Healthy Mouth?

Every dentist knows this patient.

Great home care. Minimal bleeding. Stable radiographs. Nothing particularly alarming on the periodontal chart. Maybe they’re even the patient you expect to have the best results.

Then you run a salivary test and find elevated Porphyromonas gingivalis, Fusobacterium nucleatum, or several periodontal pathogens at levels that simply don’t match the mouth you just examined.

Now what?

Is the patient healthy, or is the saliva test telling us something we’re not seeing yet? Maybe the more interesting possibility is that both things can be true.

This is where salivary diagnostics get really interesting to me. Because the more we learn about the oral microbiome, the harder it becomes to define oral health by what we can see alone.

We’re Not Measuring the Same Thing

Let’s start here: the periodontal exam isn’t going anywhere.

Probing depths, bleeding on probing, clinical attachment loss, recession, mobility, plaque, calculus and radiographic bone levels remain fundamental to periodontal diagnosis. A saliva test doesn’t replace any of that.

But it can give us a different piece of information.

Periodontitis isn’t simply a collection of deep pockets. Current models describe it as a dysbiotic, host-mediated inflammatory disease. The microbial community matters, but so does the immune response of the person hosting it.¹˒²

That distinction becomes especially important when we start testing bacteria.

Finding a periodontal-associated organism does not automatically mean we’ve found active periodontal disease. Organisms associated with periodontitis can also be detected in clinically healthy individuals. What appears to matter is not simply who is there, but microbial abundance, community structure, the environment surrounding that community, and the host response.¹˒³

So when a saliva test comes back with an unexpected result, rather than simply asking why a healthy patient has a particular bacterium, I think the more useful question is why that organism is present at that level, in that particular patient, at that particular time.

That’s a very different clinical conversation.

The Periodontal Chart Is a Snapshot. The Microbiome Is a Movie.

This is how I like to think about it.

Our periodontal examination gives us a snapshot. It tells us what the tissues look like today and, through attachment levels and radiographs, gives us evidence of what has happened over time.

The microbiome is much more dynamic. It can shift with changes in plaque ecology, salivary flow, smoking, diet, medications, hormones, systemic health, oral hygiene and periodontal treatment.

That means a patient can look clinically stable while still carrying a microbial profile we weren’t expecting.

Does that mean disease is coming? No. That’s where we need to be careful.

Microbial risk is not destiny. The oral microbiome is not simply divided into “good bugs” and “bad bugs,” and the presence of a pathogen should never be interpreted in isolation.

An unexpected result may, however, give us another reason to look more closely, follow a patient longitudinally, or ask questions we wouldn’t have asked based on the clinical examination alone.

To me, that’s where the value starts.

The Bacteria Matter. But So Does the Person Hosting Them.

Two people can carry similar periodontal-associated bacteria and have very different clinical outcomes. One may develop significant inflammation and progressive tissue destruction while the other remains clinically stable.

The difference isn’t necessarily the bacterium. The host matters too.

Host immune and inflammatory responses help determine how microbial challenge translates, or doesn’t translate, into disease. Smoking, diabetes and glycemic control, genetics, medications, immune function and other environmental and systemic factors can modify that response.²

This is also why the future of salivary diagnostics is so exciting. Much like medical testing, these technologies will continue to evolve as research advances and our understanding deepens. The tests we use today may look very different from the tests of tomorrow, expanding beyond what we currently measure to reveal new insights into both microbial activity and the body’s own biological responses.

Other studies have explored combinations of microbial and inflammatory biomarkers rather than relying on a single marker.

We’re not at the point where a saliva tube replaces a periodontal diagnosis, and I don’t think that’s the goal. What we’re moving toward is much more interesting: combining microbiology, host response, and clinical findings to create a richer picture of the individual patient.

But Where Did the Bacteria Come From?

This is the part I think deserves a much bigger conversation.

We spend a lot of time talking to patients about their behaviors. We ask about brushing, flossing, smoking, blood sugar, medical history, and their last cleaning. Those are all important questions.

