Dentist as Destiny Part 6: How many teeth do you have?

The dentist you choose is shaping your destiny. Here are Parts 1, 2, 3, 4, and 5 if you missed them.

For several weeks, I’ve asked you to imagine two people: same age, same genes, same diet.

One chose a dentist who treats the mouth as part of the whole body. The other chose a perfectly competent drill-and-fill dentist down the street.

Here’s the uncomfortable part of a career spent examining mouths. A patient would sit down in the chair at forty, looking perfectly healthy, and I had no way to prove where they were headed. 

But I usually had a clinical instinct about it…

Problems in the rest of the body tend to show up in the mouth first. After enough years of watching some patients reach their late seventies still being able to bite into an apple, sharp as ever, and others the same age ordering only soft foods and losing the thread of a conversation halfway through, that instinct stopped being a hunch. It became a pattern.

It almost always started at the gumline…

I never had the chance to test this as a controlled experiment. So for years, all I had was the pattern, and a growing body of research that kept explaining it.

If there’s one finding I want you to take from this series, it’s this. It looked like five different conditions, like cardiovascular disease, cognitive decline, blood sugar that wouldn’t stabilize, disrupted sleep, a pregnancy that ended too soon. It wasn’t five conditions. It was one condition, presenting five ways.

When the gums are inflamed, the seal between gum and tooth breaks down, leaving an open wound in the mouth. There’s a real figure behind this.

Researchers who calculated the total area of raw, bleeding tissue in a mouth with advanced periodontal disease estimated it at roughly the size of a palm (whoa).

As one review put it, a skin wound of that size would warrant an emergency room visit. In the mouth, most patients don’t even feel it.

And the effects of that wound don’t stay contained. Every time you chew or brush, some of what lives in that wound enters the bloodstream, and from there, it travels. Researchers have identified oral bacteria within arterial plaque. In 2019, they identified the periodontal pathogen Porphyromonas gingivalis, along with the toxins it produces, in the brain tissue of patients who had died with Alzheimer’s disease. The same organisms recur around the pancreas, in arthritic joints, in placental tissue. One point of entry, one slow daily leak, sustained for decades.

Count a patient’s teeth, and you have a rough indicator of life expectancy. A 2021 review of 75 studies found that patients with fewer remaining teeth carried a higher risk of all-cause mortality than those who kept theirs. (The magnitude varies by statistical adjustment, unadjusted estimates approach double the risk, fully adjusted estimates are considerably smaller, but the direction is consistent.) And it isn’t only tooth count. A 2024 study assessing bacterial diversity in the mouths of more than 8,000 patients found that a richer oral microbiome was associated with lower mortality risk in the years that followed.

What concerns me most isn’t years of life. It’s the quality of those years. Research out of Japan, following tens of thousands of older adults, found that patients who kept 20 or more of their own teeth didn’t just live longer, they spent fewer of their final years disabled and dependent. Not simply more life, but more functional life.

Now, I expect some of you are ready to tell me this is all correlation. The skeptic’s position is that the mouth isn’t causing any of this, and that unhealthy mouths simply co-occur with smoking, poverty, and poor diet, and those are the real drivers of risk. That’s a fair challenge but  doesn’t hold up once you move from observation to intervention.

Because when patients are randomly assigned to periodontal treatment, their physiology changes. In a New England Journal of Medicine trial, treating severe periodontal disease improved endothelial (blood vessel) function within six months. (In fairness: that’s a marker of vascular health, not a prevented heart attack, and the treatment transiently worsened function for a day before improving it.) Or consider antiseptic mouthwash: eliminate the bacteria on the tongue, and blood pressure rises measurably within a day in otherwise healthy people. The increase is modest (a few points) but it’s reproducible, and measured in the same individuals before and after.

We’ve seen this pattern before in medicine. For most of the last century, the accepted explanation for ulcers was stress and spicy food. A physician named Barry Marshall showed that a bacterium was responsible, drank a culture of it himself when he couldn’t get anyone to believe him, and was awarded a Nobel Prize in 2005. The clinicians certain it was “just correlation” weren’t unintelligent. They were early, confident, and mistaken. Anyone dismissing the mouth-body connection as coincidence today is standing in the same spot.

Which brings me to the point I’d emphasize most.

No one will ever prove, in a controlled trial, that a lifetime of oral care extends lifespan. That study cannot be run. There’s no product to sell at the end of it, and no ethics board will randomize a thousand patients to twenty years of dental neglect to see who dies first. So we’re left with mechanism, accumulated evidence, and clinical judgment. When the intervention is nearly free, takes ninety seconds, and carries no risk, waiting for the perfect study isn’t rigor; it’s a bad bet. It’s a much better bet to wear the seatbelt, so to speak.

