## 4 Discussion
The taper interface in the internal conical connection resists the loading and allows stable retention of position by frictional force [12; 14; 28]. Lateral forces are dissipated by the lateral wall of morse taper abutments, which also protects the abutment screw from excessive stress [12; 14; 28]. Remarkably, platform switching may also influence the location and the reestablishment of the biological width after implant placement, minimizing the marginal bone resorption [12]. This hypothesis is because the distance between the implant-abutment, micro gap contamination, and the crestal bone can be increased by a narrower abutment, controlling bone remodeling and contributing to the adequate formation of biological width [16; 29]. These data are in line with the results of this trial that showed that a smaller abutment compared to those with a diameter equal to that of the implant can produce an area responsible for reducing the invasion of the biological width [30]. Concerning the molecular analysis performed in the current study, test implants presented reduced levels of pro-inflammatory mediators (IFN-\(\gamma\), TNF-\(\alpha\), IL-6, IL-17, IL-21, IL-23, and IL-33) at 24 months compared to the control group (\(p<0.05\)). These results are supported not only by the tomographic data of this RCT, which demonstrated greater alterations in the crestal bone in control implants, but are also consistent with our clinical outcomes that showed higher PPD in this experimental group until 12 months (\(p<0.05\)). Even though the clinical data obtained during this investigation suggest, in general, a low percentage of peri-implant inflammation sites in both implant groups, it could be speculated that the control group presents an at-risk-for-harm condition due to the pro-inflammatory pattern of local molecules observed, and this condition could predispose to peri-implantitis [31]. This disturbance in local levels of pro-inflammatory mediators in implants with an external hexagonal and standard connection seems to be exacerbated with time since, in this trial, control implants showed higher levels of pro-inflammatory molecules IFN-\(\gamma\), TNF-\(\alpha\), IL-6, IL-17, IL-21, IL-23, and IL-33 at 24 months in comparison with baseline (\(p<0.05\)). Furthermore, IL-6, IL-17, IL-21, and TNF-\(\alpha\) were up-regulated at 24 months in control implants in comparison with 12 months (\(p<0.05\)). Importantly, previous data confirm that the peri-implant fluid augmented the presence of IL-6 and IL-33 in intensifying the local inflammatory process, contributing to the risk of peri-implantitis [32; 33]. Accordingly, a significantly positive association between IL-6 levels in the saliva and peri-implant disease was observed [34]. Another important pro-inflammatory marker that was up-regulated in control implants in this study was TNF-\(\alpha\), a well-established mediator related to peri-implantitis-related bone loss [35]. Remarkably, both TNF-\(\alpha\) and IL-17 are related to osteoclast formation and bone resorption, including around dental implants [36]. The biochemical outcomes of peri-implant crevicular fluid may characterize biological processes in peri-implant tissues and, according to our results, it could be assumed that external hexagonal implants placed at crestal bone level with a standard platform could harmfully modulate the local pattern of inflammatory markers in the crevicular fluid of implants, even in clinical situations of health, encouraging peri-implant bone loss. Given that a tendency to develop peri-implant diseases and complications is observed in diabetic patients [37; 38], the benefits of the use of the platform-switching concept in this patient profile could be extrapolated to, or at least be useful in, the implant success over time in type 2 diabetic individuals. However, it is necessary to highlight that one limitation of the study could be the specificity of this trial population (Brazilian ethnicity), and other populations could respond in a different pattern.