Association between Periodontal Health Status and Cognitive Abilities. The Role of Cytokine Profile and Systemic Inflammation

Abstract

Background: Contemporary neurobiology, periodontal medicine, and immunology are now focusing on the relationship between chronic periodontitis and systemic diseases, which also include Alzheimer's disease (AD). However a causative relationship between dementia and periodontitis has yet to be confirmed.

Objective: The aim of the study was to determine whether periodontal health status and cognitive abilities are correlated with the relative changes in systemic measures of pro- and anti-inflammatory cytokines as a reflection of systemic inflammation. We hypothesized that poor periodontal health status may be associated with cognitive impairment and dementia via the exacerbation of systemic inflammation.

Methods: Based on the periodontal and psychiatric examinations and the cytokine levels produced by unstimulated and LPS-stimulated PBL isolated from 128 participants, we have examined if the coexisting of these two clinically described conditions may have influence on the systemic inflammation. Mini- Mental State Examination (MMSE) and Bleeding on Probing (BoP) test results were combined into the one mathematical function U, which determines the severity of specific condition, called Cognitive and periodontal impairment state. Similarly, the levels of cytokines were combined into the one mathematical function V, whose value determines the level of Inflammatory state. The correlation between U and V was determined.

Results: These results confirm that the presence of cognitive decline and the additional source of proinflammatory mediators, like periodontal health problems, aggravate the systemic inflammation.

Conclusion: It is most likely that the comorbidity of these two disorders may deepen the cognitive impairment, and neurodegenerative lesions and advance to dementia and AD.

Keywords: Alzheimer's disease; Cognitive impairment; cytokines; dementia; periodontal disease; systemic inflammation.

Fig. (1)

Association between the averages of cytokines levels and clinical parameters BoP score (A) and MMSE score (B). Average concentrations are presented in relative scales, with minimal concentrations as a baselines (minimal concentrations taken as 1). Data presented in Table 1 and Table 2. The conditional averages of cytokines levels (points). Fitted curves were included (lines).

Fig. (2)

Correlation between Cognitive and periodontal impairment state (U), measured as the function of MMSE and BoP (see Statistical methods), and Inflammatory state (V) as a function of cytokines levels produced by unstimulated PBL ex vivo.

Fig. (3)

Correlation between Cognitive and periodontal impairment state (U), measured as the function of MMSE and BoP (see Statistical methods), and Inflammatory state (V) as a function of cytokines levels produced by LPS-stimulated PBL ex vivo.

Fig. (4)

Association between Cognitive and periodontal impairment state (U), and Inflammatory state (V) as the probability, that first person have higher Inflammatory state than the second one, if the first person has higher or lower Cognitive and periodontal impairment state than the second one. This probability is showed as a function of difference in Cognitive and periodontal impairment states between this two persons.