IADR Abstract Archives
A Novel Experimental Peri-Implantitis Model Triggers Long-Term Neuroinfllamatory and Neurodegenerative Changes in the Rat Brain
Objectives: To explore the potential link between a newly developed rat model of chronic experimentally-induced peri-implantitis (PI) and neuropathological alterations in the brain.
Methods: Chronic-type PI lesions were generated at titanium implants placed in the upper jaws of wild-type rats, after bilateral first molars extraction, by placing silk ligatures with repeated local lipopolysaccharide injections. After 24-weeks of PI progression, maxillary and brain biopsies were recovered. Rats healthy brains were used as control. PI lesions confirmation was histologically assessed by H&E staining. The hippocampus and cerebral cortex were explored for the neuroinflammatory signs, interleukin (IL)-1β, IL-6 and tumor necrosis factor alfa (TNF-α); and for microgliosis and astrogliosis, IBA-1 and GFAP area and skeletal extension, were assessed by immunohistochemistry and ELISA. To explore for signs of neurodegeneration, neuronal morphology was evaluated by means of Nissl and H&E staining. In addition, the presence of amyloid beta forms was tested.
Results: Chronic-type PI lesions were confirmed by the presence of peri-implant bone resorption accompanied by large inflammatory infiltrates. IL-1β+, IL-6+ and TNF-α+ cells and protein levels were significantly more detected within the CA1 and Dentate Gyrus regions of the hippocampus of the PI-group, than the healthy group (p < 0.05). The area occupied by activated GFAP+ astrocytes and IBA-1+ microglia, mostly at the CA2 and CA3 regions of the hippocampus were significantly increased in the PI-affected group, in comparison with the healthy group (p < 0.05). The presence of pyknotic nuclei and the presence of reduced NISSL bodies among piramidal neurons, were inconsistently present among the PI-affected group, and these were almost not detected in healthy brains. No Aβ presence was detected.
Conclusions:
Conclusions
Chronic experimentally-induced PI lesions led to detection of histomorphological signs of neuroinflammation, astrocytocis and astrogliosis, and in some cases, neurodegeneration, after 24 weeks in the rat brain.
Methods: Chronic-type PI lesions were generated at titanium implants placed in the upper jaws of wild-type rats, after bilateral first molars extraction, by placing silk ligatures with repeated local lipopolysaccharide injections. After 24-weeks of PI progression, maxillary and brain biopsies were recovered. Rats healthy brains were used as control. PI lesions confirmation was histologically assessed by H&E staining. The hippocampus and cerebral cortex were explored for the neuroinflammatory signs, interleukin (IL)-1β, IL-6 and tumor necrosis factor alfa (TNF-α); and for microgliosis and astrogliosis, IBA-1 and GFAP area and skeletal extension, were assessed by immunohistochemistry and ELISA. To explore for signs of neurodegeneration, neuronal morphology was evaluated by means of Nissl and H&E staining. In addition, the presence of amyloid beta forms was tested.
Results: Chronic-type PI lesions were confirmed by the presence of peri-implant bone resorption accompanied by large inflammatory infiltrates. IL-1β+, IL-6+ and TNF-α+ cells and protein levels were significantly more detected within the CA1 and Dentate Gyrus regions of the hippocampus of the PI-group, than the healthy group (p < 0.05). The area occupied by activated GFAP+ astrocytes and IBA-1+ microglia, mostly at the CA2 and CA3 regions of the hippocampus were significantly increased in the PI-affected group, in comparison with the healthy group (p < 0.05). The presence of pyknotic nuclei and the presence of reduced NISSL bodies among piramidal neurons, were inconsistently present among the PI-affected group, and these were almost not detected in healthy brains. No Aβ presence was detected.
Conclusions:
Conclusions
Chronic experimentally-induced PI lesions led to detection of histomorphological signs of neuroinflammation, astrocytocis and astrogliosis, and in some cases, neurodegeneration, after 24 weeks in the rat brain.