Peri-implantitis is caused by a bacterial challenge and characterized by inflammation in the peri-implant soft tissues and a progressive loss of supporting bone [1, 2]. Consequently, its treatment is cause-related and primarily aimed at arresting disease progression [3].

Based on the currently available evidence, non-surgical mechanical debridement alone seems to have a limited efficacy for the management of peri-implantitis [4, 5]. While adjunctive (i.e., local antibiotics, antimicrobial photodynamic therapy) or alternative measures (e.g. air abrasive devices, Er:YAG laser monotherapy) may improve the efficacy of non-surgical therapy, the obtained clinical outcomes appeared to be limited to a period of 6 to 12 months and were particularly compromised at advanced defect sites [4, 5]. In contrast, the efficacy of treatment was commonly improved subsequent to a surgical intervention combining open flap debridement either with adjunctive resective (e.g., apical flap, osteoplasty, implantoplasty (IP)), augmentative (e.g., bone fillers/autografts, guided bone regeneration), or a combination of resective (i.e., IP) and augmentative (refers to as combined therapy) measures [6]. Nevertheless, the reported outcomes following surgical therapy of peri-implantitis varied considerably and appeared to be influenced by a variety of different prognostic factors, such as the configuration of the bony defect [7], the physicochemical properties of the bone filler [8, 9], or the surface characteristics of the affected implants [10, 11].

Previous clinical data provide some evidence that ridge augmentation using either autogenous bone or different bone filler materials may constitute a potential risk indicator for the onset of peri-implant diseases [12, 13]. Consequently, it might be hypothesized that initial bone-grafting procedures at implant site may also influence the effectiveness of peri-implantitis treatment. Therefore, this retrospective analysis aimed at comparing the clinical outcomes following combined surgical treatment of peri-implantitis at initially grafted and non-grafted (i.e., pristine) implant sites.