Mouse maternal odontogenic infection with induces cognitive decline in offspring.

Introduction: (), a major periodontal pathogen, causes intrauterine infection/inflammation. Offspring exposed to intrauterine infection/inflammation have an increased risk of neurological disorders, regardless of gestational age. However, the relationship between maternal periodontitis and offspring functional/histological changes in the brain has not yet been elucidated.

Methods: In this study, we used a gestational mouse model to investigate the effects of maternal odontogenic infection of on offspring behavior and brain tissue.

Results: The step-through passive avoidance test showed that the latency of the acquisition trial was significantly shorter in the group ( < 0.05), but no difference in spontaneous motor/exploratory parameters by open-field test. was diffusely distributed throughout the brain, especially in the hippocampus. In the hippocampus and amygdala, the numbers of neuron cells and cyclic adenosine monophosphate response element binding protein-positive cells were significantly reduced (< 0.05), whereas the number of ionized calcium binding adapter protein 1-positive microglia was significantly increased (< 0.05). In the hippocampus, the number of glial fibrillary acidic protein-positive astrocytes was also significantly increased (< 0.05).

Discussion: The offspring of -infected mothers have reduced cognitive function. Neurodegeneration/neuroinflammation in the hippocampus and amygdala may be caused by infection, which is maternally transmitted. The importance of eliminating maternal -odontogenic infection before or during gestation in maintenance healthy brain function in offspring should be addressed in near future.