## 1 Introduction  
Dental implants are used to replace missing teeth [1]. These implants are designed to integrate with the bone, mimicking the root of a tooth. Dental implants serve as artificial tooth roots, providing a permanent base for fixed, replacement teeth [2]. The tooth is secured to the alveolar bone and gingiva via the periodontal ligament and superior soft tissue fibers [3]. However, hard and soft tissues surrounding the implant are somewhat different from the tooth and the interface between the connective tissue and the implant is devoid of fibers [4]. Within the peri-implant mucosa, collagen fibers are oriented parallel to the implant's long axis [5]. Furthermore, the mucosal region in the dental implant is characterized by a low vascular density [6]. The osteotomy procedure performed during implant placement induces tissue damage, precipitating a series of biological responses within the bone, which includes bone remodeling [7]. The subsequent weeks witness a process of modeling and remodeling of the hard tissue around the implant, culminating in the formation of new bone that surrounds the implant, a phenomenon known as osseointegration [8]. Peri-implantitis is essentially the counterpart to periodontitis [9]. Peri-implant mucositis is defined as the inflammation of the soft tissues surrounding a dental implant, whereas peri-implantitis is characterized by inflammation of the peri-implant soft tissues accompanied by bone loss around the implant [10]. A healthy peri-implant mucosa exhibits neither edema nor redness and is devoid of inflammatory markers, such as bleeding upon palpation. Both the mucosa and the superior aspect of the tooth or implant are integral components of the oral milieu, perpetually exposed to a diverse array of microorganisms [11]. Unlike the oral mucosa, which can shed epithelial cells to mitigate microbial colonization, implants and teeth lack this capability. Consequently, implants present a particularly conducive environment for bacterial adherence and biofilm formation within the grooves of the adjacent mucosa [12]. The manifestations of peri-implantitis frequently remain asymptomatic, typically identified during routine examinations through bleeding upon probing, a consistent indicator of peri-implant disease, although this may not be observed in some smokers [13]. Additional clinical indicators of this condition include suppuration, an increased probing depth compared to baseline measurements, mucosal retraction, the formation of draining sinuses, and swelling of the peri-implant mucosa [14]. Without prompt diagnosis and effective management, peri-implant disease can lead to the loss of osseointegration and ultimately, the failure of the implant [15]. The primary objective in the management of dental peri-implantitis is to mitigate the peri-implantitis lesion, thereby arresting the progression of bone support loss [16]. The treatment aims are analogous to those for periodontitis, where a successfully treated peri-implantitis site should exhibit an absence of periodontal pockets and bleeding upon probing [17]. Nevertheless, the efficacy of such treatments may be contingent upon the successful removal of biofilm from the implant surface and the accessibility of the contaminated implant surface for treatment [18]. Non-surgical approaches to biofilm removal are typically employed in conjunction with care of the upper peri-implant mucosal region [19]. Providing patients with detailed information and guidance on self-managing the infection is crucial to the overall management of peri-implant diseases in dentistry [20]. However, in instances of severe dental peri-implantitis, non-surgical methods alone may prove insufficient, necessitating a surgical intervention. Surgical modalities are employed to remediate connective tissue lesions, incorporating various mechanical techniques for biofilm elimination from the implant surface [21].