Inflammation of the periodontium associates with risk of future cardiovascular events. Issue 3 (13th February 2021)

• Record Type: Journal Article
• Authors: Van Dyke, Thomas E.; Kholy, Karim El; Ishai, Amorina; Takx, Richard A.P.; Mezue, Kene; Abohashem, Shady M.; Ali, Abdelrahman; Yuan, Neal; Hsue, Priscilla; Osborne, Michael T.; Tawakol, Ahmed
• Is Part Of: Journal of periodontology. Volume 92:Issue 3(2021)
• Page Start: 348
• Page End: 358
• Publication Date: 2021-02-13
• Subjects: atherosclerosis -- cardiovascular disease -- periodontal disease -- positron emission tomography; Periodontics -- Periodicals; 617.632
• DOI: 10.1002/JPER.19-0441
• Languages: English
• ISSNs: 0022-3492

Abstract

Abstract: 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: 18 F‐fluorodeoxyglucose positron emission tomography/computed tomography ( 18 F‐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 18 F‐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 β [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.