Chapter 3: The Ecosystem in Your Mouth¶

In which we meet the 700 species that live in your mouth, discover that most of them are trying to help, and learn why the "kill them all" approach might be making things worse

You are not alone.

I don't mean that philosophically. I mean it literally, biologically, at this very moment. Inside your mouth, right now, as you read these words, there are somewhere between 10 and 50 billion bacteria.¹ They outnumber the cells in your entire body.

This might disturb you. We've spent over a century teaching people that bacteria are the enemy—tiny invisible threats to be eliminated with antiseptics and antibiotics and vigilant hygiene. The very word "germs" carries a connotation of danger.

But here's what I've learned in my long observation of your species: the relationship between humans and their oral bacteria is far more complicated than warfare. It's more like... gardening. Or diplomacy. Or ecosystem management. The bacteria aren't invaders; they're residents. They've been there since you were born, and they'll be there until you die. The question isn't how to eliminate them—you can't—but how to maintain a community that supports your health rather than undermines it.

This is the ecological view, and understanding it changes everything.

The Oral Microbiome¶

The community of microorganisms living in your mouth has a name: the oral microbiome. And it's astonishingly complex.

Researchers have identified over 700 distinct species of bacteria that can live in human mouths,² along with various fungi, viruses, and other microorganisms. No single person hosts all 700—a typical healthy mouth contains 100-200 species at any given time. But that's still a staggering diversity.

These organisms don't live in isolation. They form complex communities, with different species occupying different niches: the tongue surface, the cheek mucosa, the gum crevices, the tooth surfaces. Each location has its own characteristic community composition, optimized for local conditions.

On tooth surfaces specifically, bacteria don't just sit there as individual cells. They organize into biofilms—structured communities embedded in a self-produced matrix of polysaccharides, proteins, and DNA. This is what we call dental plaque.

Biofilms are remarkable structures. Within them, bacteria communicate through chemical signals, share resources, exchange genetic material, and exhibit collective behaviors that no single cell could achieve. A biofilm is more like a multicellular organism than a collection of independent bacteria.

This has important implications for treatment. Bacteria in biofilms are far more resistant to antimicrobial agents than the same bacteria floating freely in solution—sometimes 100 to 1,000 times more resistant.³ The matrix protects them physically, concentrations of antimicrobials drop as they diffuse into the biofilm, and bacteria deep in the structure exist in low-oxygen, low-nutrient states that make them less susceptible to agents targeting active metabolism.

This is one reason why antiseptic mouthwashes often fail to produce the lasting results their marketing suggests. They may kill bacteria in bulk saliva and on biofilm surfaces, but the community regenerates from survivors deeper in the structure. The fundamental ecology remains unchanged.

The Good, the Bad, and the Context-Dependent¶

For most of the 20^th century, dental research focused on identifying "pathogenic" bacteria—the bad actors responsible for cavities and gum disease—with the assumption that eliminating them would solve the problem.

The arch-villain was Streptococcus mutans,⁴ identified in the 1920s and confirmed through decades of research as a primary cause of dental caries. S. mutans can metabolize sugars rapidly, producing lactic acid as a byproduct. It can survive and even thrive in acidic conditions that kill or inhibit other bacteria. And it produces sticky glucans that help it adhere to tooth surfaces and form the biofilm matrix.

If ever there was a bacterium designed to cause cavities, S. mutans is it.

But here's where the story gets more interesting. Not everyone who carries S. mutans gets cavities. And eliminating S. mutans—even if it were possible—doesn't guarantee cavity-free teeth. Something else is going on.

In the 1990s, microbiologist Philip Marsh proposed what he called the ecological plaque hypothesis.⁵ His argument was elegant:

Caries isn't caused by specific pathogenic bacteria. It's caused by an ecological shift in the entire bacterial community, driven by environmental change—specifically, by frequent exposure to sugars and the resulting acid stress.

