certain infections.
Electron microscopy showed that the microbes were entangled in beta-amyloid fibers extending from the surfaces of the fungal cells, suggesting an entrapment role for beta-amyloid. Electron microscopy of the mouse brains infected with bacteria also showed that the microbes were embedded in beta-amyloid fibers. The authors propose that beta-amyloid’s role in Alzheimer’s disease may result from dysregulation of normal immune system activity rather than abnormal processing of amyloid precursor protein as previously believed.
As more research becomes available, the standard Alzheimer’s therapy aimed at totally removing beta-amyloid plaques may need to be reconsidered.
And while gum disease can’t be said to be a direct cause of Alzheimer’s, the bacteria present in gum disease could pose a risk. All the more reason to commit yourself to optimal home hygiene and maintaining oral health.