## 9 Conclusions  
The role of OS in caries and periodontitis is not entirely understood despite many decades of studies on its role in etiopathology of these conditions. So far, numerous papers have been published to prove the potential of OS markers for screening, diagnosis and monitoring of the progress of the said diseases, but none of these methods has proven suitable for routine clinical use. From the point of view of research on the role of OS in oral diseases, an important issue is the lack of specificity--both in diagnosis and treatment. Until now, the source of free radical production is not entirely clear. Numerous reports indicate PMNs as the main source of ROS and RNS, while other researchers indicate the key contribution of bacteria (cariogenic and periopathogenic) in the development of OS in the course of caries and periodontitis [153; 154; 155]. Significant limitations of the studies conducted so far include very different methodology of biochemical tests, low number of patients in study groups, adoption of quite varied definitions of caries and periodontitis, lack of unambiguous divisions of the severity of caries and periodontitis and lack of assessment of the influence of caries and periodontitis duration as well as incomplete eradication of local and general factors affecting the tested antioxidant activity. Therefore, it is necessary to unify the inclusion and exclusion criteria of study subjects and formulate a new classification of caries and periodontitis which will more precisely and uniformly rank the severity of the disease. These solutions may enable, inter alia, the use of antioxidants in the prevention and treatment of oral diseases. Conceptualization, A.S.-R. and A.Z. ; methodology, A.S.-R. and A.Z. ; software, A.S.-R. and A.Z. ; validation, A.Z. ; formal analysis, A.Z. ; data curation, A.S.-R. and A.Z. ; writing--original draft preparation, A.S.-R. and A.Z. ; writing--review and editing, A.S.-R. and A.Z. visualization, A.S.-R.; supervision, A.Z. All authors have read and agreed to the published version of the manuscript. This work was supported by grant from the Medical University of Bialystok, Poland (grant number: SUB/1/DN/20/002/1209). \begin{table}
\begin{tabular}{l c c c} \hline \hline
**Patients** & **Analyzed Parameter** & **Results** & **Source** \\ \hline Study group: & & & \\ -242 people with CP (151 women, & & & \\ 91 men), at the age of 48-93, including: & & & \\ * group I (stage of advancement CP), & & & \\ n = 85, & & & \\ * group II (I stage of advancement CP), & & & \\ n = 79, & & & \\ * group III (III stage of advancement & & \\ CT), n = 32, & & & \\ * group IV (IV stage of advancement & & \\ CP), n = 23. & & & \\ \hline Study group: & & & \\ -20 people with gingivitis (12 women, & & \\ 8 men), at the age of 33.9 \(\pm\) 8.38, & & & \\ -20 people with CP (11 women, 9 men), & & & \\ at the age of 42.65 \(\pm\) 8.04. & & & \\ Control group: & & & \\ -20 generally healthy people (10 women, & & \\
10 men), at the age of 29.9 \(\pm\) 2.17. & & & \\ \hline
4-HNE—4 hydroxynonenal; 8-OHdG—8-hydroxy-2-deoxyguanosine; AGE—advanced glycation end products; AgP—aggressive periodontitis; ALB—albumin; AOPP—_advanced oxidation protein products_; BOP—bleeding on probing; CAT—catalasize; CP—chronic periodontitis; CuZnSGD—copper/azine SOD; FRAP—ferric reducing antioxidant power assay; GC—ggnistical vehicular fluid; GP—glutathione peroxidase; GR—glutathione reductase; MDA—malondialdehydehyde; MnSGD—manganese SOD; MPO—manguregoperoxidase; ns—mongignificant; NO—nitric oxide; NS—nonstimulated saliva; OHI—oral hygiene index; OSI—_oxidative stress_ index; PBI—papilla bleeding index; PD—pocket depth; PI—plaque index; SOD—superoxide dismutase; SRP—_scaling and root planning; SS—_stimulated saliva; TAC—total antioxidant capacity; TBARS—thiobarbituric acid reactive substances; TOS—_total oxidant status_; UA—uric acid. \(\uparrow\) increase \(\downarrow\) decrease. & \\ \hline \hline \end{tabular}
\end{table}