Acta clinica Belgica · 2026
The role of olfactory and salivary gland pathways in periodontal disease-mediated Alzheimer's disease progression: mechanistic insights and early diagnostic implications.
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Liang Hao, Yu Wenlei, Han Zeyang, Xu Bo, Zhuang Zhijie, Liu Jun
Аннотация
OBJECTIVES: Periodontal disease, characterized by subgingival biofilm dysbiosis and Porphyromonas gingivalis (P. gingivalis) colonization, has been increasingly implicated in Alzheimer's disease (AD) pathogenesis. This review systematically delineates the pathophysiological mechanisms underlying the periodontal-AD nexus, highlighting olfactory dysfunction (OD) and salivary gland hypofunction as putative prodromal biomarkers for periodontal disease-associated AD progression.
METHODS: PubMed/MEDLINE database was systematically searched for English-language articles published between January 1994 and March 2025. Search terms encompassed periodontal disease, Porphyromonas gingivalis, Alzheimer's disease, neuroinflammation, olfactory dysfunction, salivary gland hypofunction, blood-brain barrier, microglial activation, and cognitive decline.
RESULTS: Periodontal disease compromises blood-brain barrier integrity via bacterial translocation, systemic pro-inflammatory mediator dissemination, and peripheral immune cell activation, thereby potentiating microglial polarization and neuroinflammatory cascades integral to early AD neuropathology. Both OD and salivary gland hypofunction demonstrate robust associations with periodontal disease severity and constitute sensitive biomarkers for prodromal AD.
CONCLUSIONS: Periodontal disease-mediated neuroinflammation constitutes a pivotal mechanistic pathway linking oral dysbiosis to AD onset. OD and salivary gland hypofunction emerge as promising early diagnostic indicators for periodontal disease-associated AD susceptibility, warranting prospective clinical validation.
METHODS: PubMed/MEDLINE database was systematically searched for English-language articles published between January 1994 and March 2025. Search terms encompassed periodontal disease, Porphyromonas gingivalis, Alzheimer's disease, neuroinflammation, olfactory dysfunction, salivary gland hypofunction, blood-brain barrier, microglial activation, and cognitive decline.
RESULTS: Periodontal disease compromises blood-brain barrier integrity via bacterial translocation, systemic pro-inflammatory mediator dissemination, and peripheral immune cell activation, thereby potentiating microglial polarization and neuroinflammatory cascades integral to early AD neuropathology. Both OD and salivary gland hypofunction demonstrate robust associations with periodontal disease severity and constitute sensitive biomarkers for prodromal AD.
CONCLUSIONS: Periodontal disease-mediated neuroinflammation constitutes a pivotal mechanistic pathway linking oral dysbiosis to AD onset. OD and salivary gland hypofunction emerge as promising early diagnostic indicators for periodontal disease-associated AD susceptibility, warranting prospective clinical validation.