%0 Journal Article
%T Expression Profile of IL-35 mRNA in Gingiva of Chronic Periodontitis and Aggressive Periodontitis Patients: A Semiquantitative RT-PCR Study
%A Nagaraj B. Kalburgi
%A Akshay Muley
%A B. M. Shivaprasad
%A Arati C. Koregol
%J Disease Markers
%D 2013
%R 10.1155/2013/489648
%X 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. 1. Introduction Periodontal diseases are considered to be multifactorial diseases, where putative periodontopathogens trigger inflammatory and immune responses. It is characterized by irreversible loss of alveolar bone and connective tissue attachment in the periodontium which ultimately results in the loss of teeth. These pathogens are known to produce proteolytic enzymes as well as elicit signals in resident gingival cells or in immune cells infiltrating the gingival tissues that result in immune responses; these responses lead to either the successful removal of the pathogens or to host mediated destruction of the periodontal tissues [1]. Gingival inflammation is regulated by reciprocal interactions between various cell types including, leukocytes, epithelial cells, fibroblasts, and endothelial cells. Among the many immune and inflammatory mediators known cytokines have attracted special attention. Proinflammatory and anti-inflammatory cytokines play a key role in the pathogenesis of periodontal disease thereby influencing destruction, remodeling, and repair of periodontal tissues [2]. Interleukin-12 (IL-12) is one such cytokine which appears to contribute to inflammatory response in numerous physiological and
%U http://www.hindawi.com/journals/dm/2013/489648/