A major enigma remains a century after Alois Alzheimer identified the disease that bears his name.
Despite decades of research, no one understands what causes Alzheimer’s disease in the long run.
Genetic mutations, accelerated aging, immune system dysfunction, and environmental variables have all been suggested as possibilities, but experts have yet to come up with a definitive solution.
Periodontal disease is an unexpected new possibility that has emerged recently.
According to a slew of new studies, Alzheimer’s disease may develop in parallel with periodontal disease, which affects half of all persons over the age of 30.
These chronic bacterial infections are caused by organisms that burrow below the gum line and can enter the bloodstream through bleeding gums.
Heart disease, type 2 diabetes, and preterm birth have all been linked to periodontal disease.
The links to Alzheimer’s disease are less clear, but the evidence is mounting.
According to current findings, periodontal disease may exacerbate or possibly cause other prevalent ailments such as rheumatoid arthritis, colon cancer, and other gastrointestinal disorders.
Richard Lamont, a professor of oral immunology and infectious disease at the University of Louisville School of Dentistry, says, “These discoveries have spurred a new way of thinking about these illnesses and their mechanisms.”
TARGETING BACTERIAL CULPRITS
Alzheimer’s disease strikes someone in the United States every 65 seconds, and the current 6 million Americans with the disease are anticipated to increase or triple by 2050.
These sobering statistics emphasize the importance of developing innovative strategies to combat this deadly disease, which presently has no treatment.
The initial evidence of a periodontal connection came from large-scale investigations.
For example, research from Taiwan’s Chung San Medical University indicated that patients with periodontal disease had a 70 percent higher risk of getting Alzheimer’s disease than those with healthy gums over 10 years.
Another study from 2016 discovered that those with oral infections advanced six times faster than those without the disease.
Recent research has added to the evidence by finding a method via which gum diseases can influence the brain.
Gums bleed frequently when a person with periodontal disease brushes, flosses, or chews food.
This permits oral germs to enter the circulation through minute breaks in bleeding or inflamed gums, including Porphyromonas gingivalis, the disease’s main culprit.
Mia Geisinger, a professor of periodontology at the University of Alabama in Birmingham’s School of Dentistry, argues that this makes it simpler for periodontal germs to migrate from the mouth to the brain.
The microorganisms in the mouth can then get through the blood-brain barrier.
According to Geisinger, this tissue ordinarily acts as a rigorous gatekeeper, regulating which compounds reach the brain, but in Alzheimer’s and other dementias, it becomes more permeable.
P. gingivalis can damage brain neurons and increase the creation of beta-amyloid plaques, clumps of tangled proteins that are a hallmark of Alzheimer’s disease, according to a study published in Science Advances in 2019.
Gingipains, which are poisonous enzymes secreted by P. gingivalis, were discovered in 96 percent of brain samples from deceased Alzheimer’s patients and in the spinal fluid of surviving patients, according to the researchers.
Chemicals that inhibited gingipains fought off P. gingivalis infections in the brain and helped restore neurons in the hippocampus, which is important for memory formation.
A PERIODONTAL ASSOCIATION WITH COLON CANCER
Fusobacterium nucleatum, another oral microbe, has long been suspected of causing colon cancer, the second largest cause of cancer death in the United States.
F. nucleatum is well-known for its adhesiveness and participation in the production of dental plaque.
High amounts of the microorganism, on the other hand, have been detected in colon cancer tissues and have been related to more aggressive malignancy, organ metastasis, and a bad prognosis.
In 2013, Yiping Han, a professor of microbial sciences at Columbia University’s College of Dental Medicine in New York, found that F. nucleatum generates a protein called FadA adhesin, which causes inflammation and promotes the growth of malignant cells but not healthy cells.
“It looked that F. nucleatum acted as an accelerant in malignant cells, similar to pouring gasoline on a fire,” Han explains.
In 2019, the researchers discovered that F. nucleatum causes colon cells to increase the synthesis of a protein called annexin A1, which feeds cancer growth and serves as a lure for more F. nucleatum. According to Han, “basically, we established a positive feedback loop that explains why this bacterium boosts colon cancer growth and worsens its progression.”
THE ‘TWO-HIT’ MODEL AND RHEUMATOID ARTHRITIS
Rheumatoid arthritis patients are considerably more common than non-rheumatoid arthritis patients to have infected gums, suggesting that oral infections may drive and worsen rheumatoid arthritis.
Patients with rheumatoid arthritis were more than 20 times more likely than those without the disease to have infected gums, according to new case-control research.
Furthermore, the severity of rheumatoid arthritis increases as periodontal disease progresses.
Researchers have devised a “two-hit” model to explain how periodontitis may contribute to the development of joint disease.
The first blow is chronic inflammation, which is caused by a protracted immune reaction to periodontal bacteria in the mouth and circulation.
This is followed by a second blow, such as joint trauma.
According to Iain Chapple, professor of periodontology at the University of Birmingham in the United Kingdom, this double whammy appears to trigger the formation of autoimmune antibodies that attack the body’s joints and tissues.
This causes severe swelling, joint deformity, and damage to a wide range of body parts, including the heart, skin, eyes, and arteries, which are all debilitating rheumatoid arthritis symptoms.
P. gingivalis also appears to increase the susceptibility of joint tissue to the new antibodies.
According to Lamont, it generates an enzyme that partially changes proteins by converting arginine to citrulline, a process known as citrullination.
“Essentially, this puts a bullseye on the protein’s back, labeling it as potentially foreign, leading rheumatoid arthritis antibodies to attack the body’s proteins.”
Scaling, root planing, and antibiotic treatment are common dental treatments for rheumatoid arthritis symptoms, and research suggests that periodontal treatment may decrease the progression of rheumatoid arthritis.
Because these antibodies exist 10 years before symptoms appear, researchers at the Veterans Administration are now investigating at-risk relatives of people with rheumatoid arthritis to determine if treating periodontal disease can prevent them from having the joint illness in the first place.
While research linking unhealthy gums to rheumatoid arthritis, Alzheimer’s disease, and colon cancer is still in its early stages, “identifying P. gingivalis and other oral pathogens as supervillains in these diseases is a breakthrough that could result in novel treatments,” says Thomas Van Dyke, a professor of oral medicine and vice president of clinical and translational research at Harvard University.
Poor oral health is both widespread and treatable, thus the findings could lead to a new prevention paradigm that includes excellent dental care, according to Van Dyke.
