Introduction: During pregnancy, even a local response due to a localized infection like periodontitis can initiate the immune response cascade, leading to premature uterine contraction, thereby causing preterm delivery. Hence, the present study assesses the common pathways involved in periodontitis and preterm delivery. Materials and methods: Differentially expressed genes (DEGs) of periodontitis and fetal inflammation were identified from the datasets retrieved from the Gene Expression Omnibus Database. GeneMANIA was used to visualize molecular interaction networks. By ranking the scores of each node of molecular interaction, the important nodes of protein interactions were obtained. The hub genes were ranked and those with degree ≥ 20 were selected. A network of genes and their co-expression genes were analyzed. Gene ontology of the corresponding genes was also assessed. Results and discussion: 10 gene sets were significantly enriched in periodontitis samples. The most significant biological process for upregulated genes involved cytokine mediated signaling pathway, inflammatory response and chemokine signaling pathway. The most significant upregulated genes under KEGG pathway analysis are involved in cytokine-cytokine receptor interaction, viral protein interaction with cytokine-cytokine receptor and chemokine signaling pathway. Conclusions: The present study has attempted at highlighting a biological basis for common pathways occurring in both conditions: periodontitis and preterm labor. It also gives us insight into what treatment modalities must be administered to pregnant women, to reduce the chance of fetal inflammation and complications in pregnancy.
Keywords:- differentially expressed genes
- fetal inflammation
- periodontitis
- preeclampsia