Periodontal Pathogenesis and Cognitive Decline
Summary
Periodontitis is a chronic inflammatory condition of the supporting tissues of the teeth, driven by a dysbiotic biofilm dominated by pathogens such as Porphyromonas gingivalis. Local tissue destruction and microbial dissemination can provoke a systemic inflammatory response, characterised by elevated cytokines and endotoxaemia. Emerging evidence implicates periodontal pathogens and their virulence factors in compromising the blood–brain barrier, seeding neuroinflammation and accelerating neuropathological hallmarks of dementia, including amyloid-β accumulation, tau hyperphosphorylation, synaptic loss and hippocampal neurodegeneration. Both direct invasion of bacterial products into the central nervous system and indirect effects via systemic cytokine overproduction converge on microglial activation and oxidative stress, thereby impairing cognitive functions. Understanding these mechanistic pathways underscores the importance of oral health in mitigating dementia risk and suggests novel interventional targets that bridge dentistry and neurology.
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Periodontal Pathogenesis and Cognitive Decline publication trend
The graph below shows the total number of articles in periodontal pathogenesis and cognitive decline across all publications each year (not limited to Nature Index journals).
Technical terms
Porphyromonas gingivalis: Anaerobic keystone pathogen implicated in periodontitis and neurodegenerative processes.
Gingipains: Cysteine proteases produced by P. gingivalis that degrade host proteins and modulate inflammatory signalling.
Blood–brain barrier (BBB): Selective endothelial interface that restricts passage of cells and molecules from blood to brain.
Microglial activation: Innate immune response in the brain characterised by morphological changes and pro-inflammatory mediator release.
Neuroinflammation: CNS immune reaction involving glial activation and cytokine production, contributing to neuronal dysfunction.
References
- Porphyromonas gingivalis bacteremia increases the permeability of the blood-brain barrier via the Mfsd2a/Caveolin-1 mediated transcytosis pathway. International Journal of Oral Science (2023).
- Microglial DBP Signaling Mediates Behavioral Abnormality Induced by Chronic Periodontitis in Mice. Advanced Science (2024).
- IL-1β and TNF-α play an important role in modulating the risk of periodontitis and Alzheimer’s disease. Journal of Neuroinflammation (2023).
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