Predisposing conditions for retrograde peri‐implantitis, and treatment suggestions

Abstract

Background: Recent case reports introduced the term retrograde peri‐implantitis as a lesion (radiolucency) around the most apical part of an osseointegrated implant. It develops within the first months after insertion. This retrospective study aimed to find predisposing conditions for such peri‐apical lesions and to evaluate treatment strategies. Methods: All single implants (426 in the upper, 113 in the lower jaw, all Brånemark system® type) placed at the department of Periodontology of the University Hospital (Catholic University Leuven) were included in this retrospective evaluation to check the incidence of retrograde peri‐implantitis. Eventual predisposing factors such as patient characteristics (age, medical history), recipient site (local bone quality and quantity, cause of tooth loss), periodontal and endodontic conditions of neighboring teeth, implant characteristics (length, surface characteristics), and surgical aspects (guided bone regeneration, osseous fenestration, or dehiscency) were considered. Moreover, implants with retrograde peri‐implantitis were followed longitudinally to verify their treatment outcome by means of different parameters (Periotest® values (PTV), marginal bone level, radiological size of peri‐apical defect). Results: Seven implants in the upper (1.6%) and 3 in the lower jaw (2.7%) showed retrograde peri‐implantitis, before or at abutment connection. In comparison with successful implants, such peri‐apical lesions occurred preferably at sites with a history of an obvious endodontic pathology of the extracted tooth to be replaced. The incidence of retrograde peri‐implantitis was significantly higher (P<0.0001) for TiUnite® implants when compared with the machined implants (8/80 vs. 2/459). The machined implant surface, however, showed a higher failure rate (6.8%) than the TiUnite® implants (2.5%). Failures with machined surfaces preferably occurred at extraction sites of teeth with a history of endodontic pathology or sites adjacent to teeth with an obvious endodontic pathology. No other predisposing factors could be identified. A curettage of the peri‐apical lesions and the use of a bone substitute material prevented further progression of such lesions in the upper jaw (implants maintained their marginal bone and low PTV scores). A treatment in the lower jaw was less successful. Conclusions: Within the limitations of a retrospective study, these results seem to indicate that retrograde peri‐implantitis is provoked by remaining scar or granulomatous tissue at the recipient site: endodontic pathology of extracted tooth (scar tissue‐impacted tooth) or possible endodontic pathology from a neighboring tooth.