The Secretion of PGE2, IL‐1β, IL‐6, and TNFα by Adherent Mononuclear Cells From Early Onset Periodontitis Patients

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Abstract
The secretion of prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL‐1β), and interleukin 6 (IL‐6) by adherent mononuclear cells (AMNC) from 28 patients with early‐onset periodontitis was studied. The early onset‐periodontitis patients consisted of 12 patients with localized juvenile periodontitis (LJP) and 16 patients with severe generalized periodontitis (SGP). The AMNC responses to different concentrations of lipopolysaccharide (LPS) (E. coli) were determined in these 28 patients and compared to 14 healthy controls. Mediator levels in the supernatant were measured using radioimmunoassays for PGE2, IL‐1β, and IL‐6 determination and an enzyme linked immunosorbent assay for TNFα levels. The mean age of the patients was 19.9 years for the LJP group, 30.4 years for SGP, and 28.0 years for the controls. The mean number of teeth per patient with attachment loss of >6 mm was 4.75 in the LJP patients and 17.3 in the SGP group. In the absence of LPS, LJP AMNC secreted significantly more PGE2 than unstimulated control or SGP AMNC, while similar baseline amounts of IL‐1β, IL‐6, and TNFα were secreted by AMNC from the 3 patient groups. LPS stimulation resulted in the dose‐dependent secretion of significantly higher levels of PGE2 by LJP AMNC compared to SGP AMNC which in turn secreted significantly more than controls. TNFα secretion by LJP monocytes was significantly greater than the SGP and the control groups while IL‐1β secretion by the SGP AMNC was depressed compared to the other two patient groups. No significant difference in IL‐6 secretion was noted among the 3 patient groups. These data suggest that the AMNC from the peripheral blood from each of the 3 patient groups differ considerably in their capacity to secrete inflammatory mediators. It is not clear as to whether these intergroup differences in systemic AMNC responsiveness represent an intrinsic or acquired difference in LPS responsiveness. J Periodontol 1994;65:139–146.