ABSTRACT
BACKGROUND AND OBJECTIVE: Epigenetic events, as the DNA methylation, may be related to development of inflammatory diseases. Due to the important role of host's response in the pathogenesis of periodontitis, the purpose of the present study was to investigate the methylation profile of genes related to immune response in gingival tissues from patients with generalized periodontitis (GP) compared to healthy individuals. METHODS: Gingival tissues were collected from 20 individuals with GP and 20 healthy individuals. Genomic DNA was extracted and submitted to enzymatic digestions. An initial screening using a panel of genes involved with the response immune was performed in pools containing six samples of each group. Genes that presented different levels of methylation between the groups were selected for individual assays for validation. RESULTS: The array results showed an unmethylated profile in the majority of genes evaluated in both groups. MALT1, LTB, and STAT5 genes presented a profile of partial methylation in the control compared with GP group. Validation individual assays using a larger number of samples (n = 20, each group) confirmed the hypomethylation of STAT5 in the GP group compared with control group (P < .001). CONCLUSION: Generalized periodontitis is associated with hypomethylation of the STAT5 gene. Further studies are necessary to evaluate the functional impact these findings.
Subject(s)
DNA Methylation , Periodontitis/genetics , Periodontitis/immunology , STAT5 Transcription Factor/genetics , Case-Control Studies , Gingiva , Humans , Promoter Regions, GeneticABSTRACT
Objective: Central giant cell lesions (CGCL) and peripheral giant cell lesions (PGCL) occur in the jaws and containosteoclast-like giant cells and mononuclear cells positive for the macrophage marker CD68. The participationof immune-inflammatory mechanisms has been proposed in the lesions development. As IL-10 is one of the mostimportant anti-inflammatory cytokines and it is also an inhibitory cytokine to macrophage function and boneresorption, the purpose of the present study was to investigate its expression together with its receptor (IL-10Rα)in CGCL and PGCL.Study Design: Six fragments of CGCL and seven fragments of PGCL were obtained by surgical excision. Frozenspecimens were cut and subjected to immunofluorescence staining using fluorescent-labeled anti-CD68, anti-IL-10, and anti-IL-10Rα monoclonal antibodies. Microscopic analyses were performed and the percentage of positivemononuclear and giant cells for each parameter was obtained.Results: Our results revealed that all giant cells from CGCL and PGCL were CD68+ and IL-10Rα+ and that themajority was also positive for IL-10. More than 50% of the mononuclear cells from both lesions expressed IL-10Rα and the majority of these cells were CD68+ and IL-10+.Conclusion: Considering that IL-10 has inhibitory effects on the pathologic processes related to the developmentof the oral giant cell lesions, the high frequencies of cells producing this cytokine seems contradictory to theselesions growth. Investigation about the production of inflammatory cytokines as well as the IL-10 signaling pathwaysin oral giant cell lesions is required to elucidate the immunopathology of CGCL and PGCL (AU)