So here is what I’d recommend, starting tonight:

1. Treat bleeding gums as a diagnostic sign, not a cosmetic nuisance. It’s the one indicator in this entire series you can spot yourself, in the mirror. Ask your dentist directly whether you have gingival inflammation, and don’t accept a “yes” without a plan.
2. Clean between your teeth every night. Periodontal disease begins where a toothbrush can’t reach. Floss, a water flosser, interdental brushes…the method matters less to me than the habit. I love this brand new floss from Fygg.
3. Stop using antiseptic mouthwash. It kills the beneficial bacteria along with the harmful ones, including the species on your tongue that help regulate blood pressure. The goal isn’t a sterile mouth; it’s a balanced one. If you are looking for what to do instead, I love this tongue scraper and this oil pulling blend. 
4. Support the beneficial bacteria instead: leafy greens for the nitrate that tongue bacteria convert to nitric oxide, green tea, and less sugar (sugar being what feeds the underlying problem.) If the idea of eating all those leafy greens feels insurmountable, pop one of these mints.
5. Order an oral microbiome test kit. I encourage everyone to get their oral microbiome tested. You understand not only your risk for conditions like tooth decay, gum inflammation, bad breath, and gut dysbiosis, but also your body’s ability to produce nitric oxide. You’ll then receive personalized oral care and diet recommendations to balance your microbiome and improve your oral and overall health.
6. Find a dentist who treats the mouth as connected to the rest of the body. Ignore the labels of “holistic,” “biological,” “functional” which all get used loosely. Look at what the practice actually does: takes a complete medical history and applies it, assesses the airway, addresses inflammation proactively, and consults your physician when something in your mouth points to a bigger issue. My Functional Dentist Directory is a great place to start. And once you find the right practice, stay with it. A dentist who has followed your mouth for fifteen years sees change before you notice it yourself.

Warmly,

Mark

P.S. If you’ve read the whole series, you now know more about the mouth-body connection than most physicians were taught in medical school. That’s no knock on them; it simply wasn’t in the curriculum, the same way the oral microbiome wasn’t in mine when I graduated. You’re ahead of the curve.

Further Reading & Citations

Nesse, W., Abbas, F., van der Ploeg, I., Spijkervet, F. K. L., Dijkstra, P. U., & Vissink, A. (2008). Periodontal inflamed surface area: quantifying inflammatory burden. Journal of Clinical Periodontology, 35(8), 668–673. https://doi.org/10.1111/j.1600-051X.2008.01249.x

Haraszthy, V. I., Zambon, J. J., Trevisan, M., Zeid, M., & Genco, R. J. (2000). Identification of periodontal pathogens in atheromatous plaques. Journal of Periodontology, 71(10), 1554–1560. https://doi.org/10.1902/jop.2000.71.10.1554

Dominy, S. S., Lynch, C., Ermini, F., Benedyk, M., Marczyk, A., Konradi, A., … Potempa, J. (2019). Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Science Advances, 5(1), eaau3333. https://doi.org/10.1126/sciadv.aau3333

Reichert, S., Haffner, M., Keyßer, G., Schäfer, C., Stein, J. M., Schaller, H.-G., … Schulz, S. (2013). Detection of oral bacterial DNA in synovial fluid. Journal of Clinical Periodontology, 40(6), 591–598. https://doi.org/10.1111/jcpe.12102

Ye, C., Katagiri, S., Miyasaka, N., Kobayashi, H., Khemwong, T., Nagasawa, T., & Izumi, Y. (2020). The periodontopathic bacteria in placenta, saliva and subgingival plaque of threatened preterm labor and preterm low birth weight cases: a longitudinal study in Japanese pregnant women. Clinical Oral Investigations, 24(12), 4261–4270. https://doi.org/10.1007/s00784-020-03287-4

Fan, X., Alekseyenko, A. V., Wu, J., Peters, B. A., Jacobs, E. J., Gapstur, S. M., … Ahn, J. (2018). Human oral microbiome and prospective risk for pancreatic cancer: a population-based nested case-control study. Gut, 67(1), 120–127. https://doi.org/10.1136/gutjnl-2016-312580

Beukers, N. G. F. M., Su, N., Loos, B. G., & van der Heijden, G. J. M. G. (2021). Lower number of teeth is related to higher risks for ACVD and death—Systematic review and meta-analyses of survival data. Frontiers in Cardiovascular Medicine, 8, 621626. https://doi.org/10.3389/fcvm.2021.621626

Yu, J., Lin, B., Zhang, Z., Chen, W., Lv, W., & Zheng, L. (2024). Association between oral microbiome diversity and all-cause mortality: a longitudinal study of NHANES, 2009–2012. BMJ Open, 14(12), e087288. https://doi.org/10.1136/bmjopen-2024-087288

Bando, S., Tomata, Y., Aida, J., Sugiyama, K., Sugawara, Y., & Tsuji, I. (2017). Impact of oral self-care on incident functional disability in elderly Japanese: the Ohsaki Cohort 2006 study. BMJ Open, 7(9), e017946. https://doi.org/10.1136/bmjopen-2017-017946

Tonetti, M. S., D’Aiuto, F., Nibali, L., Donald, A., Storry, C., Parkar, M., … Deanfield, J. (2007). Treatment of periodontitis and endothelial function. New England Journal of Medicine, 356(9), 911–920. https://doi.org/10.1056/NEJMoa063186

Kapil, V., Haydar, S. M. A., Pearl, V., Lundberg, J. O., Weitzberg, E., & Ahluwalia, A. (2013). Physiological role for nitrate-reducing oral bacteria in blood pressure control. Free Radical Biology and Medicine, 55, 93–100. https://doi.org/10.1016/j.freeradbiomed.2012.11.013

The Nobel Prize in Physiology or Medicine 2005. NobelPrize.org — awarded to Barry J. Marshall and J. Robin Warren “for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease.” https://www.nobelprize.org/prizes/medicine/2005/summary/