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Disease Markers
Volume 35 (2013), Issue 6, Pages 819–823
Clinical Study

Expression Profile of IL-35 mRNA in Gingiva of Chronic Periodontitis and Aggressive Periodontitis Patients: A Semiquantitative RT-PCR Study

1Department of Periodontics, PMNM Dental College, Bagalkot, Karnataka 587101, India
2Department of Periodontics, Rajarajeswari Dental College and Hospital, Ramohalli Cross, Mysore Road, Bangalore, Karnataka 560060, India

Received 2 May 2013; Revised 3 August 2013; Accepted 8 October 2013

Academic Editor: Donald H. Chace

Copyright © 2013 Nagaraj B. Kalburgi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Proinflammatory and anti-inflammatory cytokines play a key role in the pathogenesis of periodontal diseases. Secretion of bioactive IL-35 has been described by T regulatory cells ( ) and is required for their maximal suppressive activity. are involved in the modulation of local immune response in chronic periodontitis patients. Objective. Hence, the present study was aimed to investigate the expression of IL-35 mRNA in chronic periodontitis and aggressive periodontitis patients. Materials and Methods. The present study was carried out in 60 subjects, which included 20 chronic periodontitis patients, 20 aggressive periodontitis patients, and 20 periodontally healthy controls. IL-35 mRNA expression in gingival tissue samples of all subjects was semiquantitatively analyzed using Reverse Transcriptase Polymerase Chain Reaction (RT-PCR). Results. The present study demonstrated the expression of IL-35 mRNA in gingival tissues of all the three groups. IL-35 mRNA expression was highest in chronic periodontitis subjects ( ) as compared to the aggressive periodontitis group ( ) and least seen in healthy patients ( ). Conclusion. The increased expression of IL-35 in chronic and aggressive periodontitis suggests its possible role in pathogenesis of periodontitis. Future studies done on large samples with intervention will strengthen our result.