Association between periodontal disease and Alzheimer's disease: a scoping review

Abstract

Background:

Alzheimer's disease (AD) is the most common type of dementia, with mild cognitive impairment (MCI) as its early reversible stage. Periodontal disease (PD) is a chronic inflammatory condition associated with systemic diseases. Recent studies suggest a potential link between PD and AD/MCI. This scoping review evaluates the existing evidence on the association between PD and AD and explores possible mechanisms.

Methods:

A literature search was conducted in PubMed, Embase, and Cochrane databases (September 2025), covering studies from 2004 to 2025. Human clinical studies, animal models, and in vitro experiments were included, while reviews were excluded. Two independent researchers performed study selection, data extraction, and quality assessment.

Results:

A total of 52 studies were included after screening 1,369 records. Among them, 25 clinical studies examined the PD-AD association, including case-control, cohort, and cross-sectional studies. Additionally, 24 studies investigated underlying mechanisms, and 3 animal studies assessed PD-related interventions for AD. Evidence suggests PD increases the risk of AD and accelerates cognitive decline. Potential mechanisms include amyloid-β (Aβ) and tau protein aggregation, neuroinflammation triggered by Porphyromonas gingivalis (Pg) infection, and gut-brain axis dysregulation. Periodontal treatment and probiotics may have protective effects against AD-related pathology.

Conclusions:

PD may be a modifiable risk factor for AD, and periodontal interventions could contribute to AD prevention and management. Further clinical studies are needed to confirm the therapeutic potential of targeting oral microbiota in AD.

1 Background

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment, cognitive decline, and behavioral disturbances, representing the leading cause of dementia worldwide and imposing a substantial burden on patients, caregivers, and healthcare systems (Alzheimer's Association, 2016, 2019; Hu et al., 2021). Neuropathologically, AD is defined by the accumulation of extracellular β-amyloid (Aβ) plaques, the formation of neurofibrillary tangles composed of hyperphosphorylated Tau protein, and subsequent synaptic dysfunction and neuronal loss (Pritchard et al., 2017; Jungbauer et al., 2022; Li et al., 2022; Mao et al., 2022; Weber et al., 2023; Wereszczyński et al., 2023; Zhao et al., 2023). In addition, chronic neuroinflammation—mediated by activated microglia, astrocytes, and proinflammatory cytokines such as IL-1β, IL-6, and TNF-α–has been recognized as a central driver of disease progression (Mao et al., 2022; Weber et al., 2023; Syrjälä et al., 2012; Pazos et al., 2018; Li et al., 2023). Emerging evidence further suggests that systemic inflammatory conditions can exacerbate neurodegenerative processes, underscoring the importance of identifying peripheral sources of inflammation as potential risk factors for AD (Kamer et al., 2008).

Periodontal disease (PD) is a chronic, multifactorial inflammatory disorder initiated by dysbiosis of the oral microbiome (Nakajima et al., 2016). It is characterized by the formation of microbial biofilms that stimulate host immune responses, resulting in periodontal tissue destruction, alveolar bone resorption, and eventual tooth loss (Lu et al., 2018). At the cellular level, PD involves infiltration of neutrophils, macrophages, and lymphocytes into periodontal tissues, accompanied by the production of proinflammatory cytokines (IL-1β, TNF-α, IL-6), prostaglandin E2, reactive oxygen species, and matrix metalloproteinases, which perpetuate tissue damage (Mirnic et al., 2024). As the disease advances, dysregulated host immunity drives chronic systemic inflammation (Wang, 2015). Importantly, periodontal pathogens such as Pg, Tannerella forsythia, and Treponema denticola can persist intracellularly, evade host defenses, and disseminate via the bloodstream (Giannini et al., 2023). Through bacteremia and infected leukocytes, microbial products (e.g., lipopolysaccharides, gingipains, bacterial DNA) may translocate to distant organs, including the brain (Banks, 2016).

