Spontaneous progression of ligatured induced peri-implantitis at implants with different surface characteristics. An experimental study in dogs II: histological observations

The aim of the present study was to analyze tissue reactions to plaque formation following ligature removal in experimental peri-implantitis at commercially available implants in dogs. Mandibular premolars and the three anterior premolars in both sides of the maxilla were extracted in six Labrador dogs. After 3 months, four implants representing four different implant systems - groups A (turned), B (TiOblast), C (SLA), D (TiUnite) - were placed in a randomized order in the right side of the mandible. Three months after implant installation, experimental peri-implantitis was initiated by placement of ligatures and plaque formation. The ligatures were removed when about 40-50% of the supporting bone was lost. After the subsequent 24-week period of continued plaque accumulation, block biopsies containing implants and their surrounding tissues were obtained and prepared for histological analysis. All types of implants exhibited extensive inflammatory cell infiltrates and large associated crater-formed osseous defects. The lesions were consistently characterized by insufficient encapsulation of pus and biofilm layers and the inflammatory cell infiltrates extended apical of the pocket epithelium. The presence of numerous osteoclasts indicated active tissue destruction. The vertical dimension and the overall surface area of the infiltrated connective tissue (ICT) were larger at implants of group D than at other implant types. It is suggested that spontaneous progression of peri-implantitis is associated with severe inflammation and tissue destruction. To cite this article:Albouy J-P, Abrahamsson I, Persson LG, Berglundh T. Spontaneous progression of ligatured induced peri-implantitis at implants with different surface characteristics. An experimental study in dogs: histological observations.Clin. Oral Impl. Res. 20, 2009; 366-371.doi: 10.1111/j.1600-0501.2008.01645.x.