Peri-implantitis was recently defined as a “pathological condition occurring in tissues around dental implants”, which is “characterized by inflammation in the peri-implant connective tissue and a progressive loss of supporting bone” [1,2,3,4].

Human biopsies confirmed the presence of plasma cells, macrophages, and neutrophils [5] and elevated expression of inflammatory cytokines [6, 7] at peri-implantitis sites. Moreover, bone matrix molecules were decreased and cells had a fibroblastic phenotype [8]. Together, human biopsies of the respective soft tissue revealed the conserved cellular and molecular principles of acute inflammatory osteolysis [9].

Peri-implantitis lesions extend apical and are commonly associated with a circumferential pattern of bone loss [1, 10]. Intraoperative clinical and radiographic assessments, however, do not fully represent the extension of peri-implantitis defects [11,12,13,14]. Moreover, the morphology of the remaining bone being exposed to masticatory forces has not been described so far. Considering that the remaining peri-implant bone has to adapt to occlusal load [15], it requires vital osteocytes to translate mechanical forces into molecular signals controlling bone adaptation [16]. It also requires vital osteocytes for inflammatory osteolysis [17]. These biological principles let us to hypothesize that the bone in peri-implantitis defects has a high density and contains vital osteocytes. Therefore, the present study reports on the characteristics of bone at sites of advanced peri-implantitis.