z-logo
Premium
Tissue Levels of Bone Resorptive Cytokines in Periodontal Disease
Author(s) -
Stashenko Philip,
Jandinski John J.,
Fujiyoshi Philip,
Rynar James,
Socransky Sigmund S.
Publication year - 1991
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1991.62.8.504
Subject(s) - beta (programming language) , tumor necrosis factor alpha , pathogenesis , alpha (finance) , interleukin , periodontal disease , mediator , interleukin 6 , cytokine , endocrinology , chemistry , medicine , immunology , pathology , biology , construct validity , nursing , computer science , patient satisfaction , programming language
T he levels of 3 bone resorptive cytokines , interleukin 1α (IL‐1α), IL‐1β, and tumor necrosis factor α (TNFα), were assessed in tissues from sites of periodontal disease. As determined by ELISA of tissue extracts, IL‐1β and TNFα were detected in all diseased sites, whereas IL‐1α was present in 8/22 sites. IL‐1β was present in highest concentration (mean ± SEM: 11,695 ± 2,888 pg/ml; 672 pM), followed by TNFα (434 ± 135 pg/ml; 26 pM), and IL‐1α (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‐1β and TNFα (r s = 0.61, P <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‐1β‐containing cells were present in approximately 5‐fold higher numbers than TNFα‐containing cells, and 40‐fold higher numbers than IL‐1α‐containing cells. Taken together with previous findings, these results indicate that IL‐1β is likely to be an important mediator in the pathogenesis of periodontal disease. J Periodontol 1991; 62:504–509 .

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here