Aderonke A Akinkugbe1, Gary D Slade2, A Sidney Barritt3, Stephen R Cole1, Steven Offenbacher4, Astrid Petersmann5, Thomas Kocher6, Markus M Lerch7, Julia Mayerle8, Henry Völzke9, Gerardo Heiss1, Birte Holtfreter6. 1. Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 2. Department of Dental Ecology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 3. Department of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 4. Department of Periodontology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 5. Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany. 6. Unit of Periodontology, Department of Restorative Dentistry, Periodontology, Endodontology, and Preventive and Pediatric Dentistry, University Medicine Greifswald, Greifswald, Germany. 7. Department of Medicine A, University Medicine Greifswald, Greifswald, Germany. 8. Department of Medicine, Ludwig-Maximilians University, Munich, Germany. 9. Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany.
Abstract
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) affects 20%-30% of adults with risk factors like obesity and insulin resistance putatively acting through chronic low-grade inflammation. Because periodontitis elicits low-grade inflammation, we hypothesized that it could contribute to NAFLD occurrence. OBJECTIVE: To investigate epidemiologic associations between periodontitis and the incidence of NAFLD among 2,623 participants of the Study of Health in Pomerania. METHODS: Periodontitis at baseline was defined as the percentage of sites (0%, <30%, ≥30%) with (i) clinical attachment level (CAL) ≥3 mm; (ii) probing pocket depth (PD) ≥4 mm. Incident NAFLD was defined as a significant increase in liver echogenicity on ultrasound relative to the kidneys, with the diaphragm indistinct or the echogenic walls of the portal veins invisible. RESULTS: After a median 7.7 years of follow-up, 605 incident NAFLD cases occurred at a rate of 32.5 cases per 1,000 person-years. Relative to participants without CAL ≥3 mm, NAFLD incidence was elevated slightly in participants with <30% of sites affected and moderately in participants with ≥30% of sites affected (multivariable-adjusted incidence rate ratio = 1.28, 95% CI, 0.84, 1.95 and 1.60, 95% CI, 1.05-2.43), respectively. A similar dose-response relationship was not observed for PD. CONCLUSION: History of periodontitis may be a risk factor for NAFLD.
BACKGROUND:Non-alcoholic fatty liver disease (NAFLD) affects 20%-30% of adults with risk factors like obesity and insulin resistance putatively acting through chronic low-grade inflammation. Because periodontitis elicits low-grade inflammation, we hypothesized that it could contribute to NAFLD occurrence. OBJECTIVE: To investigate epidemiologic associations between periodontitis and the incidence of NAFLD among 2,623 participants of the Study of Health in Pomerania. METHODS:Periodontitis at baseline was defined as the percentage of sites (0%, <30%, ≥30%) with (i) clinical attachment level (CAL) ≥3 mm; (ii) probing pocket depth (PD) ≥4 mm. Incident NAFLD was defined as a significant increase in liver echogenicity on ultrasound relative to the kidneys, with the diaphragm indistinct or the echogenic walls of the portal veins invisible. RESULTS: After a median 7.7 years of follow-up, 605 incident NAFLD cases occurred at a rate of 32.5 cases per 1,000 person-years. Relative to participants without CAL ≥3 mm, NAFLD incidence was elevated slightly in participants with <30% of sites affected and moderately in participants with ≥30% of sites affected (multivariable-adjusted incidence rate ratio = 1.28, 95% CI, 0.84, 1.95 and 1.60, 95% CI, 1.05-2.43), respectively. A similar dose-response relationship was not observed for PD. CONCLUSION: History of periodontitis may be a risk factor for NAFLD.
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