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Updated: Aug 19, 2026
Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
Published on: February 17, 2023
Spontaneous progression of experimentally induced periimplantitis
N U Zitzmann1, T Berglundh, I Ericsson
1Department of Periodontology, Göteborg University, SE-405 30 Göteborg, Sweden. n.zitzmann@unibas.ch
Background:
Periimplantitis represents an inflammatory condition that is associated with the presence of a submarginal biofilm and with advanced breakdown of soft and mineralized tissues surrounding endosseous implants. Animal models have been used to describe mechanisms involved in the pathogenesis and treatment of the soft and hard tissue lesions of periimplantitis.
Objective:
The aim of the present experiment was to study the presence and progression of inflammatory lesions in tissues surrounding implants exposed to "experimental periimplantitis".
Material And Methods:
Five Labrador dogs were used. In each dog, 2 or 3 implants were placed in both the left and right edentulous premolar regions of the mandible. Abutment connection was performed 4 months later and a plaque control regimen was initiated and maintained for 5 months. "Experimental periimplantitis" was subsequently induced by ligature placement and plaque accumulation was allowed to progress until about 40% of the height of the supporting bone had been lost. The ligatures were removed, but plaque formation was allowed to continue for an additional 12 months. Radiographs of all implant sites were obtained before and after active "experimental periimplantitis" as well as at the end of the experiment. Biopsies were harvested from the implant sites in 3 of the dogs. The tissue samples were prepared for light microscopy and the sections were used for histometric and morphometric examinations.
Results:
One implant was lost during the first 2 months of "experimental periimplantitis" and two implants were lost during the 12 months that followed ligature removal. The radiographic examination indicated that varying amounts of additional bone loss occurred in the majority of the implant sites also following ligature removal. The mucosa of all implant sites harbored inflammatory lesions that extended apically of the pocket epithelium. The lesions were separated from the marginal bone by a zone of apparently normal connective tissue.
Conclusion:
A remission of the destructive inflammatory lesion in the periimplant tissues was seen in some sites following ligature removal, but in the majority of sites additional loss of supporting bone occurred.