The concept of a “PD–brain axis” has therefore attracted increasing attention as a plausible mechanistic link between oral and neurological health (Zhang et al., 2025). Chronic periodontal inflammation elevates systemic inflammatory burden (Murakami et al., 2013), disruption of the blood–brain barrier (Furutama et al., 2020), and priming of microglial responses (Mao et al., 2022). Circulating cytokines derived from periodontal lesions may enter the central nervous system (CNS) and amplify neuroinflammatory cascades (Liu et al., 2023). Furthermore, periodontal pathogens and their virulence factors have been detected in the brain tissue of patients with AD and other neurodegenerative conditions (Olsen, 2021). In particular, Pg and its proteolytic enzymes, gingipains, have been shown to degrade neuronal proteins, promote Aβ aggregation, and enhance Tau hyperphosphorylation, thereby contributing to hallmark AD pathology (Jungbauer et al., 2022; Mao et al., 2022).

Collectively, these observations suggest that PD, through both systemic inflammation and microbial dissemination, may influence the onset and progression of AD. Considering that AD is a continuum with early preclinical changes occurring decades before clinical symptoms. Mild cognitive impairment (MCI), a condition in which cognitive function is lower than expected due to physiological aging, is a concept proposed by Petersen et al. in 1995. It is an intermediate state between normal cognition and predementia. It has also been identified as the first clinical stage of AD (Jia et al., 2020). The ability to carry out daily activities in the MCI state is still normal. A systematic review revealed that 32% of MCI patients will progress to AD within 5 years (Ward et al., 2013). However, this process is reversible (Rao et al., 2023). Interventions that eliminate related risk factors or enhance preventive factors in patients with MCI can effectively prevent AD (Nakamura et al., 2021). Understanding how periodontal inflammation interacts with neurodegenerative mechanisms is of critical importance. This scoping review aims to provide a comprehensive overview of current evidence linking PD to AD, highlight biological mechanisms underlying their interconnection, and discuss the implications of periodontal health management in the context of dementia prevention and therapy.

2 Methods

This study was designed as an exploratory scoping review with the primary aim of mapping and synthesizing the existing body of research on the association between PD and AD. The intention was not to assess intervention effectiveness or conduct meta-analyses but rather to provide a comprehensive overview of the types of evidence, study designs, and proposed mechanisms in this research field. Given its non-interventional nature and the absence of plans for a meta-analysis, formal registration (e.g., in PROSPERO) is not considered essential for this type of review. Nevertheless, to ensure transparency, the review protocol and the PRISMA-ScR Checklist have been included as Supplementary material (Appendix 1 and Appendix 2, respectively).

2.1 Data sources

A comprehensive literature search was conducted in September 2025. The databases searched included PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials to minimize publication bias.

2.2 Search strategy

The following search strategy in PubMed utilized both keyword terms in the title and abstract fields as well as in the Medical Subject Headings (MeSH) to identify possible qualifying articles: (Periodontal Diseases[Mesh] OR Disease, Periodontal[Title/Abstract] OR Diseases, Periodontal[Title/Abstract] OR Periodontal Disease[Title/Abstract] OR Parodontosis[Title/Abstract] OR Parodontoses[Title/Abstract] OR Pyorrhea Alveolaris[Title/Abstract] OR Periodontitis"[Mesh] OR Periodontitides[Title/Abstract]) OR Pericementitis[Title/Abstract]) OR Pericementitides[Title/Abstract]) AND (Alzheimer Disease[Mesh] OR Alzheimer Dementia[Title/Abstract] OR Alzheimer Dementias[Title/Abstract] OR Dementia, Alzheimer[Title/Abstract] OR Alzheimer's disease[Title/Abstract] OR Dementia, Senile[Title/Abstract] OR Senile Dementia[Title/Abstract] OR Dementia, Alzheimer Type[Title/Abstract] OR Alzheimer Type Dementia[Title/Abstract] OR Alzheimer-Type Dementia (ATD)[Title/Abstract]). This search was translated and updated for Embase and the Cochrane Central Register of Controlled Trials accordingly (Sabharwal et al., 2021). When articles were on the topic of associations between PD and AD, the reference lists of included studies were manually searched, and citations of all included studies were checked to ensure search completeness (Dickson-Swift et al., 2022).

