Guts and Gums Speak the Same Language: Meta-Analysis Links Inflammatory Bowel Disease to Periodontitis

Inflammatory bowel diseases (IBD) - ulcerative colitis and Crohn's disease - have long ceased to be a "local" gastrointestinal problem: they affect immunity, microbiota and systemic inflammation. Periodontitis - chronic inflammation of tissues around the tooth - is structured similarly: dysbiosis, hyperactivation of the immune response, inflammatory mediators. A new systematic study in BMC Gastroenterology collected disparate studies of recent years and asked a simple question: is it true that people with IBD have a higher incidence of periodontitis? The answer is yes: the risk of periodontitis in patients with IBD is approximately twice as high as in people without IBD.

Background of the study

Inflammatory bowel diseases (IBD) - ulcerative colitis and Crohn's disease - have transformed from a "Western disease" into a global burden: prevalence, life expectancy with disabling symptoms, and the number of elderly patients for whom comorbidities are particularly critical are growing. At the same time, periodontitis remains one of the most common inflammatory diseases in humans; since 2017, it has been classified according to the World Workshop staging/grading system, which allows for more accurate comparison of studies and clinical cohorts. Against this background, the question of the connection between IBD and periodontitis is not only academic: if the risks are indeed higher, dental screening and prevention should be included in the standard care of patients with IBD.

The biological plausibility of such a link has long been discussed through the prism of the “mouth-gut axis”. Periodontal inflammation leads to the expansion of oral pathobionts; some of them are able to colonize the intestine and enhance colitis-like processes in susceptible hosts. The immune architecture of both diseases is characterized by a significant role of the Th17/IL-23/IL-17 axis and proinflammatory cytokines (IL-1β, IL-6, TNF-α), which creates a common “environment” for chronicity. In other words, microbial and immune mechanisms in periodontitis and IBD do overlap, which means that an epidemiological link is expected.

There are also general modifiable and genetic risk factors. Smoking paradoxically worsens Crohn's disease and is associated with a lower risk/activity of ulcerative colitis; in periodontology, tobacco is a consistent enhancer of inflammation and attachment loss. At the genetic level, cross-references are illustrated, for example, by NOD2: a key locus of predisposition to Crohn's disease is discussed in aggressive forms of periodontitis. All this pushes towards the idea of integrated oral monitoring in patients with IBD and, conversely, careful consideration of the intestinal anamnesis in periodontal patients.

Previous reviews and meta-analyses have suggested an IBD ↔ periodontitis association, but have suffered from heterogeneous definitions of gum disease and limited sample sizes; some cohorts have produced “null” results. Therefore, updated, methodologically rigorous summaries incorporating recent studies and, where possible, separately analyzing IBD subtypes (UC vs CD) are needed by the clinical community: they clarify the magnitude of risk, help plan screening, and serve as a starting point for mechanistic and interventional work.

How the authors tested this

The team registered the protocol in PROSPERO and searched seven international databases at once (PubMed, Scopus, Web of Science, ProQuest, Embase, Cochrane, ScienceDirect) - from 1960 to December 30, 2024. They included observational studies (case-control, cross-sectional, cohort), which compared the incidence of periodontitis in adults with and without IBD. Quality was assessed using the Newcastle-Ottawa scale, meta-analysis was done in CMA, heterogeneity - by I², risk of publication bias - by Begg/Egger. In total, 11 studies were filtered, of which 10 were included in the meta-analysis.

Key elements of the methodology (short list)

• Sample: publications from 2004-2024; different designs, adult participants.
• End point: presence of periodontitis according to clinical indices (pocket, loss of attachment, etc.).
• Statistics: random effects model; primary metric - OR; sensitive "leave-one-out" analysis.
• Quality: included works are of medium/high level, NOS.
• Heterogeneity/publication bias: I² about 37.5%; Egger P=0.64 - no obvious bias is visible.

