title: Elevated expression of IL-17 and IL-12 genes in chronic inflammatory periodontal disease.
abstract: BACKGROUND
  A number of different theories have been postulated to explain the progression of gingivitis to periodontitis in the context of the Th1/Th2 paradigm. However, no consistent results have been obtained. Th17, a new T-cell subset producing IL-17, which is implicated in many aspect of inflammatory tissue destruction, overcomes many of the discrepant findings in the studies related to the Th1/Th2 hypothesis. We compared the gene expression profile of Th17-related molecules in gingivitis and periodontitis lesions showing distinct clinical entities.
  
  
  METHODS
  Gingival tissue samples were obtained from 23 gingivitis and 24 periodontitis tissues. The gene expression was measured by using quantitative real-time PCR for IL-17A, IL-17F, CCR4, CCR6, IL-12 p35 and IL-23 p19. The difference of gene expressions between gingivitis and periodontitis was analyzed by Mann-Whitney U-test. Correlations between each gene expression were also analyzed.
  
  
  RESULTS
  The expression level of IL-17A was higher than that of IL-17F and a significant difference in expression between gingivitis and periodontitis was observed only for IL-17A. CCR4 and CCR6 tended to be higher in periodontitis compared with gingivitis, although the differences were not statistically significant. Whereas the gene expression of IL-12 p35 was significantly higher in periodontitis compared with gingivitis, that of IL-23 p19 was not different between the two diseases.
  
  
  CONCLUSIONS
  This study demonstrates the elevated expression of IL-17 and IL-12 in periodontitis, i.e., the tissue destruction form of periodontal diseases, as compared with gingivitis, and provides new insight into the T-cell mediated immunopathogenesis of periodontal disease.
authors.affiliation: Center for Transdisciplinary Research, Niigata University, Niigata, Japan.
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Honda
authors.forename: Yukari
authors.initials: Y
authors.lastname: Aoki
authors.forename: Naoki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Tomoki
authors.initials: T
authors.lastname: Maekawa
authors.forename: Takako
authors.initials: T
authors.lastname: Nakajima
authors.forename: Harue
authors.initials: H
authors.lastname: Ito
authors.forename: Koichi
authors.initials: K
authors.lastname: Tabeta
authors.forename: Takafumi
authors.initials: T
authors.lastname: Okui
authors.forename: Keiko
authors.initials: K
authors.lastname: Kajita
authors.forename: Hisanori
authors.initials: H
authors.lastname: Domon
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D000328:Adult; D002908:Chronic Disease; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D018664:Interleukin-12 / Q000235:genetics*; D020381:Interleukin-17 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010510:Periodontal Diseases / Q000235:genetics* / Q000276:immunology* / Q000473:pathology; D015203:Reproducibility of Results; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D020381:Interleukin-17; D018664:Interleukin-12