The Role of Periodontitis in Increasing Cognitive Decline in Alzheimer's Disease

Abstract

Aim and background: Periodontal disease (PD), a chronic inflammatory disease of the gums, is characterized by periodontal pocket formation, bone resorption, and disruption of oral tissue integrity. This study aimed to review the literature on the potential pathogenic link between PD and Alzheimer's disease (AD), which focuses on the role of periodontal pathogens, among which is found Porphyromonas gingivalis. Methods: Recent studies and literature have linked PD to the development of systemic diseases, such as AD, a neurocognitive disorder affecting more than 6 million Americans. Given that both PD and AD are characterized by inflammation, it encourages interest in understanding how PD can influence the onset and progression of AD.

Results: These pathogens contribute to systemic inflammation by increasing the secretion of proinflammatory cytokines, such as interleukin-1β, which in turn trigger beta-amyloid accumulation plaques, increasing kinase activity involved in the hyperphosphorylation of the tau protein, and lower concentrations of brain-derived neurotrophic factor, a neuroprotective protein against neurodegeneration.

Conclusion: This review highlights a potential inflammatory feedback loop, where the immune response to oral pathogens exacerbates neurodegenerative processes in the brain, suggesting a significant intersection between PD and AD. Understanding this relationship and the mechanisms involved could open new therapeutic avenues for both diseases.

Clinical significance: The findings collectively suggest that periodontal pathogens have the potential to influence the development of AD and perpetuate inflammatory responses leading to the cognitive decline observed in AD. How to cite this article: Klonaris N, Murcia JDG, Patil S, et al. The Role of Periodontitis in Increasing Cognitive Decline in Alzheimer's Disease. J Contemp Dent Pract 2025;26(3):311-320.

Keywords: Alzheimer's disease; Brain-derived neurotrophic factor; Inflammation; Lipopolysaccharides; Periodontitis Tau protein..