The oral microbiome and periodontitis: what we know, what we are still looking for

What is meant by the oral microbiome?

The oral microbiome is the whole population of micro-organisms, mostly bacteria but also fungi and viruses, that inhabit the mouth: teeth, tongue, cheeks, saliva and the crevice between tooth and gum. More than 700 bacterial species have been identified there, making it the body's second most diverse microbial community after the gut ^[4]. This population is not an enemy to be wiped out: it helps defend against passing germs and trains local immunity.

Below the gumline, bacteria organise themselves into a biofilm, a structured, sticky layer known as dental plaque, in which they cooperate, exchange nutrients and shelter one another. As long as this community stays diverse and balanced, the gum tolerates it. When its composition tips towards species that thrive on inflammation, the result is called dysbiosis: it is this shift, not the mere presence of bacteria, that opens the door to periodontitis ^[4].

Is periodontitis caused by 'one' germ?

No. In 1998, Socransky's team analysed more than 13,000 samples of subgingival plaque from 185 people and showed that bacteria cluster into stable 'complexes'. One of them, the red complex (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola), is the one most clearly associated with deeper pockets and bleeding gums ^[2]. The association is robust; on its own, it does not say who sets off what.

In 2012, Hajishengallis and Lamont proposed going 'beyond the red complex' with the model of polymicrobial synergy and dysbiosis. Here the disease begins with a disrupted community in which certain species, called keystone pathogens, manage, even in very small numbers, to evade immune surveillance and raise the virulence of the whole biofilm; P. gingivalis is the most studied example ^[1]. The right picture is not a single culprit but an ecosystem that has changed regime.

Why the patient's response matters as much as the bacteria

It is not the bacteria that destroy bone: it is the inflammation the body mounts to contain them, once it can no longer resolve. The dysbiotic community sustains an immune response that fails to switch off; that response in turn feeds the species that thrive on the by-products of inflammation. A vicious circle sets in ^[1].

Hence the importance of the individual: two people exposed to the same biofilm do not develop the same disease. Smoking, poorly controlled diabetes, genetic traits and nutritional status modulate the intensity of the inflammatory response and the tissues' capacity to repair. The European guideline for treating periodontitis (EFP, 2020) draws the consequence: stopping smoking and controlling diabetes are part of the treatment, alongside cleaning the roots ^[3]. That is the whole point of a medical, biological and preventive periodontology: treating the biofilm, understanding the host that carries it (see periodontitis and general health).

Mouth and gut: what is research looking for?

We swallow billions of oral bacteria every day; a healthy gut resists them. Recent work asks what happens when both linings are inflamed. In 2020, a study in Cell showed, in mice, that periodontitis drives the expansion of certain oral bacteria (Klebsiella, Enterobacter) able to colonise an already inflamed gut and worsen colitis there, partly through immune cells 'trained' in the mouth that then migrate to the colon ^[6].

The result opens avenues. It remains experimental, obtained in animals. In humans, associations between periodontitis and inflammatory bowel disease have been observed; nothing, to date, shows that periodontitis causes digestive disease, or that treating it prevents one. Dr Hazout follows this work with interest, and presents it for what it is: a hypothesis under exploration.

A bacterial sample: what is it for?

A subgingival bacterial sample collects the contents of a periodontal pocket with a sterile paper point, to identify and count certain species. At the practice it is part of the first treatment session, together with a blood sample: this is Dr Hazout's protocol for understanding each patient's background. It does not replace diagnosis, which rests on the clinical examination and radiographs, and the 2020 European guideline does not make it a mandatory step of treatment ^[3].

It does, however, inform follow-up. The same guideline advises against routine adjunctive antibiotics alongside root cleaning, because of side effects and bacterial resistance, while leaving the door open for specific groups of patients, for instance severe generalised periodontitis in a young adult ^[3]. The benefit of these antibiotics exists on average but is modest: less than half a millimetre of additional pocket reduction at six and twelve months, with more side effects ^[5]. Knowing which bacteria are present then helps decide whether a prescription is justified, and which one.

• What it offers: objective evidence of a heavy load of certain species, documentation of a severe or treatment-resistant form, help in choosing an antibiotic when one is considered, comparison of the flora before and after treatment ^{[3] [5]}.
• What it does not do: make the diagnosis on its own, predict progression on its own, or replace mechanical root cleaning.
• Its place and cost are discussed on the blood tests and supplements page.

Probiotics: a complement to treatment

If the disease is an imbalance, it makes sense to try to favour the bacteria associated with health over those associated with disease: that is the principle of probiotics, most often strains of Lactobacillus reuteri. Used alongside non-surgical treatment, they have shown clinical benefits in trials, limited on average ^[7]; results vary with strains and protocols ^[8]. The 2020 European guideline does not include them among routine steps ^[3].

What really changes the microbiome

What durably alters the subgingival community is well known, and less glamorous than a capsule. First, mechanical disruption of the biofilm: root surface debridement, cleaning the roots below the gumline, removes biofilm and calculus and lets a community closer to that of health settle back in. Then daily oral hygiene, which stops the biofilm from reorganising itself in depth. Then stopping smoking and controlling diabetes, recommended by the EFP in the treatment of any periodontitis, because they change both the inflammatory background and the ecology of the biofilm ^[3].

Finally, periodontal maintenance, which repeats these steps at a suitable interval. In this frame, the microbiome is not an adversary to be eliminated but an ecosystem to be brought back, and then kept, in a state compatible with healthy gums. That is the approach Dr Victor Hazout offers at the practice in Levallois-Perret: treat, understand, prevent.

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