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Development of a peri‐implantitis model in the rat
Author(s) -
Sun Jingqing,
Eberhard Joerg,
Glage Silke,
Held Nadine,
Voigt Henning,
Schwabe Kerstin,
Winkel Andreas,
Stiesch Meike
Publication year - 2020
Publication title -
clinical oral implants research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.407
H-Index - 161
eISSN - 1600-0501
pISSN - 0905-7161
DOI - 10.1111/clr.13556
Subject(s) - peri implantitis , streptococcus oralis , implant , dentistry , dental alveolus , antibiotics , aggregatibacter actinomycetemcomitans , medicine , actinobacillus , inflammation , maxilla , bacteria , periodontitis , streptococcus , biology , surgery , microbiology and biotechnology , porphyromonas gingivalis , genetics
Objectives The aim of the present study was to establish a rodent peri‐implantitis model induced by a mixed bacterial infection characterized by bone loss and semi‐quantitative graduation of peri‐implant inflammation in histological sections. Materials and Methods Two titanium implants were implanted in Sprague‐Dawley rats, bilaterally in each maxilla. After 3 weeks healing, the rats were randomized into three groups according to different treatments over the next 3 months: Antibiotic‐Group with oral lavage of antibiotics; Bacteria‐Group with oral lavage of Streptococcus oralis and Aggregatibacter actinomycetemcomitans ; and Untreated Group with standard housing and no additional treatment. Maxillae were dissected to perform microscopic and histological analysis of bone height and peri‐implant tissues. Results The bone level, measured at one implant site per animal, in the Bacteria‐Group (2.60 ± 0.39 mm) was significantly reduced compared to the Antibiotic‐Group (2.29 ± 0.32 mm) after 3 months. The differences of bone height in the Bacteria‐Group and the Untreated Group (2.46 ± 0.27 mm) did not reach statistical significance. The inflammatory response with respect to the number of inflammatory cells and fibrous tissue compartments of the peri‐implant tissues in the Bacteria‐Group was significantly increased compared with the Antibiotic‐Group ( p  < .05). S. oralis and A. actinomycetemcomitans DNAs were detected in the Bacteria‐Group. Conclusions This rat model of peri‐implantitis used oral bacterial lavage for the induction of an inflammatory host response and bone loss. Additional bacterial treatment enhances the peri‐implant phenotype, so that significant differences to a reduced bacterial load similar to the human peri‐implantitis disease can be identified.

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