## 8 Periodontitis
[132] found that MDA concentration was significantly elevated in the saliva of CP patients compared to periodontitis healthy controls, which is consistent with the results of other studies [133; 211; 115; 116; 116; 129; 130; 134]. However, lipid peroxidation measured as TBARS was significantly higher in the AgP group compared to CP patients [13]. [PERSON] et al. [132] also noticed that MDA concentration in saliva, which was elevated compared to that in serum, indicated a more substantial local enhancement in lipid peroxidation in the periodontitis area. Interestingly, salivary 4-HNE concentration did not reveal any differences between CP and the control group, which the authors explained by dual functions of 4-HNE [132]. On the one hand, 4-HNE may prove increased oxidative lipid destruction; on the other hand, its intensified synthesis may induce an increase in leukocyte count and production of pro-inflammatory prostaglandandins and leukotrienes [135]. Another important fact is that numerous studies have shown a positive relationship between the concentration of lipid peroxidation products and the clinical status of patients [133; 132; 13, 76; 115; 129; 132] as well as a significant reduction in MDA concentration after nonsurgical therapy [132]. Interestingly, in the study by [PERSON] et al. [13], the abovementioned correlations were found only in the AgP group and not in CP patients, which suggests that OS leads to higher intensity of tissue damage in the course of AgP. In the CP group, significant positive correlations were observed between MDA concentration in the saliva and the level of C-terminal telopeptide of type I collagen, i.e., a collagen-related degradation marker used for the assessment of bone resorption [116]. [PERSON] et al. [129] observed a higher concentration of TBARS in the saliva of CP males vs. the control, and a similar--but not statistically significant--trend was observed in females. In our opinion, due to very few women (14 in the CP, 8 in the control group) and men (9 in the CP, 11 in the control group) in both groups, drawing such conclusions is burdened with high risk. As salivary advanced oxidation protein products (AOPP) and advanced glycation end products (AGEs) (markers of carbonyl stress) were not statistically different between the CP and control groups, [PERSON] et al. [129] claimed that lipid peroxidation, not protein oxidation or glycation, is a key mechanism of oxidative damage to periodontal tissues in the course of periodontitis, which is consistent with the results of [PERSON] et al. [24]. Although protein carbonyl concentration (PC, another marker of protein oxidation) in the saliva was significantly higher in the CP vs. AgP group, salivary PC values in the CP as well as AgP patients did not differ from periodically healthy individuals. Moreover, [PERSON] et at. [76] did not find any correlations between salivary AOPP and AGE and PBI in adults as well as children. The results of [PERSON] et al. [120] are in conflict with the above, although their compatibility should be noted in connection with a positive correlation of MDA with clinical parameters. The authors observed significant changes of MDA in gingival circular fluid (GCF) but not in the serum and saliva of CP patients regardless of the therapy, which--according to them--proves that lipid peroxidation level of GCF is qualitatively and quantitively distinct form that in serum and saliva. They also noticed that MDA concentration in GCF was significantly higher than in the saliva, presumably due to the presence of a large number of activated PMNs, which in turn contributed to the higher myeloperoxidase activity [56]. It appears that during the last 10 years the most frequently evaluated DNA oxidative damage parameter was 8-OHdG marker.