## 1 Introduction  
One of the key factors in the success of dental implants is the absence of progressive marginal bone loss, as its presence significantly decreases the chances of implant survival. The loss of peri-implant bone is influenced by multiple factors, with peri-implantitis being a potential contributing cause. Peri-implantitis is a bacteria-associated inflammatory disease affecting the tissues around implants, characterized by inflammation of the peri-implant mucosa and progressive loss of the supporting bone [1]. Peri-implant microbiota presents a different bacterial ecosystem compared with the microbiota in periodontitis, as it is qualitatively lower in terms of microbial diversity, but quantitatively higher for some bacterial genera [2]. Epidemiologic studies report a prevalence of peri-implantitis in 2 out of 10 implant holders and 1 out of 10 implants [3]. Three risk factors, namely patients with a history of periodontal disease, poor plaque control, or not following a regular maintenance protocol are identified with a high level of evidence. Implant surface roughness, tobacco, lack of keratinized tissue, and systemic diseases, such as diabetes, also seem to have an adverse effect, though no scientific data are available to this date [4]. One of the objectives of peri-implantitis therapy is to make an effective debridement of all granulation tissue from the area of defect and a decontamination of the exposed surfaces of an implant. Different methods of decontamination of the implant surface, involving mechanical or chemical means, are available. However, at present, no other protocol has demonstrated a higher efficacy and there is a lack of consensus in the literature [5]. The results of non-surgical therapy are inconclusive and surgical procedures demonstrated better outcomes [6]. One critical element to successfully resolve peri-implantitis is to decontaminate the implant surface and this can be affected by implant surface characteristics and geometry [7]. Implantoplasty has been proposed to eliminate the threads and smoothen the implant surface using rotatory instruments. For surgical therapy, a beneficial effect has been reported following implantoplasty associated with flap apicalisation surgery, reconstructive surgery, or a combined surgical approach [8; 9]. In addition to being an effective method of decontamination, implantoplasty could limit the risk of relapse of peri-implantitis. Following treatment of peri-implantitis, implant surfaces may become exposed to the oral environment due to bone loss and soft tissue shrinkage during healing [10]. Removal of the rough and affected surface of titanium reduces the potential for biofilm adhesion and thus its maturation on the implant surface [11; 12]. In vitro, implantoplasty reduces bacterial recolonization more than other implant surface decontamination techniques [13]. Similarly, the smoothed titanium surface exposed to the oral environment seems easier for the patient to clean and will also be easier to clean for the practitioner during supportive therapy. [PERSON] and [PERSON] suggested that smooth surfaces have an Sa value of <0.5 mm; minimally rough surfaces were identified with an Sa of 0.5-1 mm, moderately rough surfaces with Sa 1-2, and rough surfaces with an Sa of 42 mm [14]. Studies show a similar roughness between a \"machined\" implant [15] and an implant after an implantoplasty procedure (Ra = 0.39 \(\upmu\)m \(\pm\) 0.13 \(\upmu\)m) [16]. In addition, the biocompatibility of these titanium surfaces after implantoplasty seems to be preserved in vitro. Furthermore, obtaining a hydrophilic surface is conducive to bone healing [17]. Indeed, [PERSON] et al. showed that at 5 years, there were five times more relapse of peri-implantitis on implants with a rough surface compared with a machined surface [18].