IADR Abstract Archives
Periodontitis and Alzheimer’s Experimental Models: Neuroinflammation and Cognitive Status Comparison
Objectives: Periodontitis is a chronic non-transmissible disease characterized by a low-grade inflammatory state, caused by the dysbiosis of subgingival microbiota. The low-grade inflammatory state caused by bacteria associates periodontitis with others diseases, such as Alzheimer’s disease (AD). Recently, it was demonstrated that the experimental periodontitis induced by Porphyromonas gingivalis (P. gingivalis) triggers an AD-like pathology in Sprague-Dawley rats. This study aimed to determine if experimental periodontitis and an experimental model of AD display similar levels of neuroinflammation, astrogliosis and cognitive defects.
Methods: 30 Sprague-Dawley male rats 6 weeks age were divided into the following groups: 1) experimental periodontitis, induced by palatine mucosa inoculation of P. gingivalis, 2) experimental AD, induced by bilateral intra-hipocampal inoculation of amyloid β (Aβ) oligomers, 3) periodontitis control, by palatal inoculation of medium without bacteria, 4) AD control, by intra-hippocampal injection of saline solution, and 5) naïve rats. All animals were trained in the OASIS Maze task to test memory and spatial learning. The cytokines and Aβ42 levels and lipoperoxidation in serum and hippocampus were quantified. The Tau and phosphorylated Tau protein, and the morphology and number of astrocytes were observed by immunofluorescence.
Results: In both periodontitis and AD models, an increase in pro-inflammatory cytokines, Aβ42 and lipoperoxidation levels were detected compared with controls. Also, a learning and spatial memory decline was detected in both experimental models, compared to their respective controls. Finally, an increase in the Tau/pTau ratio was detected in both experimental conditions compared with controls. No significant differences were found between the experimental models investigated.
Conclusions: Periodontitis and AD models have a similar neuroinflammation, astrogliosis and cognitive decline pattern. Periodontitis trigger an AD-like pathology in a similar way than experimental AD.
Methods: 30 Sprague-Dawley male rats 6 weeks age were divided into the following groups: 1) experimental periodontitis, induced by palatine mucosa inoculation of P. gingivalis, 2) experimental AD, induced by bilateral intra-hipocampal inoculation of amyloid β (Aβ) oligomers, 3) periodontitis control, by palatal inoculation of medium without bacteria, 4) AD control, by intra-hippocampal injection of saline solution, and 5) naïve rats. All animals were trained in the OASIS Maze task to test memory and spatial learning. The cytokines and Aβ42 levels and lipoperoxidation in serum and hippocampus were quantified. The Tau and phosphorylated Tau protein, and the morphology and number of astrocytes were observed by immunofluorescence.
Results: In both periodontitis and AD models, an increase in pro-inflammatory cytokines, Aβ42 and lipoperoxidation levels were detected compared with controls. Also, a learning and spatial memory decline was detected in both experimental models, compared to their respective controls. Finally, an increase in the Tau/pTau ratio was detected in both experimental conditions compared with controls. No significant differences were found between the experimental models investigated.
Conclusions: Periodontitis and AD models have a similar neuroinflammation, astrogliosis and cognitive decline pattern. Periodontitis trigger an AD-like pathology in a similar way than experimental AD.