title: Genetic predisposition to persistent apical periodontitis.
abstract: BACKGROUND
  The proinflammatory cytokine interleukin (IL)-1 is a key regulator of host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption. Allele2 of IL-1β is associated with a four-fold increase in IL-1β production. The aim of this case-control study was to evaluate the gene polymorphism of IL-1β in the pathogenesis of endodontic failure. We hypothesized that the gene polymorphism (allele2 of IL-1β) would influence host response and enhance inflammatory reactions predisposing to persistent apical periodontitis (PAP).
  
  
  METHODS
  Subjects with at least 1 year of follow-up after root canal therapy (RCT) were recalled. Inclusion and exclusion criteria were applied, and 34 subjects with signs/symptoms of PAP with otherwise acceptable RCT were included. Sixty-one controls showed healing with acceptable RCT. Genomic DNA from buccal mucosa was amplified by polymerase chain reaction followed by restriction fragment length polymorphism to distinguish the alleles of IL-1β gene polymorphism.
  
  
  RESULTS
  A significant difference in the distribution of the polymorphic genotype among cases (70.6%) and controls (24.6%) (P < .001, Pearson χ(2)) was shown.
  
  
  CONCLUSIONS
  These findings suggest that specific genetic markers associated with increased IL-1β production may contribute to increased susceptibility to PAP.
authors.affiliation: American Board of Endodontics, Case Western Reserve School of Dental Medicine, Cleveland, Ohio, USA.
authors.forename: Jussara M
authors.initials: JM
authors.lastname: Morsani
authors.forename: Anita
authors.initials: A
authors.lastname: Aminoshariae
authors.forename: Yiping Weng
authors.initials: YW
authors.lastname: Han
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Montagnese
authors.forename: Andre
authors.initials: A
authors.lastname: Mickel
mesh_terms: D000483:Alleles; D016022:Case-Control Studies; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D054884:Host-Pathogen Interactions / Q000235:genetics; D006801:Humans; D018836:Inflammation Mediators; D053583:Interleukin-1beta / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010485:Periapical Periodontitis / Q000000981:diagnostic imaging / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012150:Polymorphism, Restriction Fragment Length / Q000235:genetics; D011859:Radiography; D012008:Recurrence; D012189:Retrospective Studies; D012390:Root Canal Therapy; D019553:Tooth, Nonvital / Q000000981:diagnostic imaging; D017211:Treatment Failure
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta