Experimental tooth loss affects spatial learning function and blood–brain barrier of mice

Abstract

ObjectiveThis study aims to investigate how experimental tooth loss affected learning, memory function, and brain pathophysiology in mice.Materials and MethodsThe mice (C57BL/6 J, 2‐month‐old, male) were divided into tooth loss and control groups. The behavioral test battery was performed at 6 and 12 months after tooth extraction. The protein levels of the tight junctions in the brains of the mice were analyzed. Hippocampal astrocyte was measured using immunohistochemical staining.ResultsThe results of behavioral tests and biochemical analysis performed during the 6 months observation period did not show significant differences between the groups. However, the escape latency in the tooth loss group was significantly longer than that in the control group at the 12 months after tooth extraction. The level of claudin‐5 decreased in the tooth loss group. Additionally, hippocampal astrogliosis was found in the tooth loss group.ConclusionsExperimental tooth loss reduced the level of claudin‐5 and caused astrogliosis in the brains of mice, which was accompanied by deterioration of learning functions. This study may provide a new insight about the association between tooth loss and cognitive dysfunction.

Risk factors of cognitive impairment: Impact of decline in oral function

“…Various mechanisms about this relationship were shown; for example, reduced masticatory function causes an impairment of the cholinergic neurotransmitter system associated with learning ability and spatial memory or reduced neurogenesis of the brain. About the influence on brain, Furukawa et al reported the possibility that decreased occlusal support in mice affect cognitive function and activity by neural activity and neuroinflammation in the hippocampus and hypothalamus [42] , and Oue et al reported that tooth loss caused astrogliosis in the brain of mice [43] . Gobel proposed a mechanism by which decreased mastication-induced sensory stimulation leading to degeneration of secondary neurons in the spatial pathway of the alveolar and trigeminal nerves and through downstream cortical-brainstem circuits, contribute to diminished cortical cholinergic function [44] .…”