The forgotten organ: Why the oral microbiome belongs in every physician's toolkit

Abstract

The oral cavity is the most densely colonised microbial niche in the human body after the gut – over 700 species and an estimated two billion bacteria (Deo and Deshmukh, 2019) – yet it remains conspicuously absent from the systemic health conversation. Mounting evidence links oral microbial dysbiosis to more than 50 systemic conditions (Peng et al, 2022), including cardiovascular disease, type 2 diabetes (Preshaw et al, 2026), adverse pregnancy outcomes, rheumatoid arthritis and Alzheimer's. Despite this, dentistry and medicine continue to operate as parallel systems, with oral health excluded from most general health screens, NHS commissioning structures and undergraduate medical curricula. This narrative review analyses current evidence on the oral microbiome and oral-systemic disease, outlines three biological mechanisms by which the oral cavity drives systemic disease, and sets out five practical, author-proposed steps physicians can take to integrate oral health into routine practice. The case for action is no longer scientific – it is structural.

Introduction: a 700-species blind spot

A patient with poorly controlled type 2 diabetes, raised CRP and a family history of cardiovascular disease walks into a GP surgery. Their HbA1c is checked, their lipids profiled, their blood pressure measured. What is almost never asked is whether their gums bleed when they brush their teeth – despite periodontitis being one of the few modifiable risk factors with bidirectional causal links to all three.

The numbers are striking. Patients with periodontal disease are 53% more likely to develop type 2 diabetes and patients with diabetes are 34% more likely to develop periodontal disease.¹ Periodontal treatment reduces HbA1c by approximately 0.5%, comparable to adding a second oral hypoglycaemic.2, 3 If any other modifiable risk factor delivered that effect size, it would be in every chronic disease guideline. Bleeding gums are not. Why?

The separation is structural, not scientific – and not new. Hippocrates, writing in around 490 BC, was reputed to have treated a woman's arthritis by extracting an infected tooth: he understood that dental disease and systemic disease were the same disease. That integration was lost. When the first US School of Medicine opened at the University of Pennsylvania in 1765, dentistry was deliberately excluded from the curriculum, and the division has hardened ever since. The oral cavity has been administratively, financially and educationally excised from the rest of the body. This article aims to summarise current evidence on oral dysbiosis and systemic disease, and proposes practical steps for integrating oral health into routine medical care.

The oral microbiome: what we know

The oral cavity contains the second most diverse microbial community in the human body – over 700 bacterial species across five distinct ecological niches: saliva, supragingival plaque, subgingival plaque, the tongue dorsum and the buccal mucosa.4, 5, 6 Unlike the gut, these niches are spatially accessible and painlessly sampled via saliva testing.⁷

In health, this community is in dynamic equilibrium. In disease, it is not. Periodontitis – affecting an estimated 19% of adults globally in severe forms, and 20–50% in some form⁸ – is now understood not as a simple infection by named pathogens, but as an exaggerated host immune response accompanied by dysbiotic shifts in the entire community, with keystone species such as Porphyromonas gingivalis orchestrating disproportionate downstream effects.⁹ We now also understand that common oral diseases such as periodontal disease reflect a complex and reciprocal interplay between the oral microbiota and the host immune response, rather than infection by named pathogens alone. The historical assumption that a broad-spectrum antimicrobial mouthwash alone could resolve oral disease has since been revised, not least because such products can also suppress components of a health-associated oral microbiota (see below).¹⁰ Similar dysbiotic principles underpin peri-implant disease, and recent systematic reviews have examined the clinical and microbiological impact of adjunctive systemic antibiotics in peri-implantitis and of non-antibiotic approaches, such as chlorhexidine-based debridement, in peri-implant mucositis, informing more judicious antimicrobial use.11, 12 The WHO's 2023 Global Oral Health Action Plan¹³ flagged that prevalence is rising globally despite a 34% increase in periodontal therapy in the US – pointing to a failure of diagnosis and prevention, not just treatment.¹³

A healthy oral microbiome: the case for symbiosis

Dysbiosis is only half of the picture. In health, the oral microbiome performs functions that benefit the host, and disrupting it indiscriminately carries its own risks. Nitrate-reducing bacteria on the tongue dorsum convert dietary nitrate to nitrite, which is subsequently reduced to nitric oxide; this oral-entero-salivary nitrate pathway is a major contributor to systemic nitric oxide bioavailability, supporting endothelial function and blood pressure regulation.¹⁰ Broad-spectrum antimicrobial mouthwashes, particularly those containing chlorhexidine, have been shown to suppress this nitrate-reducing community and to reduce nitric oxide availability and raise blood pressure in short-term studies – an effect that is distinct from, and should not be conflated with, the vascular consequences of periodontal disease itself.¹⁰ This has direct clinical implications: antimicrobial mouthwash should not be recommended reflexively or used long-term without a specific indication, and the aim of oral healthcare should be framed as restoring microbial symbiosis rather than eliminating oral bacteria altogether.

