LEVELS OF INTERLEUKIN-1-BETA IN TISSUE FROM SITES OF ACTIVE PERIODONTAL-DISEASE

Interleukin 1-beta is a potent bone resorptive cytokine which also mediates soft tissue destruction through the stimulation of prostaglandin production, and the induction of collagenase and other proteases. This constellation of activities suggests a role for IL-1-beta in the pathogenesis of human periodontitis. Levels of IL-1-beta were therefore determined in tissue obtained from (1) diseased, active (2) diseased, inactive, and (3) healthy sites from 12 patients with destructive adult periodontitis. Disease activity was defined as attachment loss of greater-than-or-equal-to 2.5 mm, as determined by sequential probing and the tolerance method. IL-1-beta was extracted from homogenates of tissue biopsies taken at surgery, and levels were quantified by ELISA. IL-1-beta was found to be present in most patient tissue samples, with levels ranging from 0-82 ng/ml. Disease active sites had higher IL-1-beta levels (p < 0.05) than inactive and healthy sites. Diseased inactive sites were divided into 2 groups, those losing small amounts of attachment (0.5-2.0 mm, worsening sites) and those which showed no change or attachment gain (stable sites). Stable diseased sites had IL-1-beta levels which were comparable to those found in healthy sites, and which were significantly different from active sites (p < 0.02). Worsening sites had IL-1-beta levels intermediate between the levels in stable and active sites. Detection of disease activity occurred more frequently at sites with IL-1-beta levels > 25 ng/ml (p < 0.01). Thus, IL-1-beta levels were positively related to changes in attachment level, but were inversely related to the presence of supragingival plaque or redness, and were unrelated to bleeding on probing or suppuration, indicating a dissociation between the presence of inflammation and IL-1-beta levels. These data indicate that IL-1-beta may have utility for the detection of sites of periodontal disease activity, and suggest that IL-1-beta may be an important mediator of attachment loss in human periodontitis.