IADR Abstract Archives
Breakdown of Periodontal Homeostasis by Dental Implants
Objectives: Objective: Peri-implantitis is a chronic inflammatory disease resulting in implant loss. To study the mechanisms of this widespread disease, a murine model was developed and used to characterize immunological parameters around dental implants at steady-state and during murine peri-implantitis.
Methods: Materials and Methods: Mice underwent implantation four weeks after extraction of the right maxillary molars. Four weeks following implantation mice were orally infected with Porphyromonas gingivalis (Pg) or vehicle only as a negative control. Mucosal tissues around implants and teeth were processed and analyzed by flow-cytometry, RT-qPCR and immunofluorescence staining. Alveolar bone loss (ABL) was evaluated using micro-computed tomography.
Results: Results: Similar to humans, Langerhans cells (LCs) were absent in the murine peri-implant epithelium, at steady-state. This was due to an alteration in epithelial expression of TGF-β1, which is known to instruct LCs differentiation. Further analyses revealed increased frequencies of neutrophils, dendritic cells, B and T lymphocytes in the peri-implant mucosa. Interestingly, implanted mice presented ABL in the contra-lateral molars where no implants were inserted, demonstrating the deleterious effect of implants on oral mucosal homeostasis. In line with this observation, higher RANKL\OPG and IL17\FOXP3 ratios were found in implanted mice, as well as elevated INF-α expression that was recently found to have pathological impact on oral immunity. Following Pg infection, ABL was significantly higher in both implants and teeth compared to control groups. This was accompanied by elevated numbers of RANKL-expressing CD4+ T cells and B cells as well as CD4+ T regulatory cells.
Conclusions: Conclusions: Implants break oral mucosal homeostasis by inducing chronic inflammation that destructs alveolar bone and results in implant loss, Pg infection accelerates this process. More importantly, such implant-driven inflammation also induces ABL in the contra-lateral otherwise healthy teeth.
Methods: Materials and Methods: Mice underwent implantation four weeks after extraction of the right maxillary molars. Four weeks following implantation mice were orally infected with Porphyromonas gingivalis (Pg) or vehicle only as a negative control. Mucosal tissues around implants and teeth were processed and analyzed by flow-cytometry, RT-qPCR and immunofluorescence staining. Alveolar bone loss (ABL) was evaluated using micro-computed tomography.
Results: Results: Similar to humans, Langerhans cells (LCs) were absent in the murine peri-implant epithelium, at steady-state. This was due to an alteration in epithelial expression of TGF-β1, which is known to instruct LCs differentiation. Further analyses revealed increased frequencies of neutrophils, dendritic cells, B and T lymphocytes in the peri-implant mucosa. Interestingly, implanted mice presented ABL in the contra-lateral molars where no implants were inserted, demonstrating the deleterious effect of implants on oral mucosal homeostasis. In line with this observation, higher RANKL\OPG and IL17\FOXP3 ratios were found in implanted mice, as well as elevated INF-α expression that was recently found to have pathological impact on oral immunity. Following Pg infection, ABL was significantly higher in both implants and teeth compared to control groups. This was accompanied by elevated numbers of RANKL-expressing CD4+ T cells and B cells as well as CD4+ T regulatory cells.
Conclusions: Conclusions: Implants break oral mucosal homeostasis by inducing chronic inflammation that destructs alveolar bone and results in implant loss, Pg infection accelerates this process. More importantly, such implant-driven inflammation also induces ABL in the contra-lateral otherwise healthy teeth.