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Oral infection with Porphyromonas gingivalis induces peri‐implantitis in a murine model: Evaluation of bone loss and the local inflammatory response
Author(s) -
TzachNahman Rinat,
Mizraji Gabriel,
Shapira Lior,
Nussbaum Gabriel,
Wilensky Asaf
Publication year - 2017
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12735
Subject(s) - porphyromonas gingivalis , peri implantitis , rankl , pathogenesis , dental alveolus , periodontitis , inflammation , medicine , molar , cytokine , dentistry , implant , immunology , surgery , receptor , activator (genetics)
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.