alexa Gingival concentrations of interleukin-23 and -17 at healthy sites and at sites of clinical attachment loss.
Immunology

Immunology

Journal of Clinical & Cellular Immunology

Author(s): Lester SR, Bain JL, Johnson RB, Serio FG

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Abstract BACKGROUND: The presence of interleukin (IL)-23 has not been reported within inflamed gingiva, so we evaluated its concentration within gingiva from normal sites and sites of chronic periodontal disease. METHODS: Gingiva was obtained prior to extraction of teeth. It was grouped based on clinical attachment loss (CAL): 0 to 2 mm (normal-slight), 3 to 4 mm (moderate), and >5 mm (severe). Tissues were solubilized, and IL-12, -23, -6, -17, and -1beta; interferon-gamma (IFN-gamma); and tumor necrosis factor-alpha (TNF-alpha) concentrations were assessed by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance, post hoc Tukey test, and Pearson correlation test. Groups were defined as significantly different when P <0.05. RESULTS: The gingival concentrations of IL-23, -17, -1beta, and -6 and IFN-gamma were significantly greater at moderate CAL sites than at normal-slight CAL sites. Gingival concentrations of IL-23, -1beta, -17, and -6 and TNF-alpha were significantly greater at severe CAL sites than at normal-slight CAL sites. In addition, the gingival concentrations of IL-23, -17, and -6 and TNF-alpha were significantly greater and the gingival concentrations of IL-12 and IFN-gamma were significantly lower at severe CAL sites than at moderate CAL sites. Gingival concentrations of IL-23, -17, -6, and -1beta and TNF-alpha correlated positively with CAL. The IL-23 gingival concentration correlated significantly with IL-17, -1beta, and -6 and TNF-alpha concentrations and correlated negatively with IL-12 and IFN-gamma concentrations. CONCLUSIONS: Our results suggested the possibility that the IL-23/IL-17 immune response was present within chronically inflamed gingiva. This is a host response that had not been reported previously in periodontal disease and may be an important factor in the chronic nature of the disease. This article was published in J Periodontol and referenced in Journal of Clinical & Cellular Immunology

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