Beware fake dental news

March 20, 2019

Why you should be skeptical of attention-grabbing headlines.

Many moons ago, while in graduate school, I studied under the late Michele L. Darby, RDH, MS, professor emeritus. She was very passionate about oral hygiene research and was able to take a snooze-worthy subject and turn it into something you didn’t want to miss. Besides being a powerful teacher and mentor, professor Darby introduced me to concepts that I’ve used in teaching and throughout my dental hygiene career. For example, when learning biostatistics, she would repeat this phrase, “There are three kinds of lies: lies, damn lies and statistics.” Data is persuasive, especially when used in ads, and often it’s used to strengthen weak arguments or to prove an opponent’s point.

I’m constantly reading about different oral/systemic links: periodontal disease and low birthweight/premature babies, cardiovascular disease and now Alzheimer’s disease. My objective in this column is to explain why it’s important to read an article with a healthy degree of skepticism.

Here’s the recent title of a recent news release from the American Academy of Periodontology: “Periodontal disease bacteria linked to Alzheimer’s disease.”

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Here’s a couple more I retrieved online:

  • “Gum disease–causing bacteria could spur Alzheimer’s”

  • “The cause of Alzheimer's could be coming from inside your mouth, study claims”

What do these headlines mean? Is it appropriate to discuss this link with patients in terms of concern about certain mouth bacteria causing Alzheimer’s disease, or do you think the headlines are a bit misleading for those who don’t understand what a link is? Let’s explore further.

Periodontal disease bacteria linked to Alzheimer’s disease

I wouldn’t be skeptical of some attention-grabbing headlines if I hadn’t studied the scientific method, research methodology and evidence-based dentistry. In undergraduate and graduate school, I learned the basics about the scientific method and biostatistics and continued my education over the years in this area. Many people have asked me how I learned to interpret the literature. All I can say is that it’s an educational process that develops over time and it requires a specific set of skills and a certain mindset. A working knowledge of evidence-based dentistry is essential for all dental hygiene professionals.

I read the recent AAP news release and the corresponding online research article in Science Advances, which uncovers a possible link between P. gingivalis and Alzheimer’s disease (AD).  P.gingivalis, a virulent periodontal pathogen in chronic periodontitis, has been identified in the brain of AD patients. Toxic proteases (enzymes) from P. gingivalis called “gingipains” have also been identified in the brain of Alzheimer’s patients, and levels are associated with tau (key brain protein) and ubiquitin (small protein) pathology. Gingipains, in vivo and in vitro, are neurotoxic with detrimental effects on tau. In this study, researchers designed and synthesized small-molecule inhibitors that targeted gingipains. The drug inhibitor reduced the P. gingivalis bacterial load, blocked amyloid beta plaques, reduced neuroinflammation and preserved neurons in the hippocampus portion of the brain. Data in the study suggests that gingipain inhibitors might be valuable for treating P. gingivalis brain infection and neurodegeneration that occurs in AD.1

P. gingivalis is found in gingival and periodontal infections but can also be found in 25 percent of healthy individuals.1 In AD, the hippocampus is one of the first sections of the brain to be damaged, but AD also causes atrophy of the cerebral cortex gray matter.1 If one or both parts of the hippocampus are damaged, the person can experience a loss of memory and a loss of the ability to make new, long-term memories. They tend to remember things that happened longer ago, before the damage occurs.

Gingipain load in the brain correlated with AD diagnosis in this study. This means that gingipain load was significantly higher in AD brains than in nondemented brains. There was also a highly significant correlation between gingipain load and tau load. Tau pathology significantly correlated with cognitive impairment with AD.

Findings of this study offer data showing that P. Gingivalis and gingipains play a role in the pathogenesis of AD and provide a unique conceptual framework for disease treatment with small molecule gingipain inhibitors.1 The researchers argue that brain infection with P. gingivalis is NOT the result of poor dental hygiene care following the onset of dementia or a consequence of late-stage disease. Instead, it’s an early occurrence that can explain the pathology in younger, middle-aged people before cognitive decline.1 The P. gingivalis load is also detected in cerebral spine fluid of clinical AD patients, which provides further evidence of P. gingivalis infection of the central nervous system. 

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P. gingivalis strains aren’t differentiated and researchers report that future studies need to differentiate between P. gingivalis strains to determine which ones are located in the brain and cerebral spinal fluid and which ones are more virulent in causing disease. Dogs can transmit a type of porphyromonas that produces gingipains called “P. gulae,” and a recent study demonstrated that dogs can transmit P. gulae to the oral cavity of their owners.2 Research is underway to determine whether P. gulae can contribute to the gingipain load in AD brains.

According to the researchers, broad-spectrum antibiotics don’t protect against P. gingivalis in vitro, but gingipains do and they’re offering an orally bioavailable brain-penetrant gingipain inhibitor that’s currently being tested in human clinical studies for AD.1

I worry about all the fake new in the spotlight, including salacious dental headlines about “potential” oral/systemic links. These titles are misleading because many professionals and patients don’t understand “links,” and I find practitioners and patients discussing, in simplistic terms, cause and effect. Patients have already told me they’ve read that oral bacteria cause AD.

If you take the time to read the research article by SS Dominy, et al., you’ll find an intricate and very detailed laboratory study with mouse brains and human brain tissue samples. If you read carefully, you’ll realize that this particular study, in terms of strength of scientific evidence, is toward the bottom of the evidence pyramid. This is where ideas and laboratory research take place and it’s an important start. Ideas turn into therapies and diagnostic tools, which are then tested with lab models and animals. It takes years for clinical trials to confirm these diagnostic tools and therapies. It’s a process and it takes time.

Early laboratory and animal/cadaver research on AD is something you can discuss with interested patients. You can talk about what we know and don’t know, and it’s a great way to get the patient’s attention. Alzheimer’s disease starts in a person’s middle years and there’s a window of time before symptoms appear, about 20 years of more. As the authors pointed out in the aforementioned research, P. gingivalis infection in the brain isn’t the result of poor dental hygiene care following the onset of dementia or late-stage AD. Instead, it’s an earlier pathology in younger, middle-aged people, and there’s even a strain of P. gingivalis in Fido, so beware playing kissy face with him until we know more!


1. Dominy SS. Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small molecule inhibitors. Science Advances. 23 Jan 2018: Vol. 5, no.1. Retrieved from:

2. Y. Yamasaki et al. Distribution of periodontopathic bacterial species in dogs and their owners. Arch. Oral Biol. 57, 1183–1188 (2012).