## 4 Discussion  
In recent years, several authors [6; 26; 27; 28] have focused their research on the diagnosis of peri-implant disease, its evolution, treatment and comparison to periodontal disease. Thus, various studies have been conducted [29; 30; 31] on immunological markers in saliva, oxidative stress [16], the volume and composition of the peri-implant crevicular fluid (PCF), the oral microbiota and its influence on the peri-implant/ periodontal condition and disease progression. Despite the promising results and the advantages of using salivary biomarkers, studies evaluating the prognosis of bone resorption/remodeling around implants with the aim of predicting the risky patients, prior to the occurrence of inflammatory disease, are scarce. Therefore, the aim of the present pilot study was to evaluate some proinflammatory cytokines, the total antioxidant status and LDH in saliva to see if the level of such parameters could predict bone loss around osseointegrated implants. Moreover, due to the lack of periodontal ligaments, acting as a cellular and vascular network, comprising mesenchymal cells of diverse differentiation levels, epithelial cell rests of Malassez, along with neural and inflammatory cells, serving as defense and \begin{table}
\begin{tabular}{c c c c c c c c c} \hline \hline \multirow{2}{*}{**mm**} & \multicolumn{8}{c}{**Group 1**} \\ \cline{2-9}  & **1** & **2** & **3** & **4** & **5** & **6** & **7** & **Mean (\(\pm\)SD)** \\ \hline Mean MBL (\(\pm\)SD) & 0.07 (\(\pm\)0.01) & 0.07 (\(\pm\)0.04) & 0.08 (\(\pm\)0.01) & 1.0 (\(\pm\)0.17) & 0.05 (\(\pm\)0.02) & 0.02 (\(\pm\)0.01) & 0.85 (\(\pm\)0.09) & 0.32 (\(\pm\)0.45) \\ \hline \hline \end{tabular}
\end{table} 
Table 4: Peri-implant marginal bone loss (MBL) measured between baseline (same day as saliva collection) and one-year follow-up. Figure 4: Analysis of correlation between one-year peri-implant bone loss (MBL) and the amount of IL-6, IL-8 and TNF-\(\alpha\) (tumor necrosis factor), total antioxidant activity (TAS) and salivary lactate dehydrogenase levels (LDH) for patients included in Group 1. The positive correlation is displayed in red and the negative correlation in blue. repair mechanisms, the dental implants are more prone to more rapid progression of bone resorption, compared to natural teeth [32; 33]. Therefore, an early diagnosis, or even better a warning in vulnerable patients who need to be closely monitored, is required. Additionally, scientific evidence for a specific bacterial biofilm composition responsible for the onset and progression of perimplantitis could not be proven. The installation of periimplantitis might depend on risk factors and the systemic condition [34], and therefore an early diagnosis of a predisposition \"pattern\" is more than welcome. Lately, saliva has become the focus as a noninvasive diagnostic fluid for oral and systemic diseases, due to its great accessibility and its non-invasive, easy and low-cost collection [19]. Many inflammatory mediators associated with peri-implant mucositis and periimplantitis, such as IL-6, IL-8, MMP-8 (matrix metalloproteinase 8), IL-1\(\beta\) and TNF-\(\alpha\), have been identified as potential biomarkers [35]. [PERSON] et al. [36] analyzed the utility of cytokines such as interleukin IL-6 and IL-10 as markers for periimplantitis. Interleukins are multifunctional proteins and glycoproteins that control intercellular relationships both locally and systemically. They are produced by immunocompetent cells such as T cells, monocytes or inflammatory infiltrates. The samples were obtained from fully edentulous patients, with at least two functional implants inserted in the mandible, but also from clinically healthy patients (control group). The results showed that there is a large difference between IL-6 and IL-10 concentrations in patients with periimplantitis compared to clinically healthy patients. Some clinically healthy patients have slightly elevated levels of IL-6.