Heart failure promotes gingival inflammation and impairs periodontal remodeling.

Authors

Martin Berger, Marta Rizk, Jaana-Sophia Kern, Ulrike Schulze-Späte, Sandra Hennecke, Maximilian Neuhaus, Florian Kahles, Julia Moellmann, Stefan Wolfart, Joachim Jankowski, Michael Wolf, Katharina Marx-Schütt, Nikolaus Marx

Published in

Scientific reports. Volume 16. Issue 1. Jul 04, 2026. Epub Jul 04, 2026.

Abstract

Observational studies suggest an association between impaired oral health and cardiovascular disease; however, the directionality and underlying mechanisms remain unclear. In particular, whether heart failure (HF) itself adversely affects oral and periodontal health has not been systematically investigated in large populations or experimental models.We examined the association between HF and self-reported oral health indicators in 502,387 participants of the UK Biobank, including 17,356 individuals with HF defined by ICD-9/10 codes. Multivariable logistic regression models adjusted for demographic factors, cardiovascular comorbidities, systemic inflammation, lifestyle, and socioeconomic status were applied. To explore causality and mechanisms, periodontal tissue remodeling and inflammation were assessed in a murine model of pressure overload-induced HF using transverse aortic constriction (TAC). Periodontal ligament (PDL) space and alveolar bone microarchitecture were quantified by micro-computed tomography, and gingival inflammatory gene expression was analyzed by RT-PCR.HF patients exhibited a significantly higher prevalence of oral health burden compared with controls (51% vs. 40%, p<0.001). HF was associated with a 1.6-fold increased risk of impaired oral health, which remained significant after full adjustment (adjusted OR 1.18, 95% CI 1.14-1.22; p<0.001). In mice, reduced left ventricular ejection fraction following TAC was strongly associated with expansion of the maxillary PDL space (R² = 0.63, p = 0.009) and alterations in alveolar bone microarchitecture (trabecular thickness R² = 0.41 p = 0.061, trabecular number R² = 0.38 p = 0.07). These structural changes were accompanied by increased gingival expression of pro-inflammatory cytokines, including Il1b (SHAM vs. TAC: 1.44 ± 1.02 vs. 3.39 ± 1.53, p = 0.06) and TNF-α (SHAM vs. TAC: 1.37 ± 0.86 vs. 5.71 ± 1.23, p = 0.002 predominantly in the maxilla.HF is independently associated with impaired oral health in a large population cohort and induces site-specific periodontal inflammation and remodelling in experimental HF. These findings support HF as an upstream driver of compromised oral-periodontal health, challenging the prevailing concept that oral disease primarily contributes to cardiovascular pathology.

PMID:
42401591
Bibliographic data and abstract were imported from PubMed on 05 Jul 2026.

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