title: Interleukin-21 expression and its association with proinflammatory cytokines in untreated chronic periodontitis patients.
abstract: BACKGROUND
  Interleukin-21 (IL-21) controls the differentiation of T-helper Th17 cells and induces the production of IL-17 in this T-cell subtype. The aim of this study is to determine the relative expression of IL-21 in gingival tissues of chronic periodontitis patients and correlate/associate this expression with proinflammatory cytokines and clinical parameters of disease.
  
  
  METHODS
  Samples of gingival biopsies were collected from chronic periodontitis patients (n = 10) and controls (n = 8). The mRNA expressions of IL-21, IL-1β, IL-6, IL-17, IL-23, IL-10, and transforming growth factor-β1 (TGF-β1) were quantified using real-time reverse transcription-polymerase chain reaction. IL-21 levels were compared between chronic periodontitis and healthy gingival tissues and correlated with cytokine and clinical parameters of tissue destruction.
  
  
  RESULTS
  A significant overexpression of IL-21, IL-1β, IL-6, IL-17, and IL-23p19 was detected in periodontal disease-affected tissues compared to healthy gingival tissues. IL-10 and TGF-β1 were, however, downregulated in periodontal lesions. IL-21 yielded significant positive correlations with probing depth, clinical attachment level, IL-1β, and IL-6. In addition, IL-21 was negatively correlated with IL-10 and TGF-β1.
  
  
  CONCLUSIONS
  IL-21 was overexpressed in chronic periodontitis gingival tissues and correlated with clinical parameters of periodontal destruction and with proinflammatory cytokines. Therefore, IL-21 might play a role in the tissue destruction that characterizes chronic periodontal disease.
authors.affiliation: Laboratory of Periodontal Biology, Department of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile. ndutzan@u.uchile.cl
authors.forename: Nicolás
authors.initials: N
authors.lastname: Dutzan
authors.forename: Rolando
authors.initials: R
authors.lastname: Vernal
authors.forename: Jose P
authors.initials: JP
authors.lastname: Vaque
authors.forename: Jocelyn
authors.initials: J
authors.lastname: García-Sesnich
authors.forename: Marcela
authors.initials: M
authors.lastname: Hernandez
authors.forename: Loreto
authors.initials: L
authors.lastname: Abusleme
authors.forename: Andrea
authors.initials: A
authors.lastname: Dezerega
authors.forename: J Silvio
authors.initials: JS
authors.lastname: Gutkind
authors.forename: Jorge
authors.initials: J
authors.lastname: Gamonal
mesh_terms: D000328:Adult; D055113:Chronic Periodontitis / Q000276:immunology*; D016207:Cytokines / Q000032:analysis*; D003774:Dental Plaque Index; D005260:Female; D005881:Gingiva / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D016753:Interleukin-10 / Q000032:analysis; D020381:Interleukin-17 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D053759:Interleukin-23 / Q000032:analysis; D053760:Interleukin-23 Subunit p19 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007378:Interleukins / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000276:immunology; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology; D053773:Transforming Growth Factor beta1 / Q000032:analysis; D000098546:Interleukin-21
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D053760:Interleukin-23 Subunit p19; D015850:Interleukin-6; D007378:Interleukins; D053773:Transforming Growth Factor beta1; D016753:Interleukin-10; D000098546:Interleukin-21