ABSTRACT
The levels of 3 bone resorptive cytokines, interleukin 1 alpha (IL-1 alpha), IL-1 beta, and tumor necrosis factor alpha (TNF alpha), were assessed in tissues from sites of periodontal disease. As determined by ELISA of tissue extracts, IL-1 beta and TNF alpha were detected in all diseased sites, whereas IL-1 alpha was present in 8/22 sites, IL-1 beta was present in highest concentration (mean +/- SEM: 11,695 +/- 2,888 pg/ml; 672 pM), followed by TNF alpha (434 +/- 135 pg/ml; 26 pM), and IL-1 alpha (342 +/- 160 pg/ml; 20 pM). The levels of all 3 mediators were significantly lower in clinically healthy tissues. There was a highly significant correlation between levels of IL-1 beta and TNF alpha (rs = 0.61, P less than 0.001), suggesting coordinated expression of these 2 mediators. The numbers of cells containing each mediator was also determined by indirect immunofluorescence on frozen tissue sections. Consistent with findings from tissue extracts, IL-1 beta-containing cells were present in approximately 5-fold higher numbers than TNF alpha-containing cells, and 40-fold higher numbers than IL-1-alpha-containing cells. Taken together with previous findings, these results indicate that IL-1 beta is likely to be an important mediator in the pathogenesis of periodontal disease.
Subject(s)
Gingiva/chemistry , Interleukin-1/analysis , Periodontitis/metabolism , Tumor Necrosis Factor-alpha/analysis , Adult , Alveolar Bone Loss/metabolism , Alveolar Bone Loss/pathology , Alveolar Process/chemistry , Alveolar Process/pathology , Cytokines/analysis , Enzyme-Linked Immunosorbent Assay , Epithelium/chemistry , Epithelium/pathology , Fluorescent Antibody Technique , Gingiva/pathology , Humans , Middle Aged , Periodontal Pocket/metabolism , Periodontal Pocket/pathology , Periodontitis/pathology , Periodontium/chemistry , Periodontium/pathologyABSTRACT
Interleukin-1 beta (IL-1 beta) is the predominant form of IL-1 produced by macrophages. IL-1 beta possesses numerous and diverse biological activities. Several of these activities, including fibroblast proliferation, potentiation of the immune response, and stimulation of bone resorption may be of relevance to the pathogenesis of periodontal disease. This study was designed to examine the presence of IL-1 beta in human periodontal tissue. An antiserum directed against the N-terminal segment (117-131) of human IL-1 beta was used to detect IL-1 beta using immunofluorescent staining techniques. IL-1 beta positive staining cells were observed in both normal and diseased tissue and were limited to the lamina propria. Brightly staining cells were increased by almost 3-fold in periodontally diseased tissue when compared to normal tissue. Low intensity staining cells were equally distributed in the normal and diseased specimens. We propose that IL-1 beta and IL-1 beta produced by cells in periodontal tissues may be related to the pathological processes associated with periodontal disease.
