Ryder 2020

From Ryder 2020*

The oral microbiome is second only to the colon in the density of microbes dwelling in those human ecosystems. DNA methods (rather than culture methods) have so far uncovered over 800 bacterial species in the oral microbiome. Just as insights into the gastrointestinal (GI) microbiome have revealed just how much destruction we have wrought on species composition with use of antibiotics, exposure to food additives like preservatives, emulsifying agents, and synthetic sweeteners, and other factors, it is now becoming clear that we have done something similar to the oral microbiome.

The use of antibacterial mouthwashes, for instance, appear to be more harmful than beneficial. Mouthwashes kill microbes indiscriminately, both beneficial and harmful. Among the effects: reduction or elimination of beneficial species has been documented to reduce microbial production of nitrites, the precursor to vasodilation (artery-relaxing) nitric oxide, from dietary nitrates, leading to higher blood pressure. Dietary carbohydrates, increased in the modern diet due to dietary guidelines and the proliferation of processed foods, alter the oral microbiome towards species, such as Streptococcus mutans, that convert sugars to acids such as lactic acid that are damaging to dental structures.

As you might guess, the oral microbiome “seeds” the esophagus and stomach with a flood of oral microbes via swallowed saliva. If stomach acid is intact, this provides an effective barrier to passage of oral microbes into the duodenum and more distal small intestine, since many oral species are not acid-tolerant. Loss of stomach acid, as occurs with stomach acid-blocking drugs, autoimmune gastritis that kills acid-producing parietal cells, or colonization with H. pylori, therefore removes the acid barrier to the descent of oral microbes into the upper GI tract (as well as barrier to the ascent of fecal microbes up from the distal small intestine and colon). Without stomach acid, the oral microbiome is therefore a major determinant of the composition of the upper GI microbiome.

Surprisingly, the oral microbiome is also a major determinant of the microbiome of amniotic fluid in a pregnant female, much more than the vaginal microbiome. It means that the composition of the oral microbiome, especially in women with poor oral hygiene, gingivitis, and periodontitis, can play roles in causing miscarriage, premature delivery, risk for necrotizing enterocolitis (a dangerous condition for newborns), and neonatal sepsis. The oral microbiome is a determinant of microbial changes in other organs including arteries, lungs, even brain.

Among the phenomena that have been documented to result from species originating from the oral microbiome are:

  • Fusobacterium nucleatum—Evidence suggests that this microbe, increased in people with gingivitis and periodontitis, is a major cause of colon cancer. Interestingly, it does not reach the colon via swallowing but through the bloodstream, an example of translocation, the ability of microbes to escape their original home (e.g., mouth, colon) and gain access to another organ. Fusobacterium has also been recovered in the amniotic fluid from women who experienced premature labor.
  • Porphyromonas gingivalis—Suspected to be a major factor in Alzheimer’s dementia, another example of translocation (as illustrated in the graphic above). It has also been associated with populating amniotic fluid in women experiencing premature labor.
  • Treponema denticola—A microbe that proliferates in people with periodontitis and root canals, this microbe has also been recovered from brains of people with dementia and is believed to “conspire” with Porphyromonas in generating the hallmark pathologies of Alzheimer’s dementia.

Changes in oral microbiome composition have also been documented in people with pancreatic cancer, type 2 diabetes, Crohn’s disease, rheumatoid arthritis, coronary disease and other conditions, but it is not yet clear whether they are cause or effect. Type 2 diabetes is an especially interesting situation: If dietary sugars cause dental disease, how about high salivary sugars that accompany diabetes, especially if blood sugar is poorly controlled? This explains why diabetes has been associated with substantial acceleration of dental decay. Diabetics especially struggle with periodontitis and tooth loss and are thereby prone to health issues resulting from a disrupted oral microbiome such as colon cancer and dementia.

In other words, this is not just about cosmetic appearance, whiter teeth, or hygiene. The oral cavity holds implications for body-wide health. If you are wheat/grain-free (thereby avoiding the amylopectin A of grains) and avoid sugars, you have take a big first step in taking back control over your oral microbiome and health.

In my DrDavisInfiniteHealth.com Inner Circle, we have been having wonderfully enlightening conversations with integrative/functional dentist, Dr. Debbie Ozment from Oklahoma. She has been sharing her wealth of knowledge on the practical aspects of dealing with the oral pathogens listed above. Dr. Ozment believes that one of the most important practices you can follow for better dental health is to disrupt tooth biofilms created by microbes with use of dental picks such as GUM Soft Picks, as well as flossing. If you’d like to hear more from Dr. Ozment, I also interviewed her for my Defiant Health podcast that can be found here or through your favorite podcast direction (Apple Podcasts, iTunes, Spotify, Google Podcasts, etc.). While conventional approaches to issues such as gingivitis and periodontitis typically involve dental procedures, fluoride, and antibiotics, I believe that we are rapidly approaching a time in which restoration of a healthy oral microbiome may prove to be a superior solution. The details of such an approach are only beginning to clarify, so stay tuned. This can be a very important conversation for both dental and overall health.

*Ryder MI. Porphyromonas gingivalis and Alzheimer disease: Recent findings and potential therapies. J Periodontol. 2020 Oct;91 Suppl 1(Suppl 1):S45-S49.