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Periodontal disease, tooth loss, and risk of oesophageal and gastric adenocarcinoma: a prospective study
  1. Chun-Han Lo1,2,
  2. Sohee Kwon2,3,
  3. Liang Wang1,4,
  4. Georgios Polychronidis1,5,6,
  5. Markus D Knudsen1,7,8,
  6. Rong Zhong1,9,10,
  7. Yin Cao11,12,
  8. Kana Wu13,
  9. Shuji Ogino1,10,14,
  10. Edward L Giovannucci1,13,15,
  11. Andrew T Chan2,3,14,15,16,
  12. Mingyang Song1,2,3,13
  1. 1Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
  2. 2Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
  3. 3Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
  4. 4Center of Gastrointestinal Surgery, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
  5. 5Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany
  6. 6Study Centre of the German Surgical Society, University of Heidelberg, Heidelberg, Germany
  7. 7Section of Bowel Cancer Screening, Cancer Registry of Norway, Oslo, Norway
  8. 8Norwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital, Oslo, Norway
  9. 9Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
  10. 10Program in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
  11. 11Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine in St Louis, St Louis, Missouri, USA
  12. 12Siteman Cancer Center, Washington University School of Medicine in St Louis, St Louis, Missouri, USA
  13. 13Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
  14. 14Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA
  15. 15Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
  16. 16Department of Immunology and Infectious Disease, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
  1. Correspondence to Dr Mingyang Song, Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA; mis911{at}mail.harvard.edu

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We read with great interest the study by Coker et al1 that provided supportive evidence for the role of oral microbiota in gastric cancer. A few studies also highlighted the possible link with oesophageal cancer.2–4 However, there is a lack of robust epidemiologic data on whether periodontal disease and tooth loss, indicators of oral microbial dysbiosis, are associated with these two cancers.

Here, we prospectively examined the association of history of periodontal disease and tooth loss with the risk of oesophageal and gastric adenocarcinoma in 98 459 women from the Nurses’ Health Study (1992–2014) and 49 685 men from the Health Professionals Follow-up Study (1988–2016). Dental measures, demographics, lifestyle, and diet were assessed using validated follow-up questionnaires. Self-reported cancer diagnosis was confirmed by review of medical records. We used Cox proportional hazards models to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs). We also examined the independent association of history of periodontal disease and tooth loss in a joint analysis.

Over 22–28 years of follow-up, we documented 199 cases of oesophageal adenocarcinoma and 238 cases of gastric adenocarcinoma. History of periodontal disease was associated with a 43% and 52% increased risk of oesophageal adenocarcinoma (multivariable-adjusted HR (aHR) 1.43, 95% CI 1.05 to 1.96) and gastric adenocarcinoma (aHR 1.52, 95% CI 1.13 to 2.04) (table …

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Footnotes

  • Contributors Study concept and design: C-HL and MS. Acquisition of the data: KW, SO, ELG, ATC and MS. Statistical analysis: C-HL. Interpretation of the data: all authors. Drafting of the manuscript: C-HL and MS. Critical revision of the manuscript for important intellectual content: all authors.

  • Funding This work was supported by the US National Institutes of Health (UM1 CA186107, P01 CA87969, U01 CA167552; K07CA218377, R21AA027608 to YC; R03 CA197879, R21 CA222940 to KW; P01 CA55075, R01 CA151993, R35 CA197735 to SO; R21 CA230873 to KW and SO; K24 DK098311, R01 CA137178, R01 CA202704 to ATC; R00 CA215314 to MS); the Siteman Investment Program (to YC); the American Institute for Cancer Research (to KW); the American Cancer Society (MRSG-17-220-01 - NEC to MS); the Project P Fund for Colorectal Cancer Research; the Bennett Family Foundation; and the Entertainment Industry Foundation through National Colorectal Cancer Research Alliance. The funders had no role in the design and conduct of the study. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funders.

  • Competing interests ATC previously served as a consultant for Bayer Healthcare and Pfizer for work unrelated to the topic of this manuscript. All remaining authors have declared no conflicts of interest.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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