## 4 Discussion
Cytokine IL-17 mRNA expression in the pulp tissue was found to be increased in inflamed dental pulp samples (\(p<0.05\)) [24], the results being in accordance with our findings. The results of the present study are also in agreement with those of [PERSON] et al. [25], who found higher levels of IL-17 in pulp samples of symptomatic teeth using immunohistochemical staining. TNF-\(\alpha\) is a proinflammatory cytokine produced mainly in response to infection, and is released by various cells that take part in the immune-inflammatory process [26]. It can also trigger the formation of the acute-phase inflammation proteins, enhance the toxicity of leucocytes, and stimulate the expression of other proinflammatory cytokines [26]. TNF-\(\alpha\), and other cytokines, can stimulate the formation and secretion of proteolytic enzymes, such as MMPs, which destroy the ECM [27]. TNF-\(\alpha\) can cause vasodilatation and increased permeability of blood vessels with leukocytes extravasation in infected areas [28]. Our results are similar to those of [PERSON] et al. [28], who reported significant higher levels (\(p=0.000\)) of TNF-\(\alpha\) protein in pulp samples from teeth clinically diagnosed with irreversible pulp inflammation compared to healthy pulp samples, using the ELISA technique. TNF-\(\alpha\) gene expression was also studied, showing statistically significant increased levels (\(p=0.002\)) in the study group consisting of irreversible pulpitis samples, as compared to healthy pulps [26]. Another study with similar results was conducted by [PERSON] et al. [29], which reported a significant increase in TNF-\(\alpha\) protein levels in the irreversible stages of pulp inflammation when compared to the control group, using a Multiplex assay (\(p<0.01\)). Although [PERSON] et al. [16] investigated the levels of TNF-\(\alpha\), using ELISA, in pulpal blood obtained from irreversible pulpitis and normal pulps, our results are in accordance with their study. SOD is one of the most important antioxidant enzymes in controlling the concentrations of ROI and, as a result, preventing excessive tissue damage under oxidative stress conditions [30]. Cellular and extracellular components are damaged if a higher production, or lesser removal, of free radicals occurs. Macrophages can produce increased levels of ROI during inflammation, which inactivate the bacteria, but, also, can damage these cells and the nearby tissue, including ECM [9]. SOD acts against free radicals by catalyzing the dismutation of the superoxide ion into oxygen and hydrogen peroxide. SOD exists in 3 isoenzymes: cytosolic Cu, Zn-SOD, mitochondrial Mn-SOD, and extracellular EC-SOD [9]. Conflicting results have been published throughout the years regarding the activity of the SOD enzyme (total, or isoenzymes Cu, Zn-SOD, Mn-SOD) in normal and inflamed dental pulps. Our results are in accordance with the reports of [PERSON] et al. [31], who found significantly elevated levels (\(p=0.0001\)) of Cu, Zn-SOD in inflamed dental pulp samples compared to healthy pulp samples obtained from adult patients. On the other hand, [PERSON] et al. [32] reported no differences in the total activity of SOD in irreversibly inflamed versus healthy pulp samples from children's permanent teeth. The observations of the present study are also similar to those of [PERSON] et al. [30], who found a significant increase (\(p<0.05\)) in both Mn-SOD and Cu, Zn-SOD mRNA expression in cases of irreversible pulpitis, and [PERSON] [33], who also reported an increased immunoreactivity in both SOD isoenzymes in inflamed dental pulp samples using immunohistochemistry. In contrast to these results, [PERSON] et al. [34] observed significantly lower (\(p<0.001\)) Cu, Zn-SOD activity in irreversibly inflamed pulp samples, as comparedto healthy dental pulp samples. The decreased Cu, Zn-SOD activity may be attributed to the progression of inflammation and depletion, or destruction, of the enzyme in oxidative stress conditions. Osteocalcin is a protein produced by osteoblasts during the matrix mineralization phase.