## 4 Discussion
[45] likewise found that the decrease in inflammatory response following periodontal treatment improves host antioxidant capacity measured both in saliva and in gingival crevicular fluid. [PERSON] et al. [46] indicated a notable decrease in 8-OHdG levels in individuals with chronic periodontitis following initial periodontal treatment. [PERSON] et al. [47] found that adequate periodontal treatment exerts a regulatory effect upon the oxidative stress levels as measured by the markers MDA and glutathione peroxidase (GSHpx). In our research, all individuals with periodontal disease were part of a periodontal maintenance program. Therefore, we believe that the lack of significant differences in salivary biomarker levels can be attributed to the fact that these individuals were not experiencing an acute or uncontrolled phase of the disease. On the other hand, increased oxidative stress levels are one of the causes underlying peri-implant disease, and treatment strategies designed to reduce oxidative stress potentially could contribute to managing peri-implant disease. [PERSON] et al. [27] observed that patients undergoing regular periodontal and implant maintenance were less likely to suffer peri-implantitis than individuals without such maintenance. [PERSON] et al. [29] in turn found salivary total antioxidant status (TAS) and the concentrations of uric acid and ascorbate were reduced significantly in individuals with peri-implant disease. This might suggest that the elevated generation production of ROS in peri-implant disease leads to a situation of excessive oxidative stress, which may be an important contributor to peri-implant tissue destruction. [PERSON] et al. [8] measured the SOD and GSHpx levels in healthy subjects and with peri-implantitis and found both markers to be markedly reduced in the individuals with peri-implantitis, evidencing a lesser capacity to combat cellular oxidative stress in these individuals. Of the 241 implants analyzed in the present study, only 7% presented some degree of peri-implant disease, and we found no changes in the salivary oxidative stress (CUPRAC, FRAP, TEACH, AOPP, and TP) between groups. This finding aligns with the results found by [PERSON] et al. [22] who measured SOD, MDA, and TAC levels in crevicular fluid and concluded that the concentrations of these three oxidative stress markers were unable to differentiate between health and peri-implant disease. The significant variability in current studies prevents us from drawing solid and definitive conclusions regarding the effectiveness of salivary biomarkers as diagnostic tools. Therefore, it is essential to enhance and conduct more research in this field. To date, no individual biomarker or conjunction of biomarkers can effectively evidence tissue destruction in the context of periodontitis and peri-implantitis, and it is still necessary to objectively identify new promising biomarkers. Until then, clinical assessment remains the method of choice. Periodontitis is a chronic disorder, and affected patients must prioritize oral hygiene. The likelihood of recurrence remains very elevated, and strict adherence on the part of the patients is necessary [19; 20; 21]. In the patients with periodontal disease, the plaque index values were significantly greater than in the healthy individuals. Adequate hygiene among patients with periodontal problems is complicated by the presence of subgingival bone defects and by the existence of enlarged interdental spaces [20]. On the other hand, our data evidence a significantly greater prevalence of smoking among patients with periodontitis (37.5%) versus healthy patients (17.5%). i.e., smokers were 2.31 times more likely to suffer periodontal disease. Smoking significantly influences bone loss around dental implants, a key risk factor. There is a debate in the scientific literature about how smoking affects early implant complications, such as postoperative infection and bone loss at the implant site.