What happened: numbers without water

Main result: IBD ↔ periodontitis, OR = 2.28 (95% CI 1.73-3.00) - that is, patients with IBD are more than twice as likely to have periodontitis than people without IBD. In subtype analysis:

• Ulcerative colitis (UC): OR = 3.14 (2.11-4.66) - the most pronounced association.
• Crohn's disease (CD): OR = 1.99 (1.40-2.83) - also significantly higher than the control.
  Formally, UC and CD did not differ in the strength of the association (P=0.09), but the trend towards higher risk in UC is noticeable and deserves mechanistic verification.

Why this might be: Common mechanisms of the "mouth and gut"

The authors discuss the intersections of immunity and microbiota: Th17 response, inflammatory mediators (IL-6, TNF-α, IL-1β), systemic circulation of CRP, and possible migration of oral microbes to the gut. Plus common risk factors - from smoking to genetic variants (e.g., NOD2/CARD15). Conversely, intestinal inflammation can "heat up" the periodontium via the blood and immune-metabolic axes. All this makes the connection biologically plausible, although causality has not yet been proven.

What was found in the clinic (besides “yes/no periodontitis”)

In a number of included studies, patients with IBD were more likely to have:

• Deeper periodontal pockets and greater attachment loss.
• More widespread mucosal and periodontal lesions.
  This fits into the idea of a more severe course of oral tissue inflammation against the background of IBD.

What does this change for practice - today

Even without a causal conclusion, the picture is clear: patients with IBD are a high-risk group for periodontitis. This means that they need early dental screening and an interdisciplinary team of a gastroenterologist and a periodontist. In practice, this means:

• At the gastroenterologist's appointment: a short questionnaire on bleeding gums, tooth mobility, hygiene, and frequency of professional cleanings.
• At the dentist: remember about IBD in the anamnesis, evaluate inflammation indices and teach hygiene (soft pastes/brushes, irrigator), plan professional cleanings more often than standard.
• In exacerbations of IBD: be careful with antibiotics/NSAIDs; if possible, synchronize periodontal therapy with control of intestinal inflammation.

Where are the weak points of research (and what to do about them)

Meta-analysis is not a "weight of evidence" if the original studies are heterogeneous. There are several limitations:

• Definitions of periodontitis varied across studies; it is important for authors and future groups to standardize criteria (eg, the 2017 consensus).
• Confounding by risk factors: Smoking increases both IBD and periodontitis and could not be accounted for consistently across samples.
• The design is observational, so the direction of the arrow (IBD → periodontitis or vice versa) cannot be determined.
• A number of meta-evaluations used crude ORs (without full adjustment) and the sample sizes in the primary articles were small. However, the robustness of the effect in the sensitivity analysis supports the validity of the overall association.

Where to go next (research roadmap)

• Longitudinal cohorts and large populations with uniform definitions of periodontitis and detailed accounting for smoking, diabetes, and IBD therapy.
• Mechanistic work: testing the mouth → gut hypothesis (microbe/metabolite translocation) and the role of the Th17 axis.
• Interventions: Can periodontitis treatment reduce IBD activity (relapse rate, inflammatory markers, steroid requirements)?
• Personalization: Identifying IBD subtypes with an “oral-inflammatory” phenotype for targeted prevention.

The main thing in three points

• IBD is associated with periodontitis: the overall risk is 2.28 times higher; by subtype - UC OR 3.14, CD OR 1.99 (without statistically significant difference between them).
• Mechanistic "bridges": Th17 response, cytokines, dysbiosis, NOD2, probable migration of oral microbes; causality not yet proven.
• For practice now: early dental screening for IBD and cooperation between a gastroenterologist and a periodontist.

Source: Naghsh N. et al. Evaluation of the association between periodontitis and inflammatory bowel disease: A systematic review and meta-analysis. BMC Gastroenterology, published 18 August 2025. Protocol registration: PROSPERO CRD42024572342. DOI: https://doi.org/10.1186/s12876-025-04181-7