How the oral cavity may drive systemic disease: three mechanisms

Oral microbial dysbiosis is proposed to contribute to systemic disease through three biologically plausible pathways, whose supporting evidence varies in strength.14, 15

Disseminated infection

Harmful bacteria can translocate from inflamed gum tissue directly into the bloodstream and seed distal sites. This is the established mechanism behind infective endocarditis, and the reason patients with certain cardiac conditions require antibiotic prophylaxis before dental procedures. UK guidance on antibiotic prophylaxis for dental procedures recently underwent it’s most significant change in nearly two decades, aligning more closely with international guidance and recommending antibiotic prophylaxis for high-risk patients on the basis of the accumulated evidence. The same principle of judicious, evidence-based antimicrobial use extends to peri-implant disease, where recent systematic reviews have examined the additional benefit of systemic antibiotics alongside mechanical debridement and underline the importance of clear boundaries between periodontal therapy, peri-implant disease management and antibiotic prescribing.11, 12 Oral bacteria are also aspirated into the lungs; improving oral hygiene in older inpatients has been shown in intervention studies to reduce pneumonia-related mortality.16, 17

Low-grade chronic inflammation and systemic inflammatory spillover

Inflamed gums produce a sustained, sub-clinical release of inflammatory mediators such as IL-1β, IL-6, IL-8, TNF-α, PGE2, CRP and LPS which enter systemic circulation and contribute to the chronic inflammatory load that worsens insulin resistance, endothelial dysfunction and metabolic syndrome. The diabetes evidence is the most striking clinical illustration: periodontal treatment reliably reduces HbA1c by 0.3–0.5%, an effect comparable to a second hypoglycaemic agent.2, 18

Disseminated injury

Microbial toxins and pro-inflammatory mediators of oral origin cause direct vascular injury. Periodontal inflammation reduces nitric oxide production and impairs endothelial vasodilation, contributing to atherosclerosis and hypertension. Patients with periodontal disease have a 25% higher risk of cardiovascular disease19, 20 and a 20% higher risk of hypertension.21, 22

If a patient bled at any other point of routine self-care such as when they rubbed their eyes, it would be investigated. The reflex to dismiss bleeding gums as normal is unique to oral health and unique to medicine.

The oral-systemic axis: clinical evidence

The mechanistic picture is reflected in the clinical literature.

Cardiovascular disease. Oral pathogens have been recovered from atherosclerotic plaques in living patients.²³ Periodontal treatment improves endothelial function in randomised trials.²⁴ A 2020 consensus from the World Heart Federation and the European Federation of Periodontology now recommends routine periodontal screening of cardiology patients.²⁵

Type 2 diabetes. The bidirectional relationship is well-characterised. Most recently, a 2026 systematic review and meta-analysis in The Lancet Public Health,²⁶ encompassing 28 longitudinal studies and more than 300,000 participants, demonstrated a bidirectional temporal association between diabetes and periodontitis. Individuals with periodontitis had a 19–26% higher occurrence of incident type 2 diabetes, while diabetes was also associated with subsequent periodontitis. Diabetes UK and the EFP issued joint guidance in 2018 recommending periodontal assessment as part of routine diabetes care.²⁷

Alzheimer's disease. In 2019, Science Advances reported Porphyromonas gingivalis and it’s gingipain virulence factors in the brains of 96% of patients with Alzheimer's. The use of gingipain inhibitors in mice has shown reduced bacterial load of an established Porphyromonas gingivalis brain infection, blocked Aβ_1–42 production, reduced neuroinflammation, and rescued neurons in the hippocampus. Human clinical trials are now underway to see if gingipain inhibitors could be valuable in treating neurodegeneration in Alzheimer’s disease.²⁸

Adverse pregnancy outcomes. Periodontitis is associated with preterm birth, low birth weight and pre-eclampsia, with oral organisms such as Fusobacterium nucleatum recovered from amniotic fluid.²⁹ A study performed in Malawi, a country with the highest rate of preterm births at 17%, found that delivering sugar free chewing gum and oral hygiene advice to 10,000 women, reduce preterm births by 24% compared to those without oral hygiene aids.³⁰

Cancer. Fusobacterium nucleatum and in particular the FnC2 strain, has been implicated in more aggressive colorectal tumour progression and chemoresistance in preclinical and translational studies,³¹ a possible contributing factor, among others, to the rising incidence of colorectal cancer in younger adults; recent work characterising Fusobacterium nucleatum subspecies suggests that distinct subspecies may carry different oncogenic potential, which may help explain the variable strength of this association across studies.³² As for pancreatic cancer, an oral microbiome study of over 122,000 participants found that elevated levels of Porphyromonas gingivalis, Eubacterium nodatum and Parvimonas micra, were associated with a statistically significant, approximately threefold increase in pancreatic cancer risk for every one standard-deviation rise in a composite microbial risk score – an association rather than an established causal mechanism.33, 32

Why we are still failing

If the evidence is this strong, why is integration so weak? Three reasons.

