Association between IL8 haplotypes and pathogen levels in chronic periodontitis

  • L. S. Finoti
  • S. C. T. Corbi
  • G. Anovazzi
  • S. R. L. Teixeira
  • J. P. Steffens
  • R. Secolin
  • Y. J. Kim
  • S. R. P. Orrico
  • J. A. Cirelli
  • M. P. A. Mayer
  • R. M. Scarel-Caminaga


Chronic periodontitis (CP) is considered to be a multifactorial disease influenced by microbial and genetic factors. The aim of the present study was to investigate whether the genetic susceptibility to CP in individuals with the IL8 ATC/TTC haplotype is associated with subgingival levels of periodontopathogens. Sixty-five individuals, grouped according to the presence (n = 28) or absence (n = 37) of the IL8 haplotype, were evaluated. After clinical periodontal evaluation, each group was subdivided according to the presence (CP) or absence (H) of periodontitis. Four subgingival samples were obtained from CP and two samples per subject from H patients. The levels and proportions of Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola were analyzed using quantitative real-time polymerase chain reaction (q-PCR). No differences were found in the proportion of periodontopathogenic bacteria between groups with the presence or absence of the IL8 haplotype. However, in the CP groups, the levels of periodontopathogens were significantly higher in the individuals without the IL8 haplotype than in the individuals with the IL8 haplotype. These results suggest that periodontal destruction may occur in patients who are considered to be genetically susceptible to CP with a lower microbial challenge because of the presence of the IL8 ATC/TTC haplotype than in patients without this haplotype.


Chronic Periodontitis Gingival Crevicular Fluid Probe Pocket Depth Clinical Attachment Loss Periodontal Destruction 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



This study was supported by the Foundation for Research Support of São Paulo State (FAPESP) grants 2003/10424-0, 2009/08773-3, and 2009/11371-4.

Conflict of interest

The authors declare no conflicts of interest with respect to the research, authorship, and/or publication of this article.


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Copyright information

© Springer-Verlag Berlin Heidelberg 2013

Authors and Affiliations

  • L. S. Finoti
    • 1
  • S. C. T. Corbi
    • 1
  • G. Anovazzi
    • 1
  • S. R. L. Teixeira
    • 2
  • J. P. Steffens
    • 3
  • R. Secolin
    • 4
  • Y. J. Kim
    • 5
  • S. R. P. Orrico
    • 1
  • J. A. Cirelli
    • 1
  • M. P. A. Mayer
    • 2
  • R. M. Scarel-Caminaga
    • 6
  1. 1.Department of Oral Diagnosis and Surgery, School of Dentistry at AraraquaraUNESP, Universidade Estadual PaulistaAraraquaraBrazil
  2. 2.Department of Microbiology, Institute of Biomedical SciencesUniversity of São PauloSão PauloBrazil
  3. 3.Department of Physiology and Pathology, School of Dentistry at AraraquaraUNESP, Universidade Estadual PaulistaAraraquaraBrazil
  4. 4.Department of Medical GeneticsUniversity of Campinas (UNICAMP)CampinasBrazil
  5. 5.Department of ImplantologySanto Amaro UniversitySao PauloBrazil
  6. 6.Department of Morphology, School of Dentistry at AraraquaraUNESP, Universidade Estadual PaulistaAraraquaraBrazil

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