Periodontitis and Inflammation: Analysis of Cytokines

Objectives: Periodontitis is initiated by bacterial infection but persists due to an inability to resolve the immune response, leading to chronic inflammation. Th17 pro-inflammatory lymphocytes respond to bacterial and fungal infections and have been implicated in various autoimmune diseases as well as in periodontitis. We hypothesize that IL23/IL17 cytokine axis is involved in periodontitis. We aim to determine the cytokine profile in periodontal gingiva compared to healthy gingiva. A longer term goal is to determine whether polymorphisms in the IL17 and IL23 receptor genes correlate with incidence of periodontitis. Methods: Gingival tissue was collected from patients undergoing extraction and placed in RNA later. RNA was extracted using an MPBio tissue homogenizer and ceramic beads and quantified by 260 nm absorbance. cDNA synthesis with MuLV reverse transcriptase was performed on normalized RNA. Expression of Cytokines IL17, IL23 and IL21 were quantified in triplicate with real-time PCR using SYBR green detection. Quantity is expressed relative to GAPDH gene expression. DNA was isolated from buccal swabs for determination of IL17A and IL23 receptor SNPs. Results: Gingival samples from 3 patients without and 4 patients with periodontitis have been analyzed to date. We find that 3 of the periodontitis patients had elevated IL17 expression compared to control patients. One periodontitis patient also had elevated expression of IL21 and IL23 genes. Conclusions: Our observations are consistent with the hypothesis that inflammation of periodontitis is mediated by the Th17 pathway