IADR Abstract Archives
Cognitive decline induced by Porphyromonas gingivalis is serotype-dependent
Objectives: Periodontitis is the most prevalent bone resorptive disease, caused by a disbiotic subgingival microbiome formed by a wide variety of bacteria. Among these bacteria, Porphyromonas gingivalis has been associated with the onset and progression of periodontitis. Recently, this bacterium has been detected in postmortem brains of individuals diagnosed with Alzheimer's disease (AD). Thus, this study aimed to determine the hippocampal-dependent spatial memory in rats affected of periodontal periodontitis induced by different encapsulated serotypes of P. gingivalis
Methods: Experimental periodontitis was induced in thirty male Sprague-Dawley rats by two palatal inoculations (days 1 and 7) of 1x1010CFU/mL containing different capsular serotypes of P. gingivalis. Sham-rats infected were used as controls. After 45 days of primary infection, OASIS Maze was performed to evaluate spatial memory and learning. Further, biological samples of palatal mucosa, maxillae, serum, cerebro-spinal fluid and hippocampus were taken for the quantification of inflammatory mediators and detection of AD histopathological hallmarks
Results: Periodontitis-affected rats infected with K1 or K2 serotypes exhibited poor performance in the OASIS Maze task compared to sham rats and those infected with K4 or K- serotypes. Also an increase in the levels of inflammatory molecules were detected in serum, hippocampus and CSF from rats inoculated with serotype K1 or K2, in comparison to the other experimental conditions. Additionally, an increase in the level of extracellular Aβ42, the oxidative stress marker, malondialdehyde and GFAP inmunoreactivity was observed in the hippocampus from rats inoculated with serotypes K1 or K2
Conclusions: Periodontitis induced by the most pathogenic serotypes of P. gingivalis, K1 or K2, could cause hippocampal damage and memory loss and constitute a risk factor for the onset of AD.
Methods: Experimental periodontitis was induced in thirty male Sprague-Dawley rats by two palatal inoculations (days 1 and 7) of 1x1010CFU/mL containing different capsular serotypes of P. gingivalis. Sham-rats infected were used as controls. After 45 days of primary infection, OASIS Maze was performed to evaluate spatial memory and learning. Further, biological samples of palatal mucosa, maxillae, serum, cerebro-spinal fluid and hippocampus were taken for the quantification of inflammatory mediators and detection of AD histopathological hallmarks
Results: Periodontitis-affected rats infected with K1 or K2 serotypes exhibited poor performance in the OASIS Maze task compared to sham rats and those infected with K4 or K- serotypes. Also an increase in the levels of inflammatory molecules were detected in serum, hippocampus and CSF from rats inoculated with serotype K1 or K2, in comparison to the other experimental conditions. Additionally, an increase in the level of extracellular Aβ42, the oxidative stress marker, malondialdehyde and GFAP inmunoreactivity was observed in the hippocampus from rats inoculated with serotypes K1 or K2
Conclusions: Periodontitis induced by the most pathogenic serotypes of P. gingivalis, K1 or K2, could cause hippocampal damage and memory loss and constitute a risk factor for the onset of AD.