# Influence of Myeloperoxidase Levels on Periodontal Disease: An Applied Clinical Study
## 4 Discussion
In accordance with the results of our study, several studies have been demonstrated that situations which may cause an increase of oxidative stress, such as CVD and periodontal disease, cause the high release of CRP, which in turn, can arouse the production of MPO in saliva and serum in order to defend tissue damage determined by oxidative stress condition [36]. In agreement with the results of the present study, [PERSON] et al. [39] demonstrated that CRP and MPO levels were higher during active phases of periodontal disease. However, while evidence has previously been demonstrated regarding high serum MPO levels as primary mediators of endothelial dysfunction or in the development of cardiovascular risk, from the authors' knowledge, there is no specific evidence to determine MPO levels in saliva in order to evaluate whether the increased expression of salivary MPO levels determines, by reflection, an increase in MPO in serum and then analyzes the salivary levels of MPO as an index of endothelial dysfunction. In this regard, however, it should be noted that this study did not reveal a significant correlation between serum and saliva MPO levels, as salivary MPO levels are influenced in patients enrolled independently only of hs-CRP and total cholesterol. This explanation can be determined by the way that MPO salivary levels may be due to an exclusive local oral production of MPO. In this regard, it should be noted that, from the studies currently present in the literature, while the effect of MPO at a systemic level mediated by the reduction of NO on endothelial damage has been previously highlighted, the impact of MPO activation orally (e.g., in saliva) is less clear. However, there are studies that show that periodontal disease is positively correlated with high levels of NO and therefore with related stress-oxidative damage [19; 24]. The presence of high levels of NO at salivary level can be explained as NO is produced orally in response by the host as a specific salivary defense in the presence of periodontal pathogenic bacteria that are exacerbated during periodontitis [12; 40; 24]. Furthermore, some studies suggested that decreasing activities of NO and some other enzymatic antioxidants, such as superoxide dismutase catalase, were associated with periodontitis and high levels of MPO, whereas others claim that antioxidants function as protective agents against free radicals during CP progression [19; 24; 41]. However, there is no unanimous consensus in the literature on the effects of NO levels on tissue damage during periodontitis. Some reports have shown high levels of NO in periodontal tissue in the active periodontal period [39; 42] while, on the other hand, other authors have shown lower levels of NO in saliva of subjects with periodontal disease [25; 43]. However, results in the literature may have been determined by the different homogeneity of the patients enrolled in the studies, by the different age ranges of the patients analyzed, or by the excessive presence of patients who smoke; in fact it has been shown that smoking can cause a high increase in salivary NO salivary levels [44; 45; 46]. Another explanation for the different results found in the literature can be determined by the different salivary sampling method performed in the different studies. Furthermore, the cause of the different expression of MPO at the salivary and serum level may be due to a different production of NO at the oral level which may be different from the serum one. As an explanation of the results of the present study, it should be highlighted that the dysfunctional damage at the endothelium level found in patients with periodontitis and with CVD can be determined by a specific inflammatory and immune pathway in which MPO modulates a response towards pathogenic bacteria of the oral biofilm which are exacerbated during the active phases of periodontal damage.