I recently had a patient ask me whether gum disease caused dementia. I told her that I was not sure if there was a direct correlation, but that I know that I have read some things that indicate that there is a link between the two. I promised to research it further and get her more information. And, in truth, I wanted to know the answer. My grandmother had early onset Alzheimer’s and it was devastating.
Alzheimer’s disease is an irreversible, progressive brain disorder and is the most common cause of dementia in adults. Brain cell connections and the cells themselves degenerate and die, eventually destroying memory, thinking skills and ultimately the ability to carry out even simple tasks. Memory loss and confusion are the main symptoms. No cure exists, but medications and management strategies may temporarily improve symptoms. While Alzheimer’s Disease is not considered a normal part of aging, the greatest known risk factor is increasing age, and the majority of people with Alzheimer’s are 65 and older. But it is not just a disease of old age. Approximately 200,000 Americans under the age of 65 have younger-onset Alzheimer’s disease (also known as early-onset Alzheimer’s).
The most common early symptom of Alzheimer’s is difficulty remembering newly learned information because Alzheimer’s changes typically begin in the part of the brain that affects learning. As Alzheimer’s advances through the brain it leads to increasingly severe symptoms, including disorientation, mood and behavior changes; deepening confusion about events, time and place; unfounded suspicions about family, friends and professional caregivers; more serious memory loss and behavior changes; and difficulty speaking, swallowing and walking.
It is the destruction and death of nerve cells that causes memory failure, personality changes, problems carrying out daily activities and other symptoms of Alzheimer’s disease. Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques are deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells. Tangles are twisted fibers of another protein called tau (rhymes with “wow”) that build up inside cells. Though autopsy studies show that most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more and in a predictable pattern, beginning in the areas important for memory before spreading to other regions.
In January of 2019, a study was published in the Journal of Science Advances1, where the brain tissue of deceased people with Alzheimer’s disease was studied. Researchers consistently found Porphyromonas gingivalis (p. gingivalis) one of the main pathogens responsible for periodontal disease. They also detected the p. gingivalis bacterium’s DNA in spinal fluid taken from living Alzheimer’s patients. In addition, toxic enzymes made by the bacterium — called gingipains — showed up in many of the Alzheimer’s brain samples.
In addition to the human brains, experiments in mice were also done which suggested a connection between the bacterium p. gingivalis and Alzheimer’s disease. When the research team infected the gums of healthy mice with P. gingivalis, the bacterium was later isolated from the brains of the animals. In addition, damage to neurons and higher than normal levels of the protein beta-amyloid in the mice brain tissue were found. Beta-amyloid proteins clump together to form plaques in the brains of people with Alzheimer’s disease. Researchers were able to clear the P. gingivalis infection in the brains of mice using a molecule that binds to and blocks the gingipains. This also reduced the production of beta-amyloid and some of the neuronal damage. The findings of this study offer evidence that P. gingivalis and gingipains in the brain play a central role in the pathogenesis of Alzheimer’s Disease.
Infection may also play a role in the disease process. Studies are being done to see if beta-amyloid is the brain’s way of protecting itself against microbes. The theory is that beta-amyloid could be an antimicrobial peptide that is part of the normal immune response against brain infections. The mechanism of action could be that the plaques are actually trying to envelop the microbes to protect the brain. However, ultimately it is suspected that more than one toxic agent will be found.
While the scientific study shows a clear link between the two diseases, researchers are quick to point out that the study does not provide strong enough evidence to state that there is a cause and effect relationship between p. gingivalis and Alzheimer’s Disease. They pointed out the small size of the study and the need to reproduce the results. Hence, it is too early to say that if you didn’t floss your teeth, you’re going to get Alzheimer’s disease; Or, if you do floss your teeth, that you won’t get Alzheimer’s.
The bigger take away from this theory is that mouth health should not be disassociated from the health of the rest of the body. It is refreshing to see that scientists are no longer ignoring dental disease as a contributing factor in systemic diseases. Overall wellness relies on oral health. So, while there may not be a direct correlation, there is enough of a connection to discuss this with your patients as another reason to brush, floss, and make bi-annual visits to your office.
1. Dominy et al., Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors Sci. Adv. 2019; 5: 23 January 2019