Observation of Inflammation, Oxidative Stress, Mitochondrial Dynamics, and Apoptosis in Dental Pulp following a Diagnosis of Irreversible Pulpitis.

Abstract

Mitochondrial dynamics play a pivotal role in maintaining the homeostasis of the dental pulp. Inflammation and oxidative stress can trigger changes in mitochondrial dynamics, leading to cell death in the dental pulp. This study aimed to investigate inflammation, oxidative stress, mitochondrial dynamic alterations, and cell death in inflamed pulpal tissues compared to healthy pulp tissues. Pulpal tissues were collected (n=15 per group) from: 1) healthy people as the control and 2) people with clinically diagnosed irreversible pulpitis. Proteins indicating inflammation, oxidative stress, mitochondrial dynamics, and cell death markers were investigated by western blot analysis. A Student's t-test was used to analyse differences between the healthy and irreversible pulpitis groups. A probability of 0.05 was used to indicate statistical significance (p<0.05). The expression of the proteins, tumour necrosis factor-alpha (TNF-α) and nuclear factor kappa-lightchain-enhancer, by activated B cells (NF-κB) from inflamed pulp tissues were significantly higher than those of control. Compared to controls, 4 hydroxynonenal (4HNE) and dynamin-related protein 1 (Drp1) were significantly higher, while mitofusin 2 (MFN2) and optic atrophy type 1 (OPA1) were significantly lower in inflamed pulp tissues. Bcl-2-associated X protein (Bax), cleaved caspase-3, and cytochrome c were significantly higher in inflamed pulpal tissues compared to controls. In inflamed pulpal tissues, we found a significant increase in the expression of receptor-interacting serine or threonine-protein kinase 1 (RIPK1) but not receptor-interacting serine or threonine-protein kinase 3 (RIPK3). Irreversible pulpitis is associated with inflammation, oxidative stress, alterations in mitochondrial dynamics, and apoptosis in pulpal tissues. (EEJ-2022-01-014).