Expression of chronic pain genes in apical periodontitis tissues

• Published in: International endodontic journal Vol. 56; no. 8; pp. 991 - 999
• Main Authors: Francio, Jordano, Neves, Glaucia T., Souza, Leticia C., Carneiro, Everdan, Silva, Renato M., Letra, Ariadne
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.08.2023
• Subjects: apical periodontitis; Chronic pain; endodontic pathosis; Gelatinase B; Gene expression; Gum disease; Periodontal ligament; Periodontitis; Tissue inhibitor of metalloproteinase 1; chronic pain; endodontic pathosis; apical periodontitis; gene expression
• ISSN: 0143-2885; 1365-2591
• DOI: 10.1111/iej.13932

Aim To evaluate the expression of genes involved in chronic pain conditions in apical periodontitis (AP) tissues. Methodology An electronic search was performed in Scopus and MEDLINE (via PubMed) databases to identify articles (n = 173) related to genes involved in chronic pain conditions. Full‐text reviews of the selected articles allowed the prioritization of 16 genes to be investigated with regards to their expression in AP tissues. Periapical lesions (n = 42) were collected during surgical endodontic procedures and processed for mRNA extraction and investigation of target genes via RT–qPCR. Healthy periodontal ligament tissues obtained from third molar extractions were used as controls. Relative levels of target gene expression in AP and control tissues were normalized to GAPDH expression and compared using the 2−ΔΔCt method. Data analysis was performed using the Mann–Whitney U test with a statistical significance threshold set at p < .05. Results mRNA expression levels of MMP9, TIMP1, TNFA, CAMK4 and COMT were significantly increased in AP tissue samples compared with controls (p < .05). Positive correlations were observed between the expression of TIMP1 with COMT and CAMK4, TNFA with TIMP1 and CAMK4, COMT with CAMK4. Conclusions This study confirms the upregulation of MMP9, TIMP1, TNFA in AP tissues and reports for the first time, the expression of CAMK4 and COMT as suggestive of their involvement in AP pathogenesis.