Distinctive genes and signaling pathways associated with type 2 diabetes-related periodontitis: Preliminary study

• Published in: PloS one Vol. 19; no. 1; p. e0296925
• Main Authors: Duarte, Poliana Mendes, Gurgel, Bruno César de Vasconcelos, Miranda, Tamires Szeremeske, Sardenberg, Juliana, Gu, Tongjun, Aukhil, Ikramuddin
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 19.01.2024; Public Library of Science (PLoS)
• Subjects: 1-Phosphatidylinositol 3-kinase; Adrenomedullin; AKT protein; Analysis; B cells; Biopsy; Biosynthesis; Care and treatment; Cholesterol; Complications and side effects; Denosumab; Diabetes; Diabetes mellitus (non-insulin dependent); Diabetics; Gene expression; Genes; Genetic aspects; Gum disease; Immunohistochemistry; Inositol phosphate; Inositol phosphates; Inositols; Medical research; Medicine, Experimental; Pathogenesis; Periodontitis; Physiology, Pathological; Prevention; PTPN2 protein; Risk factors; Signal transduction; Teeth; Transcriptomes; Transcriptomics; Transfer RNA; tRNA; Type 2 diabetes; United States; California; United Kingdom > UK; England; United States > US
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0296925

The biological mechanisms underlying the pathogenesis of type 2 diabetes (T2DM)-related periodontitis remain unclear. This cross-sectional study evaluated the distinctive transcriptomic changes between tissues with periodontal health and with periodontitis in patients with T2DM. In this cross-sectional study, whole transcriptome sequencing was performed on gingival biopsies from non-periodontitis and periodontitis tissues from non-diabetic and diabetic patients. A differentially expressed gene (DEG) analysis and Ingenuity Pathway Analysis (IPA) assessed the genes and signaling pathways associated with T2DM-related periodontitis. Immunohistochemistry was performed to validate selected DEGs possibly involved in T2DM-related periodontitis. Four hundred and twenty and one thousand five hundred and sixty-three DEGs (fold change ≥ 2) were uniquely identified in the diseased tissues of non-diabetic and diabetic patients, respectively. The IPA predicted the activation of Phagosome Formation, Cardiac β-adrenergic, tRNA Splicing, and PI3K/AKT pathways. The IPA also predicted the inhibition of Cholesterol Biosynthesis, Adrenomedullin, and Inositol Phosphate Compounds pathways in T2DM-related periodontitis. Validation of DEGs confirmed changes in protein expression of PTPN2 , PTPN13 , DHCR24 , PIK3R2 , CALCRL , IL1RN , IL-6R and ITGA4 in diseased tissues in diabetic subjects. Thus, these preliminary findings indicate that there are specific genes and functional pathways that may be involved in the pathogenesis of T2DM-related periodontitis.