The divide is structural, not scientific. In the UK, NHS dentistry sits outside primary care commissioning. GPs cannot refer into NHS dental care and most undergraduate medical curricula contain fewer than two hours on oral health across five years.³⁴ When professional and commissioning structures do not support collaboration between medicine and dentistry, closer integration becomes structurally difficult to achieve.

Prevention is undervalued where it is most valuable. Oral diseases remain the most prevalent non-communicable diseases globally, affecting 3.5 billion people, with steep socioeconomic inequalities. The Lancet's 2019 series called this ʻa public health failure of staggering proportions’³⁵ – and very little has changed since. In the UK, most patients follow the philosophy that they will only visit the doctor when or if they are sick whereas most patients will see their dentist annually for a regular check up whether or not they feel they have any issues. This makes the dental practice the prime location for screening and prevention of not only oral diseases, but also systemic diseases. Imagine being able to go to your dental practice and get your blood pressure checked? Or your HbA1C or vitamin D checked? Imagine if your dentist could refer you to the doctor when you were pre diabetic for dietary support as opposed to when you had diabetic foot? The system needs to shift from a reactive system that is primed for urgent care and disease, to a preventative system that rewards early detection and prevention. For this to happen, we need to work together as one team.

Different languages. The number of times I have tried to explain to a doctor or even a patient their oral issues and not be understood is countless. Dentists speak a different language to most other clinicians. Much of how we diagnose is based on qualitative symptoms and radiographs whereas our medical doctors will often rely on quantitative results such as bloods to diagnose disease. In order for us to communicate effectively, we must speak the same language. This is where salivary testing could offer the conversion of what was once qualitative symptoms or issues to quantitative diagnoses. For example, microbiome testing to assess the levels of pathogenic bacteria in the oral cavity or testing how an oral infection such as a dental abscess is raising CRP levels.

Five things physicians can do tomorrow

None of what follows requires new equipment, legislation or funding. The first four recommendations reflect actions already supported by existing clinical guidance; the fifth relates to an emerging technology whose clinical role is still being defined.

• 1.Ask the question. ʻDo your gums bleed when you brush or floss?’ takes ten seconds and identifies the single best clinical proxy for periodontitis. Add it to the diabetes review, the cardiovascular review and the antenatal booking visit.
• 2.Refer with intent. When a patient with diabetes, cardiovascular disease or pregnancy answers yes, refer them – and explain why. A vague ʻsee your dentist’ is dismissed. ʻYour gum inflammation is making your diabetes harder to control’ is acted upon.
• 3.Treat oral health as a vital sign in chronic disease. Build periodontal status into shared care records the way smoking status is. We measured smoking until measuring it became unremarkable, and behaviour followed measurement.
• 4.Advocate for curricular reform. Medical and dental schools should share at least one joint module on the oral-systemic axis. The Royal Colleges are well placed to drive this; the GMC and GDC are well placed to mandate it.
• 5.Use the microbiome carefully. Salivary microbiome testing is clinically available and increasingly affordable. It currently provides a snapshot of microbial composition rather than a validated predictive or risk-reduction tool however many companies are aiming to achieve this. A more immediate, evidence-based application is awareness of the oral cavity as a reservoir for antimicrobial resistance genes: judicious antibiotic prescribing in both medicine and dentistry, informed where relevant by microbiome and resistance data, is an area where physicians and dentists can act together now.¹¹

Conclusion: the oral cavity is not optional

For many years we have questioned whether the oral systemic links referenced to in this article are merely correlation or whether there is any causative link. The evidence reviewed here varies considerably by condition: for some – periodontitis and diabetes, and to a lesser extent cardiovascular disease – the case for a bidirectional, and in places causal, relationship is now well supported by mechanistic and intervention data; for others – Alzheimer's disease, adverse pregnancy outcomes and cancer – the evidence remains associative and mechanistically plausible rather than proven. What can be said with more confidence is that the oral cavity is not isolated from the rest of the body, and that oral health deserves a more consistent place in general medical assessment and preventive care.

The oral microbiome will not solve every problem in chronic disease management, and translating this evidence into practice will require clearer referral pathways between medicine and dentistry, shared clinical records, and careful, evidence-led use of emerging diagnostic tools such as salivary testing. Treating the oral cavity as separate from the rest of the body however is increasingly difficult to justify clinically, structurally or financially.

The oral cavity has been forgotten for long enough. It is time for medicine to remember it.

CRediT authorship contribution statement

Victoria Sampson: Writing – original draft.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Declaration of Competing Interest

The author is the founder of THS Labs, a company developing saliva-based oral microbiome diagnostics. No commercial product is endorsed in this article.