Diet is currently considered in the context of nutrient absorption by an animal’s lower gut. The upper gut, home to the second most abundant microbial population in the mammalian body, is also fully capable of mechanical and enzymatic digestion and nutrient absorption.

Due to the rapid transit time of food through the mouth, however, oral microbes must manufacture enzymes to process the food quickly and effectively. Then they must wait for broken-down nutrients to recirculate in saliva and crevicular fluid, as food is processed in the lower gut and absorbed into the host’s bloodstream.1

The billions of microbes attached to every single square millimeter of oral tissue, particularly on the tongue and subgingival spaces, are continuously bathed with waxing and waning levels of nutrients that they require for growth. However, this can be harmful to the animal host.


Omnivores, such as humans, canines, and swine, are prone to gingivitis and gum disease at rates of 47% to 71%, 70%, and 50%, respectively.2-4 It is no surprise that dental disease is so prevalent in these species, as the omnivore diet is rich in carbohydrate and microbially-metabolized sugars, leading to inorganic acid, mineral acid, organic acid, and other proinflammatory waste product production.5

Surprisingly, we also see non-omnivores with dental disease. Indeed, gingivitis, gum disease, and abscesses are also found in over 50% of middle-aged large cats, equines, and bovines, all with very divergent diets and gut anatomies.6


Genetic, behavioral, and many others factors likely drive dental disease in animals. A very established driver is the ingestion of dietary carbohydrates. Although acceptable for the lower gut, they are not ideal for the oral cavity. Hidden carbohydrates exist as bulking agents found in kibble and many feeds; these carbohydrates are quickly realized and metabolized by oral microbes.

Why call out carbohydrates? The inflammation-causing oral microbes can quickly utilize carbohydrates, convert them to stronger acids and organic acids, which lower the tissue pH and elicit an immune response; this can then weaken the barrier function of the animal’s mucosal epithelia.7 The most relevant repercussion is that inorganic and organic acids can favor the growth of acid-tolerant dental pathogens.8-10 The problem is that the host animals do not have such defense mechanisms.

Persistent activation can manifest as periodontal disease, stomatitis, or abscess formation. More troubling, the consequences are not limited to the mouth. Inflammation and subgingival overgrowth of microbes can alter reproduction, shorten lifespan, and/or lead to downstream systemic conditions (cardiovascular, GI, liver, kidney, joint, etc). A depiction of staged disease processes is presented in the adapted image shown below.6

We have recently initiated preclinical work on equine oral microbial biofilms. Interestingly, we are finding correlations similar to trends observed in humans, canines and felines:

  1. The older the animal, the more dysbiosis is observed.
  2. The more feed given to the animal, instead of naturally foraged foods, the higher the oral pathogen count.
  3. Both factors seem to strongly link to the presence or patient history of dental disease in that animal.






6Journal of Periodontology, Volume: 89, Issue: S1, Pages: S17-S2.





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Emily Stein, Ph.D. founded Primal Health (TEEF for Life) in 2017 to focus on improving the dental health of both humans and animals by producing oral microbiome modulation products. She has spent 12 years developing Selective Microbial Metabolism Regulation Technology (SMMRT™) at Primal Therapies, Inc., which is focused on using metabolic influencers to re-engineer disease-causing bacterial biofilms into those that are health-promoting, to decrease inflammation and to improve outcomes. Prior to that, she spent 7 years as a research fellow at Stanford University in Rheumatology and Immunology focused on the neuro-endocrine-immune axis in autoimmune and chronic inflammatory diseases. She holds a Ph.D. in Microbiology from the University of California at Berkeley where she studied inter- and intra-cellular signaling pathways involved in stress response and community development in bacteria and received her B.S. in Microbiology and Immunology at the University of Iowa where she studied the interaction between M. tuberculosis and innate immune cells.


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