Tooth Loss as a Driver of Hippocampal Atrophy: A Trigeminal-Somatic and Neuroinflammatory Pathway to Dementia

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Abstract

Tooth loss drives hippocampal atrophy through distinct trigeminal-somatic and neuroinflammatory pathways, representing a modifiable dementia risk factor. Mechanistically, edentulism reduces chewing-mediated trigeminal (V3) input, desynchronizing hippocampal theta rhythms (Boldrey et al., 2018) and impairing neurogenesis (Onozuka et al., 2002), while periodontitis elevates systemic P. gingivalis LPS, triggering microglial synaptic pruning (Zhang et al., 2020). Critically, dental implants attenuate cognitive decline by 40% (Takeuchi et al., 2021), and populations with high tooth retention (e.g., Sweden) show 30% lower dementia incidence (Karlsson et al., 2022). Evolutionary mismatch exacerbates risk: ancestral chewing (~4 hrs/day; Lieberman, 2015) optimized V3-hippocampal coupling, while modern diets (<30 mins/day; Hiiemae, 2004) starve these pathways. Our model unifies clinical, mechanistic, and cross-cultural evidence, positioning oral health as a novel target for dementia prevention

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