Here's how it works:

In a healthy mouth (low sugar intake, reasonable pH):

The bacterial community is diverse
Many species produce alkali as part of their metabolism, neutralizing acids
S. mutans is present but represents only a small fraction of the community
Acid-producing species don't dominate
Net pH stays above critical threshold most of the time
Remineralization exceeds demineralization

Under sugar stress (frequent sugar exposure):

Each sugar episode produces acid, dropping pH
Acid-sensitive species decline (they can't tolerate the low pH environment)
Acid-tolerant species like S. mutans gain competitive advantage
The community composition shifts toward acidogenic (acid-producing) and aciduric (acid-tolerant) species
These species produce more acid, further lowering pH
A self-reinforcing cycle develops
Demineralization begins to exceed remineralization

The critical insight is that the environment selects for the community composition. You don't get cavities because you "caught" S. mutans from someone. You create the conditions under which S. mutans can dominate by repeatedly exposing your mouth to sugar and acid.

This ecological view changes how we think about prevention. Killing bacteria is treating a symptom. Changing the environment is treating the cause.

The Helpful Residents¶

Once you start looking at the oral microbiome as an ecosystem rather than an enemy camp, you start noticing the beneficial players.

Streptococcus sanguinis is sometimes called a "pioneer colonizer"—one of the first species to establish itself on a clean tooth surface. It produces hydrogen peroxide, which inhibits S. mutans. It also possesses the arginine deiminase system (ADS),⁶ which metabolizes arginine (an amino acid common in saliva and foods) to produce ammonia:

Arginine → Ornithine + NH₃ + CO₂ + ATP

That ammonia directly neutralizes acid, raising local pH. S. sanguinis essentially manufactures its own antacid while living in your mouth.

Streptococcus gordonii has similar capabilities—arginine metabolism, alkali production, and competitive activity against cariogenic species.

Streptococcus salivarius prefers to colonize the tongue rather than teeth. Some strains produce bacteriocins—natural antibiotics that target competing bacteria, including some pathogens. S. salivarius strains K12 and M18 are now used in commercial oral probiotics.

Veillonella species can't metabolize sugars directly, but they can metabolize lactate—the very acid that S. mutans produces. They convert lactic acid to weaker acids like propionic and acetic acid, effectively detoxifying the main weapon of cariogenic bacteria.

Certain Actinomyces species are important early colonizers that help establish healthy biofilm architecture.

When you use an antiseptic mouthwash that kills 99.9% of bacteria indiscriminately, you're not just killing S. mutans. You're killing S. sanguinis and S. gordonii and Veillonella—the species that were helping maintain ecological balance. You're creating a blank slate that may be recolonized by whatever community can establish itself fastest, which may or may not be healthier than what was there before.

The Nitrate-Reducing Revelation¶

Here's something that might surprise you: some of your oral bacteria are performing a service that affects not just your mouth but your entire cardiovascular system.

Certain oral bacteria—including some Veillonella, Actinomyces, and Rothia species—can reduce dietary nitrate to nitrite:

NO₃⁻ → NO₂⁻

This might seem like irrelevant biochemistry, but it's not. The nitrite these bacteria produce is swallowed, enters your stomach, and is converted to nitric oxide—a molecule that relaxes blood vessels and lowers blood pressure.

This is called the entero-salivary nitrate-nitrite-nitric oxide pathway, and it turns out to be a significant contributor to cardiovascular health. Dietary nitrate (found in leafy greens, beets, and other vegetables) has blood pressure-lowering effects, and those effects depend on oral bacteria performing the first step of the conversion.

Here's where it gets concerning: antiseptic mouthwashes kill nitrate-reducing bacteria.

A 2020 study in Free Radical Biology and Medicine found that twice-daily use of antiseptic mouthwash was associated with increased systolic blood pressure compared to controls.⁷ Other studies have found that antiseptic mouthwash use can blunt the blood pressure-lowering effects of exercise (which also works partly through nitric oxide).

Let me be direct: regular use of antiseptic mouthwash may be raising your blood pressure.

This is a case where the "kill all germs" approach has consequences that extend far beyond the mouth. The oral microbiome isn't just relevant to oral health—it's a functioning organ system with metabolic activities that affect your whole body.

Dysbiosis: When the Garden Goes Wrong¶

Dysbiosis is the term for a microbial community that has shifted away from a healthy configuration. In the mouth, this can take several forms.

Cariogenic dysbiosis involves the shift toward acid-producing, acid-tolerant species we discussed above. Environmental drivers include frequent sugar exposure, low saliva flow, poor buffering capacity.

Periodontal dysbiosis involves a shift toward different organisms—anaerobic species like Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola that thrive in the oxygen-poor environment of deep gum pockets. These organisms trigger inflammatory responses that destroy the tissues supporting teeth.

