Interleukin-1 concentrations within gingiva during the progression of periodontal disease

Interleukin-1 isoform concentrations within gingiva during the progression of periodontal disease. S. R. Lester, J. Bain, R. B. Johnson and F. G. Serio, Department of Periodontics and Preventive Sciences, University of Mississippi, Jackson, MS.

Objectives: To evaluate Interleukin-1 isoform concentrations within gingiva obtained from normal and sites of periodontal inflammation..

Methods: An interdental gingival papilla was obtained prior to extraction of adjacent teeth. The tissue was grouped based on adjacent pocket depth and bleeding on probing (BOP). Gingiva adjacent to a ≤ 3 mm sulcus without BOP was classified as "normal"(N); gingiva adjacent to a 3 mm sulcus with BOP was classified as "diseased, slight"(DS). Gingiva adjacent to a 4-6 mm sulcus featuring BOP was classified as "diseased, moderate"(DM) and gingiva adjacent to > 6 mm sulci was classified as "diseased, severe"(DSev). Tissues were solubilized and IL-1-b, IL-1-¦Á, IL-1-ra, and IL-6 concentrations were assessed by ELISA. Data were compared by factorial ANOVA, post-hoc Tukey, and the Pearson's correlation test. Groups were defined as significantly different when p<0.05. Results: Gingival concentrations of IL-6, IL-1ra, IL-1-¦Á, and IL-1-b were significantly greater adjacent to DS than adjacent to H, DM or DSev sites (p<0.05). In addition, the gingival concentrations of IL-1ra and IL-1-¦Á were significantly greater within gingiva adjacent to > 6mm DSev than adjacent to DM sitesp<0.05).

Conclusions:Our data indicate nearly equivalent concentrations of the three IL-1 isoforms at H, DS, DM, and DSev and significantly higher concentration of each isoform at DM (compared to H and DS) and IL-1- alpha and beta at DSev (compared to DM). These data are not similar to those from GCF obtained from sites of periodontal inflammation; in particular, gingival tissue contains lower concentrations of IL-1ra than that reported within GCF. These data could explain why addition of IL-1ra to sites of inflammation promotes healing.