IADR Abstract Archives
Association between Alzheimers Disease and Periodontitis: Pilot study
Objectives: The bacteria in the disbiotic microbiome of periodontitis (PE) exacerbate the production of proinflammatory mediators having the potential to spread to the systemic circulation and trigger neuroinflamation wich plays a fundamental role in the onset and progression of Alzheimers Disease (AD). The aim of this study was to quantify the levels of Th1, Th17, Th2 and T-reg cytokines, load of P. gingivalis (P.g) and ApoE-ε4 in Gingival Crevicular Fluid (GCF) of controls, PE and PE and AD subjets and correlate them with the cognitive status.
Methods: A cross sectional study was carried out. Each of the subjects included were classified according to their periodontal (AAP 2017) and their congnitive (MoCa Test). Biological samples of GCF and subgingival microbiota were taken to quantify cytokine profiles (Multiplex immunoassay, Invitrogen™ Cytokine 25-Plex Human Panel), ApoE-ε4 (Invitrogen™ Apolipoprotein ε4 Human ELISA Kit) and bacterial load of P. g (qPCR, FavorPrepTM Tissue Genomic DNA extraction Mini Kit).
Results: Cognitive status was dependent on the study group, significant difference (p<0.05) was found in the clinical parameters of PE between groups. A correlation was found between cognitive impairment and higher levels of Th1 and Th17 citokynes (r=-0.919, p<0.05) while Th2 ant Treg citokynes increases as the cognitive status improves (r=0.97, p<0.05). The bacterial load of P. gingivalis increased as the cognitive status decline (r=-0.996, p<0.05). ApoE-ε4 , a known risk factor of AD, secretion was detectable in GCF of all subjets and higher in impaired cognitive status (r=-0.939, p<0.05).
Conclusions: Association between periodontal citokyne, bacterial load, ApoE-4ε and cognitive status were established. This data supports recent studies about the relationship between this two diseases. This is the first clinical study to quantify the secretion of ApoE-ε4 in GCF. With this it is suggest that a greater control of periodontal status could modify the cognitive status in AD.
Methods: A cross sectional study was carried out. Each of the subjects included were classified according to their periodontal (AAP 2017) and their congnitive (MoCa Test). Biological samples of GCF and subgingival microbiota were taken to quantify cytokine profiles (Multiplex immunoassay, Invitrogen™ Cytokine 25-Plex Human Panel), ApoE-ε4 (Invitrogen™ Apolipoprotein ε4 Human ELISA Kit) and bacterial load of P. g (qPCR, FavorPrepTM Tissue Genomic DNA extraction Mini Kit).
Results: Cognitive status was dependent on the study group, significant difference (p<0.05) was found in the clinical parameters of PE between groups. A correlation was found between cognitive impairment and higher levels of Th1 and Th17 citokynes (r=-0.919, p<0.05) while Th2 ant Treg citokynes increases as the cognitive status improves (r=0.97, p<0.05). The bacterial load of P. gingivalis increased as the cognitive status decline (r=-0.996, p<0.05). ApoE-ε4 , a known risk factor of AD, secretion was detectable in GCF of all subjets and higher in impaired cognitive status (r=-0.939, p<0.05).
Conclusions: Association between periodontal citokyne, bacterial load, ApoE-4ε and cognitive status were established. This data supports recent studies about the relationship between this two diseases. This is the first clinical study to quantify the secretion of ApoE-ε4 in GCF. With this it is suggest that a greater control of periodontal status could modify the cognitive status in AD.