Porphyromonas gingivalis is particularly interesting because it's been described as a "keystone pathogen"⁸—an organism that can reshape the entire community at concentrations too low to cause direct damage. It manipulates host immune responses in ways that create favorable conditions for other periodontal pathogens.

The ecological principle remains the same: these organisms don't cause disease by overwhelming healthy defenses. They cause disease when conditions shift in ways that allow them to gain dominance.

Restoring Ecological Balance¶

If dysbiosis is the problem, what's the solution?

The first answer is environmental management—changing the conditions that drove the shift in the first place:

Reduce sugar frequency to decrease acid stress
Support saliva flow and buffering to maintain pH
Allow adequate time for remineralization between acid challenges

The second answer is competitive dynamics—supporting the beneficial species that naturally keep pathogens in check:

Arginine supplementation feeds the alkali-producing bacteria
Xylitol selectively disadvantages S. mutans (it can't metabolize xylitol effectively, wasting energy trying)
Probiotics introduce beneficial strains directly

The third answer, emerging from research, is targeted ecological intervention—more sophisticated approaches that manipulate community composition without wholesale destruction:

Probiotic strains that produce bacteriocins against specific pathogens
Prebiotic substances that selectively feed beneficial species
Eventually, perhaps, genetically modified organisms designed to colonize and protect

We'll explore these approaches in detail in later chapters. For now, the key understanding is that the goal isn't sterilization. You can't sterilize your mouth and wouldn't want to. The goal is to maintain—or restore—an ecological balance that supports oral health.

What This Means for You¶

Here are the practical implications of the ecological view:

Stop trying to kill everything. That approach is based on outdated science and may be causing harm. Reserve antiseptic products for specific therapeutic situations (active periodontal disease, post-surgical care) rather than daily maintenance.

Feed the good bacteria. Diets rich in arginine (found in meat, fish, dairy, nuts) support alkali-producing species. Nitrate-rich vegetables (leafy greens, beets) feed the cardiovascular-protective nitrate reducers.

Starve the bad bacteria. Reduce sugar frequency rather than obsessing over total amount. Consider xylitol products that specifically disadvantage S. mutans.

Create favorable conditions. Maintain good saliva flow, support pH buffering, give your mouth time to recover between acid challenges.

Consider probiotics. The evidence is still developing, but oral probiotics (especially S. salivarius strains) show promise for shifting community composition in beneficial directions.

Your mouth is a garden. You're the gardener. The question isn't whether bacteria will grow—they will. The question is whether you'll cultivate the plants you want or let weeds take over.

Speaking of ecological niches, there's one major bacterial habitat in your mouth that we haven't discussed yet: the tongue. Let's go there next.

Dewhirst, F. E., et al. (2010). The human oral microbiome. Journal of Bacteriology, 192(19), 5002-5017. The oral cavity harbors approximately 10 billion bacteria. ↩
Human Oral Microbiome Database (HOMD) — A curated database documenting over 770 bacterial species found in the human oral cavity. ↩
Stewart, P. S., & Costerton, J. W. (2001). Antibiotic resistance of bacteria in biofilms. The Lancet, 358(9276), 135-138. Biofilm bacteria can be 100-1000 times more resistant to antibiotics than planktonic cells. ↩
Streptococcus mutans — Wikipedia. First isolated from carious lesions by J. Kilian Clarke in 1924. ↩
Marsh, P. D. (1994). Microbial ecology of dental plaque and its significance in health and disease. Advances in Dental Research, 8(2), 263-271. The ecological plaque hypothesis proposes that environmental changes drive shifts in microbial community composition. ↩
Burne, R. A., & Marquis, R. E. (2000). Alkali production by oral bacteria and protection against dental caries. FEMS Microbiology Letters, 193(1), 1-6. The arginine deiminase system generates ammonia that neutralizes acids in dental plaque. ↩
Bondonno, C. P., et al. (2015). Antibacterial mouthwash blunts oral nitrate reduction and increases blood pressure in treated hypertensive men and women. American Journal of Hypertension, 28(5), 572-575. ↩
Hajishengallis, G., et al. (2012). Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement. Cell Host & Microbe, 10(5), 497-506. P. gingivalis acts as a keystone pathogen that can dysregulate host immunity. ↩