Journal
JOURNAL OF CLINICAL PERIODONTOLOGY
Volume 41, Issue 9, Pages 853-861Publisher
WILEY
DOI: 10.1111/jcpe.12286
Keywords
adaptive immunity; gingival tissue; matrix metalloproteinase; periodontitis; RANKL; T-helper cytokines
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Funding
- National Institute of Health [P20GM103538, UL1TR000117]
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Aim: Variations in the expression of cytokines during the progression of periodontitis remain ill-defined. We evaluated the expression of 19 cytokine genes related to T-cell phenotype/function during initiation, progression and resolution of periodontitis, and related these to the expression of soft and bone tissue destruction genes (TDGs). Materials and Methods: A ligature-induced periodontitis model was used in rhesus monkeys (M. mulatta) (n = 18). Gingival tissues were taken at baseline pre-ligation, 2 weeks and 1 month (Initiation) and 3 months (progression) post ligation. Ligatures were removed and samples taken 2 months later (resolution). Total RNA was isolated and the Rhesus Gene 1.0 ST (Affymetrix) used for gene expression analysis. Significant expression changes were validated by qRT-PCR. Results: Disease initiation/progression was characterized by overexpression of Th17/Treg cytokine genes (IL-1 beta, IL-6, TGF beta and IL-21) and down-regulation of Th1/Th2 cytokine genes (IL-18 and IL-25). Increased IL-2 and decreased IL-10 levels were seen during disease resolution. Several Th17/Treg cytokine genes positively correlated with TDGs, whereas most Th1/Th2 genes exhibited a negative correlation. Conclusion: Initiation, progression and resolution of periodontitis involve over-and underexpression of cytokine genes related to various T-helper subsets. In addition, variations in individual T-helper response subset/genes during disease progression correlated with protective/destructive outcomes.
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