THE RELEASE OF INTERLEUKIN-1-BETA, TUMOR NECROSIS FACTOR-ALPHA AND INTERFERON-GAMMA BY CULTURED PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM PATIENTS WITH PERIODONTITIS

The extracellular release of IL‐1β by cultured peripheral blood monocytes from 26 periodontitis patients and 26 control subjects was measured by radioimmunoassay. Unstimulated monocytes from periodontitis patients released significantly more IL‐1β than controls during 24 h of culture; there was a wide variation in the amount of IL‐1β released (0.45–13.00 ng/ml per 106 cells) which did not correlate with either the degree of bone loss or pocket formation observed clinically. When stimulated with lipopolysaccharide (LPS; Actinobacillus actinomycetemcomitans; 5 μg/ml) monocytes from periodontitis patients produced significantly more IL‐1β than those from control subjects. Monocyte culture supernatants from another 10 periodontitis patients and 10 control subjects were also assayed for both IL‐1β and TNF‐α by enzyme‐linked immunosorbent assays. Spontaneous and LPS‐stimulated (Bacteroides gingivalis; 5 μ/ ml) IL‐1β release were again significantly higher for periodontitis patients. TNF‐α was detected in the periodontitis cultures (0–765 pg/ml per 106 cells), but the mean value was not significantly different from controls. LPS‐stimulated TNF‐α release, however, was significantly higher than for control subjects, and there was a strong correlation between spontaneous IL‐1β and TNF‐α release by monocytes from the periodontitis group. Measurement of interferon‐γ (IFN‐γ) in lymphocyte cultures from these patients by immunoradiometric assay showed that IFN‐γ levels in periodontitis cultures were consistently low, but not significantly so when compared to controls; both groups responded equally to concanavalin‐A (5 μg/ml). Although the precise roles of IL‐1β and TNF‐α in periodontitis remain unclear, these data provide evidence that both cytokines may participate in the pathogenesis of the disease. Copyright © 1990, Wiley Blackwell. All rights reserved