## 1 Introduction  
Dental implants are now considered as an effective and predictable treatment modality for the functional and aesthetic rehabilitation of either partially or completely dedentulous patients [1, 2]. This rehabilitation method has a success rate of more than 90% for implants in function for more than five years [3]. However, despite the high success rates associated with implant rehabilitation, biological complications may arise in the peri-implant soft tissues, such as peri-implantitis, which can compromise the permanence of the implant [4]. Peri-implantitis is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and progressive loss of supporting bone [5; 6]. This definition is in accordance with the more recent classification of periodontal and peri-implant diseases (American Academy of Periodontology--AAP and European Federation of Periodontology--EFP 2018) [6]. According with the Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions, there is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis, which is assumed to precede peri-implantitis [6]. Data indicate that patients diagnosed with peri-implant mucositis may develop peri-implantitis, especially in the absence of regular maintenance care. However, the features or conditions characterizing the progression from peri-implant mucositis to peri-implantitis in susceptible patients have not been identified [6]. With a growing number of dental implants inserted, the potential number of sites for implant-associated diseases increases [7]. But the actual value of the incidence/prevalence of this disease is uncertain since the method of classifying peri-implantitis has varied between authors over the years and, in addition, few studies follow up and evaluate the sample for several years [8]. The characteristics of the populations included also vary between studies, which may influence the results [8]. In a systematic review carried out by [PERSON] et al., the prevalence of peri-implantitis obtained per patient was 18.8% while the prevalence per implant was 9.6% [9]. [PERSON] et al. conducted a systematic review and meta-analysis, that included forty-seven articles, and concluded that the mean prevalence of peri-implantitis, at implant and subject level was 9.25% and 19.83%, respectively [10]. There are some similar features in the sequence of immunopathological events in peri-implant and periodontal infections [11]. Both are initiated primarily by Gram-negative anaerobic bacteria, while the inflammatory process goes faster and deeper around implants than around natural teeth and thus is a more significant problem for patients with dental implants [12]. However, [PERSON] et al. in a study in which the transcriptome profiling using mRNA from patients suffering from either peri-implantitis or periodontitis was compared, the authors observed that these two pathologies react in a different way [13]. These differences may be explained by the anatomy, which is very different comparing the scar tissue in peri-implantitis with the specialized fibers inserting the surface of the teeth. In peri-implantitis tissue, transcripts associated to innate immune responses, and defense responses were dominating, while in periodontitis tissues, bacterial response systems prevailed [13]. Research evidence indicates that implant complications tend to be clustered in a subset of individuals rather than being randomly distributed in the population implying that patient's host response might play a role for the implant success [14; 15]. Interleukin-1 (IL-1) is the pivotal mediator of the immune-inflammatory response that acts both in response to bacterial infection and in bone metabolism [16].