4.5 Article

Inflammation of the periodontium associates with risk of future cardiovascular events

Journal

JOURNAL OF PERIODONTOLOGY
Volume 92, Issue 3, Pages 348-358

Publisher

WILEY
DOI: 10.1002/JPER.19-0441

Keywords

atherosclerosis; cardiovascular disease; periodontal disease; positron emission tomography

Funding

  1. NIH [R01HL122177, R01HL137913, R01HL129856, T32HL076136, R01DE02520, KL2TR002542]
  2. Genentech

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The study showed that inflammation of the periodontium, independently predicted future cardiovascular events through heightened arterial inflammation. The relationship between periodontal inflammation and cardiovascular events was found to be primarily mediated by arterial inflammation, providing important support for a link between periodontal disease and cardiovascular disease.
Background While growing evidence suggests a link between periodontal disease (PD) and cardiovascular disease (CVD), the independence of this association and the pathway remain unclear. Herein, we tested the hypotheses that: (1) inflammation of the periodontium (PDinflammation) predicts future CVD independently of disease risk factors shared between CVD and PD, and (2) the mechanism linking the two diseases involves heightened arterial inflammation. Methods F-18-fluorodeoxyglucose positron emission tomography/computed tomography (F-18-FDG-PET/CT) imaging was performed in 304 individuals (median age 54 years; 42.4% male) largely for cancer screening; individuals without active cancer were included. PDinflammation and arterial inflammation were quantified using validated F-18-FDG-PET/CT methods. Additionally, we evaluated the relationship between PDinflammation and subsequent major adverse cardiovascular events (MACE) using Cox models and log-rank tests. Results Thirteen individuals developed MACE during follow-up (median 4.1 years). PDinflammation associated with arterial inflammation, remaining significant after adjusting for PD and CVD risk factors (standardized beta [95% CI]: 0.30 [0.20-0.40], P < 0.001). PDinflammation predicted subsequent MACE (standardized HR [95% CI]: 2.25 [1.47 to 3.44], P <0.001, remaining significant in multivariable models), while periodontal bone loss did not. Furthermore, mediation analysis suggested that arterial inflammation accounts for 80% of the relationship between PDinflammation and MACE (standardized log odds ratio [95% CI]: 0.438 [0.019-0.880], P = 0.022). Conclusion PDinflammation is independently associated with MACE via a mechanism that may involve increased arterial inflammation. These findings provide important support for an independent relationship between PDinflammation and CVD.

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