Comparison of transcriptomes of tissue samples from chronic and aggressive periodontitis patients

Comparison of Transcriptomes of Tissue Samples from Chronic and Aggressive Periodontitis Patients The destruction in periodontal disease begins with a bacterial challenge that triggers the immune response of a susceptible host. Genetic factors modulate how individuals interact with many environmental agents, including biofilm, to determine periodontitis susceptibility. Based on the hypothesis that there may be differences in the tissue response of aggressive and chronic periodontitis, which are combined under the title of "periodontitis" according to the 2017 periodontal disease classification, and that there may be differences in gene expressions due to the genetic background even if clinical improvement is observed, the aim of our study is; to reveal the similarities and differences between these two diseases at the level of gene expression by comparing the transcriptomes of the tissue samples obtained in the active period of the disease and in the period of clinical improvement in patients with aggressive and chronic periodontitis. Among the microarray datasets that were diagnosed with periodontitis and studied on gingival tissue in the GEO database, using the keywords "Periodontitis", "Homo sapiens", "gingival tissue", the datasets were found among the results obtained by selecting the study type "expression profiling by sequence". Pairwise comparisons of sample groups in the GEO2R were performed for the four datasets GSE79705, GSE10334, GSE16134 and GSE23586 that met the inclusion criteria. Venn diagram was used to identify overlapping and non-shared genes within the identified DEGs. Differential gene expression (fold change), gene ontology (GO; biological process), pathway enrichment and protein-protein interaction network analyzes were performed. An increase in the expression of genes (NDUFA1, NDUFA11, NDUFA12, NDUFA13, NDUFA2, NDUFA3, NDUFA7, COX7A2, COA6, ROMO1) associated with mitochondrial activity, oxidative phosphorylation and ROS production was observed in healthy tissues with a history of aggressive periodontitis. In addition, in common with the active disease period; antigen processing and presentation, osteoclast differentiation, apoptosis, NK-mediated cytotoxicity-related genes (IL-6, TLR2, IFNAR1, TNFSF11, LY96, CD40, FCGR2A) increased expression, while decreased expression of epithelial differentiation, epithelial development, cell-cell signaling was observed. In healthy tissues with a history of chronic periodontitis, there was no increased response to inflammatory processes, but decreased expression of pathways related to antigen processing and presentation, regulation of leukocyte-mediated cytotoxicity, and systemic processes. The increase in the expression of inflammatory response-related genes in healthy tissues with a history of aggressive periodontitis, similar to the active disease period, revealed that although it is clinically healthy, it can no longer be considered healthy in terms of tissue response. Keywords: aggressive periodontitis, chronic periodontitis, comparative transcriptome analysis