## 1 Introduction  
Implant-anchored restorations have become, over the years, a very predictable alternative to conventional prosthetic restorations [1]. Although it is generally considered a safe, risk-free surgical procedure, with a high success rate, inserting an implant can lead to immediate failure, depending mostly on the surgical technique used, or late failure due to complications occurring over time [2]. Most of the complications can be solved without problems when diagnosed early. However, in some cases, an inflammatory process can lead to implant and bone loss or other, more severe, complications such as mandible bone fracture or oronatral communications [3, 4].  
Peri-implant inflammation manifests itself as peri-implant mucositis, a reversible inflammation of peri-implant soft tissues around a functional dental implant with bleeding on gentle probing, increased probing depth, erythema and/or suppuration and perimplantitis, with additional irreversible loss of hard and soft tissues around the implants, recession of the mucosal margins and radiographic detectable bone loss [5; 6; 7].  
The mechanisms of peri-implant mucositis and periimplantitis are mostly based on biofilm-induced inflammatory lesions around dental implants. The host reaction, reflected by the intensity of the inflammatory response to bacterial products, is crucial in the peri-implant bone destruction. [PERSON] and [PERSON] [8] examined the survival rate of implants and observed a small number of patients losing many implants. Based on this finding, they estimated that patients who had one implant lost were 1.3 times more likely to lose more implants. This observation led to the hypothesis that host factors affect implant survival, and therefore, genetic predisposition may be involved in the development of periimplantitis. Most of the recent studies highlighted that the polymorphisms of cytokines play a vital role in the immune response, but no decisive results have been shown to recommend genetic testing prior to implants' insertion [9; 10].  
Cytokines are, however, considered as markers of inflammation, with the immune response to plaque pathogens being regulated by the balance between pro- and anti-inflammatory cytokines [11]. These mediators are also involved in modulating osteoclast and maintaining bone homeostasis by regulating osteoclast and osteoblast differentiation and activation [12]. Their identification and dosage could, therefore, predict peri-implant bone remodeling.  
As oxidative stress and inflammatory processes lead to tissue destruction, and extracellular lactate dehydrogenase (LDH) is a marker of cell death and tissue degradation, its level in saliva is a useful biomarker for periodontal disease diagnosis and monitoring [13].  
The increased oxygen consumption in the inflammatory process will determine the overproduction of free radicals, leading to the damage of oral tissue cells. Normal saliva contains enzymatic and non-enzymatic antioxidants for neutralizing the free radicals, and their concentration is claimed to be significantly decreased in periodontal patients compared to healthy individuals [14; 15; 16].  
Due to its great accessibility, requiring non-invasive collection methods, saliva is a very good tool in assessing and diagnosing different oral and systemic diseases, has high availability, is painless and does not require special equipment for collection [17].  
There are several studies investigating the salivary concentration of cytokines in the cases of peri implantitis [5; 18; 19]. However, studies predicting disease, mainly marginal bone loss (MBL), an essential component of prevention, are scarce.  
The aim of this pilot study was to measure total antioxidant status, the amount of IL-6, IL-8 and TNF-\(\alpha\) (tumor necrosis factor), salivary lactate dehydrogenase levels and the correlation with one-year peri-implant bone loss.