## 4 Discussion
In contrast, IL-10 has not been found in clinically healthy patients, as it is only found in patients with periimplantitis. Similar to the authors' findings, in our study, the highest level of IL-6 was observed in the two patients with the greater MBL loss at one-year follow-up. [PERSON] et al. [37], evaluating peri-implant and gingival samples of patients with failing implants, severe periodontal disease and healthy controls, for TNF-\(\alpha\), IL-1\(\alpha\), IL-6, platelet-derived growth factor A (PDGF-A) and transforming growth factor alpha (TGF-\(\alpha\)), reported much higher levels of TNF-\(\alpha\), IL-1\(\alpha\) and IL-6 in patients with periimplantitis and periodontal compromised patients compared to healthy patients. [PERSON] et al. [10] analyzed the single nucleotide polymorphisms in the IL-2 gene at position \(-330\) and the IL-6 gene at position \(-174\) in 34 patients with failing implants and 40 patients with healthy implants. The analysis established that these genes do not pose a genetic risk and cannot be correlated with early implant failure. [PERSON] and co-workers [38] studied the levels of cytokines (IL-8, IL-1\(\beta\), IL-6, IL-10, TNF-\(\alpha\) and IL-12p70) in the gingival crevicular fluid (GCF) in relation to subginguival bacterial species, for both healthy teeth and implants. The results showed an increase in all cytokines in implants and teeth with high bacterial load. However, inflammatory cytokines (especially IL-1\(\beta\) and TNF-\(\alpha\)) were produced even in sites with minimal bacterial accumulation. The in vitro study by [PERSON] et al. evaluated the fibroblasts of patients with periimplantitis, marginal periodontitis and healthy patients. The results showed that fibroblasts, in patients with periimplantitis and marginal periodontitis, had a pronounced proinflammatory and synthesized higher amounts of IL-6 and IL-8 [39]. Three cytokines were selected to be assessed in the present pilot study: IL-6, IL-8 and TNF-\(\alpha\). IL-6 is a proinflammatory cytokine with a central role in host defense, being produced by many cell types, such as monocytes, macrophages, fibroblasts, endothelial cells, T cells and mast cells [40]. IL-6 plays an important role in T-lymphocyte proliferation, B-lymphocyte differentiation and complement cascade activation, and in addition, can induce bone resorption [10]. Its salivary value is significantly higher in patients diagnosed with periimplantitis or periodontal disease compared to healthy controls [40; 41; 42]. IL-8 is a pro-inflammatory chemokine that may be produced by macrophages, epithelial cells, mesenchymal stem cells (MSCs), mast cells and endothelial cells, near the surface of titanium implants [43; 44]. Its presence was established in periprosthetic tissues with implant debris and was confirmed as a biomarker of peri-implant osteolysis. Moreover, implant debris can induce the production of IL-8 by human osteoblasts [43; 45]. IL-8 attracts activated macrophages and neutrophils (PMNs), and together with osteoclasts, determines bone loss over time [43]. The statistically significant direct correlation between one-year bone loss and the level of IL-8, in spite of the lack of inflammation, could be explained by this mechanism. However, the highest level of IL-6 and IL-8 was observed in patients 4 and 7 from Group 1 (Table 1). The same patients registered significant peri-implant bone loss at one-year follow-up (Table 4), with the pattern of resorption noticed for these two implants leading to qualify them as unsuccessful, according to [PERSON]'s implant success criteria (vertical bone loss less than 0.2 mm/year after the first year post-implantation) [46]. TNF-\(\alpha\), a key biomarker of bone remodeling, was highlighted by several studies as a potential tool for the prognosis and progression of periimplantitis and periodontitis due to its increasing values with disease progression [5; 47]. [PERSON] and co-workers found a significantly higher concentration of TNF-\(\alpha\) in individuals who developed periimplantitis after 5 years [5].