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Aim To investigate the effects of N‐acetyl cysteine (NAC), Biodentine, ProRoot MTA and their combinations, on cell viability, mitochondrial reactive oxygen species (mtROS) production, mineralization and on the expression of genes related to inflammatory cytokine production, mitochondrial dynamics and cell apoptosis of lipopolysaccharide (LPS)‐induced human dental pulp cells (hDPCs). Methodology Isolated hDPCs were exposed to 20 μg mL−1 of Escherichia coli (E. coli) LPS for 24 h, before the experiment, except for the control group. Eight experimental groups were assigned: (i) control (hDPCs cultured in regular medium), (ii) +LPS (hDPCs cultured in LPS medium throughout the experiment), (iii) −LPS/Media, (iv) −LPS/BD, (v) −LPS/MTA, (vi) −LPS/NAC, (vii) −LPS/BD + NAC and (viii) −LPS/MTA + NAC. Cell viability was measured using Alamar blue assay at 24 and 48 h. Production of mtROS was evaluated at 6 and 24 h by MitoSOX Red and MitoTracker Green. The expressions of IL‐6, TNF‐α, Bcl‐2, Bax, Mfn‐2 and Drp‐1 genes were investigated at 6 h using reverse transcriptase‐polymerase chain reaction (RT‐PCR). For differentiation potential, cells were cultured in the osteogenic differentiation media and stained using Alizarin red assay at 14 and 21 days. The Kruskal–Wallis test, Mann–Whitney U test and one‐way anova were performed for statistical analysis. Results NAC was associated with significantly greater LPS‐induced hDPC viability (P < 0.05). Both Biodentine and MTA extracts promoted cell survival, whereas the combination of NAC to these material extracts significantly increased the number of viable cells at 24 h (P < 0.05). Biodentine, MTA or NAC did not alter the mtROS level (P > 0.05). NAC supplementation to the MTA extract significantly reduced the level of IL‐6 and TNF‐α expression (P < 0.05). Regarding mitochondrial dynamics, the use of NAC alone promoted significant Mfn‐2/Drp‐1 expression (P < 0.05). Most of the groups exhibited a level of Bcl‐2/Bax gene expression similar to that of the control group. The increases in mineralization productions were observed in most of the groups, except the LPS group (P < 0.05). Conclusions The antioxidant effect of NAC was not evident under the LPS‐induced condition in DPC in vitro. NAC combined either with Biodentine or MTA improved LPS‐induced hDPCs survival at 24 h. The combination of NAC with MTA promoted mineralization.

Long-term consumption of a high-fat diet (HFD) causes not only obese-insulin resistance, but is also associated with mitochondrial dysfunction in several organs. However, the effect of obese-insulin resistance on salivary glands has not been investigated. We hypothesized that obese-insulin resistance induced by HFD impaired salivary gland function by reducing salivation, increasing inflammation, and fibrosis, as well as impairing mitochondrial function and calcium transient signaling. Male Wistar rats (200–220 g) were fed either a ND or an HFD (n = 8/group) for 16 weeks. At the end of week 16, salivary flow rates, metabolic parameters, and plasma oxidative stress were determined. Rats were then sacrificed and submandibular glands were removed to determine inflammation, fibrosis, apoptosis, mitochondrial function and dynamics, and intracellular calcium transient signaling. Long-term consumption of an HFD caused obese-insulin resistance and increased oxidative stress, fibrosis, inflammation, and apoptosis in the salivary glands. In addition, impaired mitochondrial function, as indicated by increased mitochondrial reactive oxygen species, mitochondrial membrane depolarization, and mitochondrial swelling in salivary glands and impaired intracellular calcium regulation, as indicated by a reduced intracellular calcium transient rising rate, decay rates, and amplitude of salivary acinar cells, were observed in HFD-fed rats. However, salivary flow rate and level of aquaporin 5 protein were not different between both groups. Although HFD consumption did not affect salivation, it caused obese-insulin resistance, leading to pathophysiological alteration of salivary glands, including impaired intracellular calcium transients, increased oxidative stress and inflammation, and salivary mitochondrial dysfunction.

Our findings suggest that an increase in peripheral innervation may lead to increased inflammation, which is part of the immunopathogenesis of OLP. Differences in nociception between OLP-R and OLP-E arise from the pathogenesis of each lesion, not from the differences in peripheral innervation.

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