title: Cytokine analysis in lesions refractory to endodontic treatment.
abstract: BACKGROUND
  Failure in endodontic treatment is often caused by the persistence of microorganisms in the root canal after therapy. When treatment fails, an immune response develops that is characterized by an extensive network of immunologic mechanisms that lead to the production of cytokines and chemokines.
  
  
  METHODS
  The objective of this study was to determine the relative messenger RNA (mRNA) expression of IFN-γ, TNF-α, IL-1β, IL-17A, IL-10, and MCP-1 in periapical dental lesions refractory to treatment. Clinical samples were taken from teeth presenting periapical lesions refractory to endodontic treatment (the experimental group) or from healthy teeth with pulp vitality (the control group). Three paper points passing through the root apex (2 mm) were used to collect the samples. The total RNA was extracted from each sample, complementary DNA was synthesized, and quantitative polymerase chain reaction analysis was performed. The Mann-Whitney U test was used to determine the statistical significance of our findings (P < .05).
  
  
  RESULTS
  Significant differences in the levels of IFN-γ, TNF-α, IL-17A, and MCP-1 mRNA expression were observed in cases refractory to endodontic treatment as compared with the control group. The expression of IL-1β mRNA was not significantly different between the groups. The expression of IL-10 mRNA was insignificant in both the experimental and control groups.
  
  
  CONCLUSIONS
  A significantly increased expression of TNF-α, IFN-γ, IL-17A, and MCP-1 mRNA was observed in the periapical immune response in cases of endodontic failure. These results suggest that a proinflammatory cytokine profile predominates in these types of dental lesions.
authors.affiliation: Departamento de Odontologia Restauradora, Faculdade de Odontologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Luiz Carlos Feitosa
authors.initials: LC
authors.lastname: Henriques
authors.forename: Luciana Carla Neves
authors.initials: LC
authors.lastname: de Brito
authors.forename: Warley Luciano Fonseca
authors.initials: WL
authors.lastname: Tavares
authors.forename: Leda Quércia
authors.initials: LQ
authors.lastname: Vieira
authors.forename: Antônio Paulino
authors.initials: AP
authors.lastname: Ribeiro Sobrinho
mesh_terms: D000293:Adolescent; D000328:Adult; D018932:Chemokine CCL2 / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D003782:Dental Pulp / Q000276:immunology; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D020381:Interleukin-17 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010483:Periapical Diseases / Q000276:immunology*; D012333:RNA, Messenger / Q000032:analysis; D060888:Real-Time Polymerase Chain Reaction; D012008:Recurrence; D012390:Root Canal Therapy; D019227:Tooth Apex / Q000276:immunology; D017211:Treatment Failure; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D055815:Young Adult
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016207:Cytokines; C508609:IL10 protein, human; C508717:IL17A protein, human; D020381:Interleukin-17; D053583:Interleukin-1beta; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma