Levels of interleukin 1β in tissue from sites of active periodontal disease

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Abstract
Interleukin Iβ 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‐1β in the pathogenesis of human periodontitis. Levels of IL‐1β 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 ≥2.5 mm, as determined by sequential probing and the tolerance method. IL‐1β was extracted from homogenates of tissue biopsies taken at surgery, and levels were quantified by ELISA. IL‐1β was found to be present in most patient tissue samples, with levels ranging from 0–82 ng/ml. Disease active sites had higher IL‐1β 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‐1β 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‐1β levels intermediate between the levels in stable and active sites. Detection of disease activity occurred more frequently at sites with IL‐1β levels >25 ng/ml (p < 0.01). Thus, IL‐1β 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‐1β levels. These data indicate that IL‐1β may have utility for the detection of sites of periodontal disease activity, and suggest that IL‐1β may be an important mediator of attachment loss in human periodontitis.