Periodontitis as a Modifiable Risk Factor for Dementia: Mechanistic Pathways Linking Oral Inflammation to Neurodegeneration

Emerging evidence increasingly implicates chronic periodontal disease as a contributor to age-related cognitive decline and dementia, including Alzheimer's disease (AD). Periodontitis is defined by persistent oral microbial dysbiosis, ulcerated gingival epithelium, repeated bacteremia and sustained systemic inflammatory signaling - factors that plausibly influence neuroimmune pathways and cerebrovascular integrity. This review synthesizes findings from epidemiological studies, systematic reviews, mechanistic analyses and experimental models to examine the biological links between oral inflammation and neurodegeneration. Collectively, the literature suggests a stepwise oral-brain axis: first gingival inflammation promotes local and systemic pro-inflammatory cytokine release, second repeated bacteremia allows oral pathogens and microbial byproducts to enter circulation, third these signals and agents access and compromise the blood-brain barrier, then fourth microglia in the brain become primed and hyper-reactive and at last enhanced neuroinflammation accelerates amyloid-β and tau pathology. Although causal inference remains limited by the predominance of observational data, emerging intervention studies and mechanistic evidence suggest that periodontal health is a potentially modifiable factor in dementia prevention strategies.