Studies were deemed eligible if they met the following criteria: (i) original clinical or experimental investigations conducted in human participants or animal models; (ii) explicitly examined the association between periodontal disease and Alzheimer's disease or explored potential underlying mechanisms; and (iii) published in English between January 2004 and February 2024. Excluded from consideration were systematic reviews, narrative reviews, and conference abstracts without full-text availability.

2.3 Data flustering

The search results were then saved and exported into EndNote, a bibliographic software program, to store, organize, and manage all the results (Dickson-Swift et al., 2022). After removal of duplicates, titles were examined by one author, and articles unrelated to PD and AD were removed. For the retained articles, clinical human and animal studies in which associations between PD and AD were explored or a potential mechanism was elucidated were included. Systematic and retrospective reviews were excluded.

Individual studies were tabulated, and brief descriptions of the following parameters were provided: name of the first author, year of publication, number of participants, country of study participants, study design, study population (human or animal), objective of the study, and outcomes, including statistical parameters and conclusions (Tables 1–3).

3 Results

The initial search yielded 1,369 results. After deduplication, 1,035 articles were further evaluated, 455 of which were excluded for being systematic or retrospective reviews. The remaining 580 full-text articles were assessed, and after excluding studies where PD and/or AD were not the primary variable of interest, 52 studies were included in the summary tables. A PRISMA flow chart showing the study selection at each stage is detailed in Figure 1. Twenty-five studies explored the correlation between PD and AD through clinical research (Table 1). The studies were undertaken in the following regions: China n = 3, Finland n = 1, Germany n = 1, India n = 1, Italy n = 1, Japan n = 1, Korea n = 3, Pomerania n = 1, Spain n = 1, Sweden n = 1, Turkey n = 1, United Kingdom n = 1, USA n = 6, Mendelian randomization studies = 3. The highest number of studies were carried out in USA (n = 6), Korea (n = 3) and China (n = 3). And the studies included 7 case-control studies, 8 cohort studies, 6 cross-sectional studies, 3 Mendelian randomization studies and 1 quasi-experimental study. Twenty-four studies explored the potential mechanism underlying the correlation between PD and AD (Table 2). And the studies included 6 clinical studies conducted in Austria, the United Kingdom, China, Japan, Spain and the United States, 14 animal experiments and 4 cell experiments. Among the 6 clinical studies, 3 were cross-sectional studies, 2 were case-control studies and 1 Cross-sectional study. Three animal studies reported treatment progress based on the potential mechanism underlying the correlation between PD and AD (Table 3).

Figure 1

4 Discussion

This review systematically summarizes the existing evidence on the association between PD and AD, highlighting potential biological mechanisms underlying this relationship and discussing the implications of periodontal management in AD prevention and treatment. While accumulating epidemiological and experimental studies suggest a link between PD and an increased risk of cognitive decline, the causal relationship remains unclear. Further well-designed longitudinal studies and mechanistic investigations are required to establish a definitive connection and explore targeted interventions.

4.1 The correlation between PD and AD

PD has been identified as a chronic inflammatory condition associated with systemic health consequences, including cardiovascular disease, diabetes, and more recently, neurodegenerative disorders such as AD (D'Aiuto et al., 2025). Epidemiological studies have reported that individuals with PD exhibit a higher prevalence of AD and mild cognitive impairment (MCI) (Schwahn et al., 2022; Chen et al., 2017; Holmer et al., 2018). Several cohort and case-control studies have found that markers of PD (Syrjälä et al., 2012; Ma et al., 2022; Schwahn et al., 2022; Choi et al., 2019; Carballo et al., 2023; Fu et al., 2023; Ide et al., 2016; Panzarella et al., 2022; Noble et al., 2014; Yoo et al., 2023; Laugisch et al., 2021; Saito et al., 2022; Karaduran et al., 2023), such as clinical attachment loss and probing depth, are significantly associated with poorer cognitive performance. However, due to the observational nature of most studies, the directionality and causality of this association remain to be fully established.

Some studies propose that PD may contribute to AD pathogenesis by exacerbating neuroinflammation and promoting amyloid-beta (Aβ) deposition (Karaduran et al., 2023). Conversely, it is also plausible that AD-related cognitive decline leads to compromised oral hygiene, thereby increasing susceptibility to PD (Syrjälä et al., 2012; Martande et al., 2014). The bidirectional nature of this relationship warrants further investigation, particularly through longitudinal cohort studies and Mendelian randomization analyses to determine whether PD plays a causal role in AD progression.

4.2 Potential mechanisms of PD and AD

4.2.1 PD and Aβ/tau protein aggregation

According to the amyloid hypothesis, abnormal accumulation of Aβ in specific brain regions triggers microglia-mediated inflammation, leading to neuronal damage and ultimately AD. PD may exacerbate this process by inducing systemic inflammation and allowing microbial components to cross the blood–brain barrier (BBB), thereby promoting Aβ deposition (Ahmad et al., 2019). In addition, PD may induce abnormal tau phosphorylation and the formation of neurofibrillary tangles (NFTs), further accelerating AD pathology (Ryder and Xenoudi, 2021). Several studies have demonstrated that PD enhances microglial activation (Díaz-Zúñiga et al., 2019; Kantarci et al., 2020; Ilievski et al., 2018; Qian et al., 2021) induces neuroinflammatory responses, and leads to neuronal injury, while animal models of PD also exhibit tau hyperphosphorylation and NFT formation (Ilievski et al., 2018). Thus, interventions aimed at mitigating excessive microglial activation might offer potential benefits in slowing AD progression.

4.2.2 The role of Porphyromonas gingivalis (Pg) in AD

Pg is a key periodontal pathogen implicated in PD and has been detected in the brain tissues of AD patients (Poole et al., 2013). Studies (Sato et al., 2022; Gu et al., 2020) have shown that Pg lipopolysaccharide (LPS) is present in AD brains, whereas it is absent in cognitively normal individuals. Animal experiments (Ilievski et al., 2018; Bahar et al., 2021) further indicate that oral infection with Pg can induce AD-like neuropathological changes, including Aβ deposition, neuroinflammation, and neuronal loss. However, there is still debate regarding the specific toxic components of Pg: while some studies attribute the neurotoxicity to Pg LPS (Sato et al., 2022; Gu et al., 2020), others suggest that phosphoglycerol dihydroceramide produced by Pg may play a more crucial role (Yamada et al., 2020). Further research is required to pinpoint the primary virulence factor of Pg in AD pathogenesis and to develop targeted therapeutic strategies against Pg infection.

4.2.3 Microbial invasion routes

Multiple routes may allow periodontal pathogens to invade the central nervous system (CNS). Periodontal pathogens, particularly Pg, produce virulent factors: specifically, gingipains: that compromise the integrity of the blood-brain barrier, allowing bacteria and inflammatory mediators to enter the central nervous system (Kim and Pang, 2025). Oral pathogens may also migrate directly to the brain via cranial nerve routes, such as the trigeminal or olfactory nerves (Sakane et al., 2020). Additionally, secondary routes—particularly the gastrointestinal tract—may be involved. PD-induced oral dysbiosis can alter gut microbial composition, promoting systemic inflammation and neuroinflammation through the gut–brain axis (Xue et al., 2020; Lu et al., 2022). These pathways likely act in combination, enhancing CNS vulnerability in the context of chronic oral infection.

4.2.4 Periodontal microbiome dysbiosis and metabolic abnormalities

Beyond direct microbial invasion, PD-associated dysbiosis alters host metabolism. Metabolomic studies have identified specific PD-related metabolites (e.g., galactinol, D-mannitol) that predict AD progression (Leblhuber et al., 2020; Qiu et al., 2024). Gut microbiome disturbances induced by PD have also been linked to neuroinflammation and cognitive decline in animal models (Xue et al., 2020; Lu et al., 2022). However, clinical validation remains limited, and further studies are needed to confirm whether microbiome-targeted therapies can mitigate AD risk.

4.3 The correlation between PD treatment management and AD

Given that there are currently no disease-modifying therapies for AD and that existing treatments offer only transient symptomatic relief, early intervention is critical (Di Santo et al., 2013). PD has been proposed as a modifiable risk factor for AD, suggesting that its treatment might provide a novel approach for AD prevention and management (Dominy et al., 2019). Several studies have demonstrated that periodontal therapy—such as scaling and root planning—may reduce systemic inflammatory markers and potentially improve cognitive outcomes.

For instance, Schwahn et al. (2022) indicated that periodontal treatment might mitigate AD-related brain atrophy, while Saito et al. (2022) reported a lower risk of AD among individuals who received long-term periodontal care. Additionally, preclinical studies (Zhao et al., 2023) have shown that gingipain inhibitors can reduce Aβ production, dampen neuroinflammation, and protect hippocampal neurons, and that probiotics such as Nisin can ameliorate AD-like pathology by restoring microbial balance. More recently, nanotechnology-based strategies have emerged; an animal study (Liu et al., 2025) demonstrated that Pg-stimulated macrophage membrane-coated platinum nanoclusters (Pg-M-PtNCs) exhibited good biocompatibility, effectively inhibited Pg growth, and reduced bacterial load and neuronal injury in vivo, thereby improving AD-like cognitive impairment. Collectively, these findings highlight the therapeutic potential of periodontal treatment and novel experimental approaches, although their efficacy requires confirmation in large-scale clinical trials.

4.4 Conflicting findings and limitations

Despite accumulating evidence, inconsistencies remain. Some studies report no significant association between PD and AD after adjusting for confounders such as age, education, and comorbidities, suggesting that residual confounding cannot be excluded. Additionally, the majority of studies are cross-sectional or retrospective, which limits causal interpretation. Heterogeneity in study populations, PD diagnostic criteria, and cognitive assessment tools further complicates comparisons across studies. It is important to note that this scoping review provides a valuable mapping of existing evidence but offers a lower level of evidence compared to systematic reviews or meta-analyses. This distinction should be kept in mind when interpreting the findings. Another limitation is language and publication bias: this review only included English-language and peer-reviewed articles, excluding gray literature, which may have led to omission of relevant data. Incorporating gray literature in future reviews may reduce bias and provide a more balanced synthesis.

4.5 Future directions

Future research should prioritize longitudinal and interventional studies to clarify causality and mechanisms. Standardization of PD and AD diagnostic criteria, along with harmonized outcome measures, would facilitate cross-study comparisons. Integration of microbiome profiling, metabolomics, and neuroimaging could provide new insights into biological pathways. Importantly, evaluating periodontal treatment as part of multidomain AD prevention strategies warrants exploration in clinical trials.

5 Conclusion

This review synthesizes current evidence on the association between PD and AD. Epidemiological studies consistently demonstrate that individuals with PD have a higher prevalence of cognitive decline and AD, although most available data are observational and causality has not been established. Experimental studies provide mechanistic insights, suggesting that PD may contribute to AD pathology through chronic systemic inflammation, amyloid-β and tau aggregation, neuroinvasion of Pg, and oral–gut–brain microbiome dysregulation. Limited but emerging evidence also indicates that periodontal treatment may attenuate systemic inflammation and potentially improve cognitive outcomes.

Taken together, these findings highlight PD as a potential modifiable risk factor for AD. While current evidence supports biological plausibility and a consistent association, robust longitudinal and interventional studies are still needed to determine whether improving periodontal health can reduce the incidence or progression of AD.

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