## 1 Introduction  
Dental implants represent an excellent treatment option for the rehabilitation of atrophic jaws; nevertheless, even this clinical option is not free from complications [1]. Similarly, for natural teeth undergoing periodontal problems (periodontitis), dental implants could be affected by peri-implant mucositis (inflammation of soft tissues, reversible) or peri-implantits (involvement of hard and soft tissues) [1].  
A recent change in the classification of peri-implantitis has lead to an increased difficulty in the interpretation of the prevalence of this disease [2]. Nowadays, we can assume for peri-implantitis the presence of bleeding or supuration with gentle pressure on probing and some variations from previous examinations, such as increased probing depth and increased bone loss; in the case of the absence of previous examinations, peri-implantitis is defined as presence of bleeding and/or supuration on gentle probing, probing depths \(\geq\)6 mm, and bone levels \(\geq\)3 mm apical to the most coronal portion of the intraosseous part of the implant, as stated by the American Academy of Periodontology and the European Federation of Periodontology [3].  
This consensus report attempts to overcome the limits derived from a variety of different classifications that resulted in a wide range of prevalence reported, limiting the possibility of a real evaluation of peri-implantitis spread [4].  
Risk factors generically recognized are history of periodontitis, smoking, diabetes and patient compliance, while other conditions discussed in the literature are the presence or absence of keratinized mucosa around implants, bone augmentation procedures, type of implant surface and implant positioning [5].  
A recent study drew attention to the differences of bacterial biofilm between natural teeth and implants: in fact, [PERSON] et al. reported that peri-implantitis are resistant to beta-lactam antibiotics, which are effective against periodontal communities even as monotherapies [6].  
The primary goal of peri-implantitis treatments is the reduction of bacteria from implant surfaces, achieving deep decontamination; in order to obtain this result, both a non-surgical and surgical approach to implant surfaces have been proposed [5].  
The main treatment options are represented by:  
* Antiseptic and antibiotic therapies (local or systemic) [6,7]
* Mechanical debridement: curettes, ultrasonic, air abrasive, rotary titanium brushes [5]
* Laser treatments: diode, Er:YAG, CO\({}_{2}\), Nd:YAG, Er,Cr:YSGG [8, 9, 10, 11, 12, 13, 14, 15, 16]
* PDT: photodynamic therapy [15]
* Chemical agents: H\({}_{2}\)O\({}_{2}\), H\({}_{3}\)PO\({}_{4}\), EDTA [5]  
In the surgical treatment, the aim of decontamination is obtained through an open flap in order to perform deep sanitization and to create an implant morphology easier to clean, with the further possibility of obtaining guided bone regeneration [5].  
The above-mentioned treatments could be combined in order to enhance clinical results.  
Laser treatments for peri-implantitis show increasing attention in the literature; PDT seems to be effective only in the reduction of inflammatory status, but as a result of its scarce peak power (<2 W), PDT has only limited possibility of eliminating bacteria from implant surfaces, due to poor penetration capacity of the laser light in tissues imbibed with photosensitizer [17,18].  
In order to overcome these limitations, [PERSON] [12, 13, 14, 15] proposed a modified protocol, named OHLLT (oxygen high-level laser therapy), combining a 980 nm laser (Wiser, Doctor Smile) with hydrogen peroxide, leading to higher bioavailability and deeper penetration in the biofilms; moreover, this protocol has reduced interference of the irradiation performed respect to photoactivating agents with absorption within the visible band (Figure 1).  
The aim of this retrospective controlled study is to assess clinical outcomes of OHLLT alone in a non-surgical approach and OHLLT adjunct to a surgical approach.