# Peri-Implant Tissue Behaviour Next to Different Titanium Surfaces: 16-Year Post-Trial Follow-Up
In a recent systematic review of the Literature, [PERSON] et al. [3] underlined the osteogenic potential of rough dental implant surfaces, the latter facilitating the migration, adhesion, and proliferation of osteogenic and fibrobl cells. A consensus report published in 2009 stated that \"moderately rough and rough surfaces provide enhanced bone integration compared with smooth and minimally rough surfaces\" [13]. There is an increasing promotion of new engineered designs of implant surface, and several techniques are available today to increase surface roughness. Among the physical modifications the following can be cited: sandblasting, plasma spray, magnetron co-sputtering, wire electrical discharge machining, thermal treatment, laser surface modification, non-thermal plasma and ultraviolet (UV) functionalization, etc. [14; 15]. In the present study, acid-etched surfaces were used. Acid etching by strong acids is a commonly used chemical treatment to increase roughness and modify surface properties. According to a recent study by [PERSON] et al. [16], dual acid-etched (DAE) surfaces increased peri-implant endosseous healing properties in the native bone of the examined posterior maxilla, showing improved histological behaviour and histomorphometric bone response, and higher rates of removal torque, in comparison to machined surfaces. It has been estimated that implant osseointegration is achieved when implant surface roughness is at least 1-1.5 \(\upmu\)m [3]. However, at the same time, the increased roughness can facilitate bacterial adhesion and biofilm accumulation, especially in case of peri-implant tissue recession, with consequent exposure of the rough surface of the implant neck into the oral cavity [17]. Some studies have indicated that below a certain critical roughness of implant surface, called \"threshold R(a)\" (0.2 \(\upmu\)m), no further reduction of bacterial accumulation could be expected, and there is not any major impact on the supra- and subgingival microbial composition [18; 19]. Some authors have related plaque accumulation to the development of peri-implantitis, and considered plaque control the most important way to prevent peri-implant disease and implant failure [20; 21; 22]. However, there is a lack of evidence about a clear effect of implant surface on the onset of peri-implantitis [23]. Other recent studies [24; 25] have shown that, even if a correlation between plaque accumulation and mucositis can be found, this does not apply to peri-implantitis. Bone resorption and so called peri implantitis have a multifactorial etiology and are influenced by a multitude of factors besides the implant features, including characteristics of the receiving site, surgical technique, prosthodonic material and design, individual susceptibility of the host (e.g., history of periodontitis), systemic conditions (e.g., diabetes mellitus, positive interleukin-1 genotype, uncontrolled HIV positivity, intravenous bisphosphonate, immunosuppressive), and behavioral factors (e.g., smoking, parafunction, adherence to supportive therapy), etc. All these conditions can potentially affect oral tissues, interfering with implant healing and bone maintenance over time [26; 27; 28; 29]. In the current literature, several studies investigated the clinical outcomes of implants with different surface modifications, but most of them were parallel arm clinical trials [30] or retrospective studies [31]. There is a lack of randomized controlled clinical trials (RCT) designed according to a split-mouth method investigating the clinical performances of implants with different titanium surfaces. There is also a lack of clinical studies with a long-term follow-up. In particular, randomised controlled clinical trials typically have a relatively brief in-trial follow-up period which can underestimate the effects of a device and fail to detect long-term outcomes, which may take years to appear [32].