Can treating gum disease improve or slow down Alzheimer and other neurodegenerative diseases and boost longevity?

A healthy smile has often been associated with good overall health as well as with confidence, social status, physical and mental vigour and overall attractiveness and likeability. Healthy clean teeth boost confidence whilst both Alzheimer and periodontitis sap confidence, trigger health complications and shorten lifespan. Alzheimer and periodontitis seem to be closely linked and as recent studies show bi-directional relationships between periodontitis and inflammatory diseases (such as rheumatoid arthritis and certain cardiovascular diseases) – will it be long until studies underway show a similar bi-directional link between gum disease and Alzheimer? In other words, could treating periodontitis improve Alzheimer symptoms or slow down the onset?

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Irene Petre

2/27/20263 min read

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How about the link to Alzheimer and other neurodegenerative studies?

Studies have shown a connection between bacteria associated with periodontal disease and the progression of Alzheimer’s disease. Gum disease bacteria may be able to travel to the brain and be a factor in the development of Alzheimer’s disease (1).

Preliminary results for the effect of periodontal health on cognitive decline were presented (poster presentation) at Alzheimer's Association International Conference (AAIC) 2020 in Amsterdam, the Netherlands (2).

Emerging evidence from a study in 2022 shows that both poor periodontal health and tooth loss adversely impacts cognition, increasing the risk of both cognitive decline and dementia. However, the available evidence is rather patchy (e.g., highly heterogenous, lacking robust methodology) for now and not possible to draw firm conclusions just yet. Authors call for further well-designed studies involving standardized periodontal and cognitive health assessment and for addressing reverse causality.

Systematic reviews and meta‑analyses of longitudinal studies report that the worse the periodontal health (clinical periodontitis, tooth loss/edentulism) is, the higher the risk of cognitive decline, dementia, and mortality in older adults (3). Results vary by how periodontal disease and cognition are measured, length of follow‑up, and how well studies adjust for smoking, diabetes, socioeconomic status, and other shared risk factors.

Many animal and laboratory studies showed a positive relationship

Experimental lab and animal models have shown that periodontal pathogens or their toxins can accelerate brain inflammatory responses and Alzheimer‑like pathology; such studies support the mechanistic case but cannot on their own prove clinical benefit in humans. Successful trials in animals do not always correlate with successful trials in humans, especially when it comes to brain related investigations.

A 2025 analysis of 19 recent pilot and small‑scale clinical studies found that elevated systemic inflammatory markers and oral microbiome disturbances were associated with increased risk of Alzheimer’s disease (AD) (4). Periodontal therapy in these studies was linked to reductions in systemic inflammation and to stabilisation of cognitive decline, supporting a plausible pathway that connects periodontal disease and Alzheimer through chronic inflammation and microbial translocation. These findings point to oral health maintenance as a potentially important preventive strategy and underscore the need for integrated medical–dental care and larger longitudinal research to confirm causality and long‑term benefit.

Chronic periodontitis raises circulating levels of pro‑inflammatory cytokines such as IL‑1β, IL‑6, and TNF‑α, which can cross the blood–brain barrier, activate microglia, and sustain neuro-inflammatory processes implicated in AD pathology. Periodontal pathogens, notably Porphyromonas gingivalis, have been detected in brain tissue and their virulence factors (gingipains) are hypothesised to promote amyloid‑β aggregation, tau hyperphosphorylation, and neuronal injury. Biomarker studies report associations between periodontitis and elevated plasma p‑Tau and Aβ1‑40, characteristic shifts in the oral microbiome (for example, relative increases in Firmicutes and decreases in Bacteroidetes), and salivary metabolites such as galactinol that correlate with cognitive decline. Clinically, periodontal treatment has been observed to lower systemic inflammatory burden, slow cognitive deterioration, and reduce measures of brain atrophy in some cohorts, positioning gum disease as a modifiable risk factor for Alzheimer. Severe gum disease and tooth loss have been associated with a 6–16% higher risk of Alazheimer, with this risk amplified by pro‑inflammatory diets and vitamin D deficiency.

Technological advances in neuroimaging, molecular profiling, and systems biology will likely clarify shared mechanisms and causal pathways. Investigating targeted anti‑inflammatory and antimicrobial interventions that address periodontal pathogens may open new and exciting therapeutic or preventive routes for Alzheimer and overall neurodegenerative diseases, which affect nearly 60m people worldwide (5). The accumulating evidence linking periodontal disease and Alzheimer’s disease highlights the systemic nature of neurodegeneration and the value of cross‑disciplinary approaches that integrate dentistry, neurology, immunology, and public health.

Larger randomized trials are needed and remain key to shifting policy focus and reimbursement

At least one registered trial, Centre Hospitalier Universitaire de Liege, Belgium is explicitly testing whether periodontal treatment affects Alzheimer‑related outcomes (for example the PETAL trial evaluating periodontal treatment and Alzheimer outcomes). Results from these larger, well‑designed trials are needed to establish causality and clinical benefit (6).

These studies matter above all because of their prevention potential and research and policy implications.

If gum disease contributes causally to Alzheimer (and maybe other neurodegenerative diseases), then routine oral care and timely periodontal treatment could become relatively low-cost strategies to reduce dementia incidence or at least delay onset. They could inform policy makers and drive a shift in wider national reimbursement of periodontal treatments, but also focus efforts towards targeted communication campaigns.

There are studies that indicate that good gum disease improves healthspan and equally that Alzheimer correlates with morbidity and mortality, so improving the symptoms of both these diseases and relenting the onset of Alzheimer is likely to have a positive impact on lifespan and longevity as well.