title: Gingival crevicular interleukin-1 and interleukin-1 receptor antagonist levels in periodontally healthy and diseased sites.
abstract: Interleukin-1 (IL-1) molecules, IL-1 alpha and IL-1 beta are cytokines involved in the acute-phase response against infection and in the pathogenesis of periodontal destruction. Administration of exogenous IL-1 receptor antagonist (IL-1ra) is effective in reducing the inflammatory reactions mediated by IL-1. However, the relationship between these three naturally occurring IL-1 molecules and periodontal diseases has been poorly characterized. We investigated the correlation of gingival crevicular IL-1 molecules and the clinical status of patients with different severities of periodontitis. IL-1 alpha, IL-1 beta, IL-1ra and the total IL-1/IL-1ra ratio (IL-1 activity index; IL-1AI) were measured in 75 gingival crevicular fluid (GCF) samples from non-inflamed gingiva sites in 2 healthy subjects and diseased sites in 7 patients with several types of periodontitis. IL-1 alpha, IL-1 beta and IL-1ra were measured by specific non-cross-reactive enzyme linked immunosorbent assay. The probing depth, gingival index and alveolar bone loss of each site was recorded at the time of GCF sampling. The total amount of IL-1 alpha, IL-1 beta and the IL-1AI, but not total IL-1ra, were found to be correlated with alveolar bone loss score. Three IL-1 molecules were also measured in the gingival tissue of patients with periodontitis. A similar progressive decrease of the IL-1AI was detected in gingival tissue with periodontitis. These results suggest that the amounts of both crevicular IL-1 and IL-1AI are closely associated with periodontal disease severity.
authors.affiliation: Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Nagoya, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ishihara
authors.forename: T
authors.initials: T
authors.lastname: Nishihara
authors.forename: T
authors.initials: T
authors.lastname: Kuroyanagi
authors.forename: N
authors.initials: N
authors.lastname: Shirozu
authors.forename: E
authors.initials: E
authors.lastname: Yamagishi
authors.forename: M
authors.initials: M
authors.lastname: Ohguchi
authors.forename: M
authors.initials: M
authors.lastname: Koide
authors.forename: N
authors.initials: N
authors.lastname: Ueda
authors.forename: K
authors.initials: K
authors.lastname: Amano
authors.forename: T
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000210:Acute-Phase Reaction / Q000276:immunology; D000328:Adult; D000368:Aged; D016301:Alveolar Bone Loss / Q000276:immunology / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005881:Gingiva / Q000276:immunology; D005883:Gingival Crevicular Fluid / Q000276:immunology*; D005891:Gingivitis / Q000276:immunology; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000473:pathology; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000473:pathology; D010518:Periodontitis / Q000276:immunology* / Q000473:pathology; D010519:Periodontium / Q000276:immunology*; D017472:Receptors, Interleukin-1 / Q000032:analysis / Q000037:antagonists & inhibitors*
chemical_list: D007375:Interleukin-1; D017472:Receptors, Interleukin-1