But there’s another variable that rarely makes it onto the periodontal chart: who are they sharing saliva with?

Your patient doesn’t live in a microbial bubble.

Partners kiss. Parents kiss their children. Families share food, drinks, and utensils. Caregivers sometimes clean a pacifier with their own mouth. People live together for years, sometimes decades.

And oral bacteria can be shared.

This is called horizontal transmission, and the concept has been documented for decades. Early molecular studies found indistinguishable strains of P. gingivalis in spouses, supporting person-to-person transmission of periodontal-associated organisms.⁵˒⁶ Later studies continued to identify shared strains among couples and family members, although the frequency of transmission varies among populations and organisms.⁷˒⁸

A systematic review and meta-analysis examining P. gingivalis among cohabiting family members found that shared detection was moderately frequent. Importantly, estimates changed substantially depending on whether culture, PCR, or strain-level genotyping was used.⁹

More recently, large-scale metagenomic research has given us an even more fascinating look at microbial sharing. A 2023 Nature study analyzing more than 9,700 human microbiomes found extensive bacterial strain sharing among individuals. Oral microbiome transmission occurred largely horizontally, and strain sharing increased with the duration of cohabitation. The median oral strain-sharing rate among cohabiting individuals was approximately 32%.¹⁰

In other words, the people we live with may help shape our microbial ecosystem.

Before everyone goes home and starts testing their spouse, though, there is an important distinction: transmission is not disease.

Sharing a periodontal-associated bacterium does not mean someone will develop periodontitis. The organism still has to exist within an incredibly complex microbial community. The environment has to support it, and the host response, behaviors, genetics and salivary environment may all influence what happens next.

The same microbial exposure can therefore have very different biological consequences in two different people.

But think about the patient who is doing everything we ask. They floss, brush, clean interproximally, come in for maintenance, and genuinely change their habits, yet their microbial profile continues to surprise us.

Could repeated microbial exposure from a partner or household member be one piece of that puzzle?

I think it’s a question worth asking.

Maybe oral health isn’t always an individual project. Maybe sometimes it’s a family plan.

I Was the Patient Who Didn’t Make Sense

This subject became personal for me long before it became something I wrote about.

Following my own pregnancy loss, I eventually decided to test my saliva. I expected the result to be pretty boring.

I had excellent home care. I didn’t have the bleeding, calculus, or obvious clinical picture that I would have associated with a concerning periodontal microbial profile.

Then my results came back.

Fusobacterium nucleatum was above the laboratory reporting reference lines.

That result stopped me, but not because it gave me an answer about my pregnancy loss. It didn’t. The presence of F. nucleatum cannot establish causation for an obstetric complication, and I think we have to be extremely responsible about saying that, especially when discussing pregnancy loss.

What the result gave me was curiosity.

I started thinking differently about why an organism might be present at an unexpected level, how long it may have been there, whether the microbial environment had changed over time and how my own host response influenced what that organism actually meant for me. I also started thinking about microbial exposure from the people closest to us and, more broadly, what could be happening biologically before we can see it clinically.

I didn’t suddenly have answers. I had better questions, and those questions changed the trajectory of my career.

An Elevated Result Isn’t a Diagnosis. It’s Information.

I think this distinction becomes increasingly important as salivary testing becomes more accessible.

We can’t take every elevated organism and turn it into disease. That’s not precision medicine. That’s overinterpretation.

A microbial result has to live inside the patient’s entire clinical picture: probing depths, bleeding, attachment levels, radiographic findings, previous periodontal history, systemic health, medications, salivary flow, hormonal influences, smoking or vaping, implants, and other potential microbial niches.

And increasingly, I think longitudinal information matters too. A single result is a snapshot of biology at one point in time. A persistent pattern may tell us something different.

Perhaps we should also begin considering what oral health looks like within the household, not because we’re diagnosing a spouse from our patient’s saliva, but because once we understand that the oral microbiome is dynamic and partially shaped by our environment, the person sitting in our chair becomes part of a much larger biological story.

Maybe “Healthy” Needs More Context

Dentistry has become incredibly good at documenting what has already happened. We measure the pocket, identify attachment loss, see bone loss, and restore the cavity.

Precision medicine pushes healthcare toward a different question: what can we understand about someone’s biology before irreversible damage occurs?

I think saliva gives dentistry an extraordinary opportunity to participate in that conversation.

Not because saliva has all the answers. It doesn’t. And not because bacterial testing should replace the clinical examination. It shouldn’t.

But microbial DNA, host inflammatory markers, and other salivary biomarkers are giving us another layer of information that didn’t previously exist chairside.

The future probably isn’t one bacterium, one inflammatory marker, or one test. It’s the integration of clinical findings, microbial ecology, host response, medical history, behavior and environment, and perhaps even the microbial communities of the people with whom we share our lives.

So when the clinically healthy patient gets an unexpected saliva result, maybe we don’t have to decide which one is “right.”

Maybe both are telling us something. One tells us what we can see. The other gives us a glimpse of biology we couldn’t see before.

And sometimes the most valuable thing a diagnostic test can do isn’t give us an answer.

It makes us curious enough to ask a better question.

 References

  1. Hajishengallis G, Lamont RJ. Polymicrobial communities in periodontal disease: their quasi-organismal nature and dialogue with the host. Periodontol 2000. 2021;86(1):210-230.
  2. Hajishengallis G, Chavakis T, Lambris JD. Current understanding of periodontal disease pathogenesis and targets for host-modulation therapy. Periodontol 2000. 2020;84(1):14-34.
  3. Abusleme L, Dupuy AK, Dutzan N, et al. The subgingival microbiome in health and periodontitis and its relationship with community biomass and inflammation. ISME J. 2013;7(5):1016-1025. doi:10.1038/ismej.2012.174.
  4. Domokos Z, Simon F, Uhrin E, et al. Evaluating salivary MMP-8 as a biomarker for periodontal diseases: a systematic review and meta-analysis. Heliyon. 2024;10(22):e40402. doi:10.1016/j.heliyon.2024.e40402.
  5. van Steenbergen TJM, Petit MDA, Scholte LHM, van der Velden U, de Graaff J. Transmission of Porphyromonas gingivalis between spouses. J Clin Periodontol. 1993;20(5):340-345. doi:10.1111/j.1600-051X.1993.tb00370.x.
  6. Saarela M, von Troil-Lindén B, Torkko H, Stucki AM, Alaluusua S, Jousimies-Somer H, Asikainen S. Transmission of oral bacterial species between spouses. Oral Microbiol Immunol. 1993;8(6):349-354. doi:10.1111/j.1399-302X.1993.tb00610.x.
  7. Asano H, Ishihara K, Nakagawa T, Yamada S, Okuda K. Relationship between transmission of Porphyromonas gingivalis and fimA type in spouses. J Periodontol. 2003;74(9):1355-1360. doi:10.1902/jop.2003.74.9.1355.
  8. Van Winkelhoff AJ, Boutaga K. Transmission of periodontal bacteria and models of infection. J Clin Periodontol. 2005;32(Suppl 6):16-27. doi:10.1111/j.1600-051X.2005.00805.x.
  9. Bennani M, Rangé H, Meuric V, Mora F, Bouchard P, Carra MC. Shared detection of Porphyromonas gingivalis in cohabiting family members: a systematic review and meta-analysis. J Oral Microbiol. 2020;12(1):1687398. doi:10.1080/20002297.2019.1687398.
  10. Valles-Colomer M, Blanco-Míguez A, Manghi P, et al. The person-to-person transmission landscape of the gut and oral microbiomes. Nature. 2023;614:125-135. doi:10.1038/s41586-022-05620-1.

Dr. Neusha Najafi
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