## 4 Discussion  
In our sample of 160 patients with 241 dental implants, we evaluated a number of salivary oxidative stress biomarkers (CUPRAC, FRAP, TEACH, AOPP, and TP) and found no significant changes between the groups studied. Statistical analysis revealed no substantial differences between the groups studied. Nevertheless, it must be noted that the review of the literature yielded few studies on the correlation between clinical parameters and oxidative stress in patients of this kind. Saliva contains a variety of substances that can indicate the presence of periodontal disease in its early stages. Oxidative stress, identified as a major factor in the likelihood of developing periodontal issues, is indispensable the progression of this condition through a variety of mechanisms, many of which are still in the process of being fully understood. This relationship has led to the use of salivary oxidative stress biomarker analysis as a valuable diagnostic tool for identifying not only periodontal disease but also a range of systemic and local disorders. Significantly, a well-documented relationship has been established linking periodontal disease to various comorbidities, including diabetes, neurological disorders, rheumatological conditions, cardiovascular diseases, and metabolic syndrome. This link underscores the importance of a comprehensive understanding of oral health in relation to an individual's health and overall well-being [2; 4; 40; 41; 42]  
[PERSON] et al. [43] analyzed 292 subjects (58 with periodontal disease and 234 healthy individuals) to assess the oxidation of DNA, lipids, and proteins. These authors measured 8-OHdG (hydroxyl radical-mediated damage to DNA), 8-epi-PGF2 alfa (lipid peroxidation), protein carboxyl group content (protein oxidation), and TAC (total antioxidant capacity), and recorded a notable augmentation in all of these parameters in the participants with periodontal conditions versus the healthy individuals. [PERSON] et al. [15] analyzed the saliva of 42 patients (19 patients with periodontal disease and 23 healthy), and found that lipid peroxidation in periodontitis appears to be caused by an augmented production of reactive oxygen species (ROS) in males and a decrease in antioxidant status in females. The research of [PERSON] et al. [14] identified the mean levels of malondialdehydeehyde (MDA), a lipid peroxidation biomarker, to differ significantly between healthy patients and those with periodontitis, with confirmation of increased ROS production on the part of the inflammatory cells in periodontitis. \begin{table}
\begin{tabular}{c c c c c} \hline \hline  & \multicolumn{2}{c}{**Risk of Implant Failure**} & \multicolumn{2}{c}{**Univariant Logistic Regression**} \\ \cline{2-5}  & **No** & **Yes** & **OR (IC 95\%)** & \(p\)**-Value** \\ \hline Group. \(n\) (\%) & & & & \\ Healthy & 112 (92.6) & 9 (7.4) & & \\ Periodontitis & 112 (93.3) & 8 (6.7) & 0.89 (0.33–2.39) & 0.815 \\ Location. \(n\) (\%) & & & & \\ Mandibula & 103 (92) & 9 (8) & & \\ Maxilla & 121 (93.8) & 8 (6.2) & 0.76 (0.28–2.03) & 0.580 \\ Years implant placement. mean (St) & 2.8 (2.1) & 3.6 (3.5) & 1.14 (0.95–1.38) & 0.168 \\ Width (mm). mean (St) & 3.85 (0.38) & 3.8 (0.37) & 0.71 (0.19–2.62) & 0.603 \\ Length (mm). mean (St) & 10.2 (1.1) & 10 (1) & 0.84 (0.52–1.34) & 0.461 \\ Mesiovestibular probing. mean (St) & 2 (1) & 2 (1) & 1.35 (0.91–2.02) & 0.138 \\ Bleeding. \(n\) (\%) & & & & \\ No & 214 (93.4) & 15 (6.6) & & \\ Yes & 10 (83.3) & 2 (16.7) & 2.85 (0.57–14.22) & 0.201 \\ \hline \hline \end{tabular} St = standard deviation.  
\end{table} 
Table 7: Results in relation to the presence of peri-implantitis. [PERSON] et al. [44] reported that non-surgical therapies can rehabilitate and regulate the patient's antioxidant capacity by modifying salivary oxidative stress markers such as MDA, total oxidative stress, and superoxide dismutase (SOD). [PERSON] et al.