Rinat Tzach-Nahman1,2, Gabriel Mizraji1,2, Lior Shapira1, Gabriel Nussbaum2, Asaf Wilensky1. 1. Department of Periodontology, Faculty of Dental Medicine, The Hebrew University-Hadassah Medical Center, Jerusalem, Israel. 2. The Institute of Dental Sciences, Faculty of Dental Medicine, The Hebrew University-Hadassah Medical Center, Jerusalem, Israel.
Abstract
AIM: Peri-implantitis is a major health concern, with unclear pathogenesis, and with no accessible animal models. Our aim was to establish a mouse model for peri-implantitis and to investigate mediators of inflammation. MATERIALS AND METHODS: Mice were divided into implanted versus non-implanted groups. Implants were inserted immediately following the extraction of the upper first molar. Four weeks following implantation, implanted and non-implanted mice were challenged with either Porphyromonas gingivalis or vehicle (eight mice in each subgroup, 32 mice in total). Alveolar bone loss and expression of inflammatory mediators in the soft tissue were assessed 42 days following infection. RESULTS: Porphyromonas gingivalis infection induced greater bone loss around implants than around teeth. In non-infected animals, the presence of the implant correlated with elevated expression of Il-10, Foxp3 and Rankl/Opg ratio, while Tnf-α levels were decreased relative to tissue around teeth. Six weeks following infection, Tnf-α increased significantly while the expression of Foxp3 decreased in the tissue around the implants. No significant differences in anti- or pro-inflammatory mediators were found around teeth of infected, relative to non-infected mice. CONCLUSIONS: Oral infection with P. gingivalis of mice with implants induced bone loss and a shift in gingival cytokine expression. This mouse model enables exploration of the pathogenesis of peri-implantitis and testing of novel treatments.
AIM: Peri-implantitis is a major health concern, with unclear pathogenesis, and with no accessible animal models. Our aim was to establish a mouse model for peri-implantitis and to investigate mediators of inflammation. MATERIALS AND METHODS:Mice were divided into implanted versus non-implanted groups. Implants were inserted immediately following the extraction of the upper first molar. Four weeks following implantation, implanted and non-implanted mice were challenged with either Porphyromonas gingivalis or vehicle (eight mice in each subgroup, 32 mice in total). Alveolar bone loss and expression of inflammatory mediators in the soft tissue were assessed 42 days following infection. RESULTS:Porphyromonas gingivalisinfection induced greater bone loss around implants than around teeth. In non-infected animals, the presence of the implant correlated with elevated expression of Il-10, Foxp3 and Rankl/Opg ratio, while Tnf-α levels were decreased relative to tissue around teeth. Six weeks following infection, Tnf-α increased significantly while the expression of Foxp3 decreased in the tissue around the implants. No significant differences in anti- or pro-inflammatory mediators were found around teeth of infected, relative to non-infected mice. CONCLUSIONS:Oral infection with P. gingivalis of mice with implants induced bone loss and a shift in gingival cytokine expression. This mouse model enables exploration of the pathogenesis of peri-implantitis and testing of novel treatments.
Authors: S Hiyari; A Naghibi; R Wong; R Sadreshkevary; L Yi-Ling; S Tetradis; P M Camargo; F Q Pirih Journal: J Periodontal Res Date: 2017-10-17 Impact factor: 4.419
Authors: Khaled Mukaddam; Monika Astasov-Frauenhoffer; Elizaveta Fasler-Kan; Laurent Marot; Marcin Kisiel; Roland Steiner; Fabien Sanchez; Ernst Meyer; Joachim Köser; Michael M Bornstein; Sebastian Kühl Journal: Nanomaterials (Basel) Date: 2022-03-24 Impact factor: 5.076