gms | German Medical Science

50. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds)
12. Jahrestagung der Deutschen Arbeitsgemeinschaft für Epidemiologie (dae)

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie
Deutsche Arbeitsgemeinschaft für Epidemiologie

12. bis 15.09.2005, Freiburg im Breisgau

Inverse Association Between Atopic Diseases and Periodontitis – the Study of Health in Pomerania (SHIP)

Meeting Abstract

  • Nele Friedrich - Institute of Epidemiology and Social Medicine, Greifswald
  • Henry Völzke - Institute of Epidemiology and Social Medicine, Greifswald
  • Christian Schwahn - Unit of Periodontology, Greifswald
  • Axel Kramer - Institute of Hygiene and Environmental Medicine, Greifswald
  • Michael Jünger - Department of Dermatology, Greifswald
  • Torsten Schäfer - Institute of Social Medicine, Lübeck
  • Ulrich John - Institute of Epidemiology and Social Medicine, Greifswald
  • Thomas Kocher - Unit of Periodontology, Greifswald

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie. Deutsche Arbeitsgemeinschaft für Epidemiologie. 50. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 12. Jahrestagung der Deutschen Arbeitsgemeinschaft für Epidemiologie. Freiburg im Breisgau, 12.-15.09.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc05gmds100

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter:

Veröffentlicht: 8. September 2005

© 2005 Friedrich et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.




In 1989 Strachan [1] found a strong relation between hay fever and family size and postulated the “hygiene hypothesis”, which suggests that infections in early infancy may have protective effects against the development of allergic diseases. In this context we investigate the independent relation between Periodontitis as oral infection and the risk of atopic diseases.

Materials and Methods

The Study of Health in Pomerania (SHIP) is a cross-sectional epidemiological survey of the adult population in the northeast of Germany [2]. 2837 of the 4310 participants were included in the analyses.

According to the presence or absence of house dust mite allergy, hay fever or asthma, 446 were classified as persons with atopic diseases. Periodontitis was measured by attachment loss and categorised according to the percentage of surfaces (max. 14 teeth at four surfaces) which exceeding 3mm attachment loss [healthy periodontal conditions: 0-7.7%, low: 7.8-28.6%, moderate: 28.7-63.9%, severe: >63.9%]. Odds ratios (OR) for the effect of periodontitis on atopic diseases were calculated using logistic regression.


After adjustment for age, gender, school education, smoking, alcohol consumption, number of teeth and family history for allergies or asthma these analysis revealed an inverse association between periodontitis and atopic diseases. Participants with healthy periodontal conditions had an increased risk for atopic diseases (OR for healthy, low, moderate attachment loss; 1.97 [95%-CI 1.49-2.59]; 1.79 [95%-CI 1.40-2.30]; 1.81 [95%-CI 1.39-2.36]) compared to subjects with severe periodontitis.


Periodontitis-inducing bacteria were detected in dental plaque of children [3], [4] , so promotive conditions for periodontitis already emerged in childhood. This early infection elicits an immune response.

In the aetiology of periodontal disease the involvement of T-cell subsets is equivocal. One aetiology model suggests that periodontitis is Th2-mediated and the production of interleukin-1 mediate the tissue destruction. A second model, Th1 cells and the produced IFN-γ are responsible for tissue destruction [5]. The hygiene hypothesis is based on the Th1/Th2 paradigm and the inverse relation between Th1-mediated (infections) and Th2-mediated (allergies) immune responses [6].

Inverse associations between atopy and Th1-mediated infections like tuberculosis, measles and hepatitis A were demonstrated [7], [8], [9], but also an inverse relation between a Th2-mediated infection by helminths and allergy were detected [10].

Among periopathogenic micro-organisms factors such as smoking, diabetes, male gender or genetic predisposition are important for the pathogenesis of periodontitis [11]. The resulting complex interactions cause the pathogenesis and the severity of periodontitis. In conclusion the present findings support the hygiene hypothesis.


SHIP is part of the Community Medicine Net ( of the University of Greifswald, which is funded by grants from the German Federal Ministry of Education and Research (BMBF, grant 01ZZ96030); the Ministry for Education, Research, and Cultural Affairs; and the Ministry for Social Affairs of the Federal State of Mecklenburg–West Pomerania. The contributions to data collection made by field workers, study physicians, ultrasound technicians, interviewers, and computer assistants are gratefully acknowledged.


Strachan DP. Hay fever, hygiene, and household size. Bmj 1989;299(6710):1259-60.
John U, Greiner B, Hensel E, Ludemann J, Piek M, Sauer S, et al. Study of Health In Pomerania (SHIP): a health examination survey in an east German region: objectives and design. Soz Praventivmed 2001;46(3):186-94.
Tanner AC, Milgrom PM, Kent R, Jr., Mokeem SA, Page RC, Riedy CA, et al. The microbiota of young children from tooth and tongue samples. J Dent Res 2002;81(1):53-7.
Umeda M, Miwa Z, Takeuchi Y, Ishizuka M, Huang Y, Noguchi K, et al. The distribution of periodontopathic bacteria among Japanese children and their parents. J Periodontal Res 2004;39(6):398-404.
Yamazaki K, Yoshie H, Seymour GJ. T cell regulation of the immune response to infection in periodontal diseases. Histol Histopathol 2003;18(3):889-96
Mosmann TR, Coffman RL. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu Rev Immunol 1989;7:145-73.
Shirakawa T, Enomoto T, Shimazu S, Hopkin JM. The inverse association between tuberculin responses and atopic disorder. Science 1997;275(5296):77-9.
Shaheen SO, Aaby P, Hall AJ, Barker DJ, Heyes CB, Shiell AW, et al. Measles and atopy in Guinea-Bissau. Lancet 1996;347(9018):1792-6.
Matricardi PM, Rosmini F, Ferrigno L, Nisini R, Rapicetta M, Chionne P, et al. Cross sectional retrospective study of prevalence of atopy among Italian military students with antibodies against hepatitis A virus. Bmj 1997;314(7086):999-1003.
van den Biggelaar AH, van Ree R, Rodrigues LC, Lell B, Deelder AM, Kremsner PG, et al. Decreased atopy in children infected with Schistosoma haematobium: a role for parasite-induced interleukin-10. Lancet 2000;356(9243):1723-7.
Nunn ME. Understanding the etiology of periodontitis: an overview of periodontal risk factors. Periodontol 2000 2003;32:11-23.