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Dementia is among the most pressing public health challenges of the 21st century. An estimated 57 million people worldwide were living with dementia in 2021, and this number is projected to reach 153 million by 2050 as populations age. In the absence of disease‐modifying therapies for most forms of dementia, identifying and mitigating modifiable risk factors across the life course has become a central strategy for reducing the population burden of cognitive decline. The 2024 Commission on dementia prevention, intervention, and care identified 14 modifiable risk factors that collectively account for 45% of cases. Although oral health was not formally included as a standalone risk factor in the Commission's framework, a growing body of epidemiological evidence implicates poor oral health, and tooth loss in particular, as a potentially important contributor to cognitive decline., , A recent correspondence in argued that the population‐attributable fraction for edentulism (4.64%) exceeds that of several risk factors currently included in the framework. Meta‐analyses have consistently demonstrated that tooth loss is associated with a 28% to 48% increased risk of cognitive impairment and a 14% to 55% increased risk of dementia,, , , with evidence of a dose‐response relationship in which each additional missing tooth incrementally elevates risk., Several biological mechanisms have been proposed but evidence has been limited by small sample sizes, convenience sampling, or reliance on animal models., , , Chronic periodontal infections generate sustained systemic inflammation, with elevated circulating levels of C‐reactive protein, interleukin‐6, and tumor necrosis factor‐α, which can compromise the blood‐brain barrier and activate neuroinflammatory cascades., , , Periodontal pathogens, notably , have been identified in postmortem Alzheimer's disease (AD) brains and shown to promote amyloid‐β (Aβ) production and neuroinflammation., , Tooth loss also impairs masticatory function, leading to reduced intake of protective nutrients, and diminishes sensory input through the trigeminal nerve to the hippocampus, a structure critical for memory formation., In addition, two recent UK Biobank studies have linked poor oral health to white matter injury, and shown that circulating proteomic markers partially mediate this association, although both examined neuroimaging markers of brain integrity rather than incident dementia.