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.
Materials and Methods: Mice underwent implantation four weeks after extraction of the right maxillary molars. 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: 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.
Conclusions: Implants break oral mucosal homeostasis by inducing chronic inflammation that destructs alveolar bone and results in implant loss. More importantly, such implant-driven inflammation also induces ABL in the contra-lateral otherwise healthy teeth.
Clinical Significance: Dental clinicians should take into consideration the impact of implant placements on patient’s periodontal status.