Gum Bacteria isn’t Just About Dental Health
Keeping your teeth clean doesn’t only freshen your breath and prevent tooth decay – it might actually save your life.
The bacteria that cause gingivitis (gum disease) is called Porphyromonas gingivalis and is highly mobile throughout the body. People without any notably gum disease can carry the bacteria – it is found in low levels in about one-quarter of the population, so it’s relatively common.
But Porphyromonas gingivalis travels through the body easily. Common dental procedures appear to shake it loose, and given the right conditions, it may move into the liver and coronary arteries. In fact, another study found that it had colonized 100 percent of patients with cardiovascular disease. Porphyromonas gingivalis can also migrate to the brain, raising the risk of Alzheimer’s disease and even fuel the condition to progress even faster.
According to the study researchers, the connection between the Porphyromonas gingivalis doesn’t appear to be because of poor dental hygiene due to dementia, but rather a result of the bacteria invading the central nervous system during middle age – well before symptoms show.
While these facts can sound daunting, they illustrate the connections throughout the body for overall health – no one system is truly separate from the other. Proper dental care is about much more than keeping an attractive smile – it’s about keeping something to smile about.
Abstract:
Dominy SS, Lynch C, Ermini F, et al. Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Sci Adv. 2019;5(1):eaau3333.
Porphyromonas gingivalis, the keystone pathogen in chronic periodontitis, was identified in the brain of Alzheimer’s disease patients. Toxic proteases from the bacterium called gingipains were also identified in the brain of Alzheimer’s patients, and levels correlated with tau and ubiquitin pathology. Oral P. gingivalis infection in mice resulted in brain colonization and increased production of Aβ1-42, a component of amyloid plaques. Further, gingipains were neurotoxic in vivo and in vitro, exerting detrimental effects on tau, a protein needed for normal neuronal function. To block this neurotoxicity, we designed and synthesized small-molecule inhibitors targeting gingipains. Gingipain inhibition reduced the bacterial load of an established P. gingivalis brain infection, blocked Aβ1-42 production, reduced neuroinflammation, and rescued neurons in the hippocampus. These data suggest that gingipain inhibitors could be valuable for treating P. gingivalis brain colonization and neurodegeneration in Alzheimer’s disease.
