Systemic inflammation linking chronic periodontitis to cognitive decline

Brain Behav Immun. 2019 Oct:81:63-73. doi: 10.1016/j.bbi.2019.07.002. Epub 2019 Jul 4.

Abstract

Persistent inflammation in the systemic immune system can impose detrimental effects on the central nervous system (CNS). Neuroinflammation might be a result of this to accelerate the progressive deterioration of neuronal functions during aging. In this regard, controlling inflammation through delaying and/or preventing chronic inflammatory diseases may be a potential strategy to prevent or modify the progression of Alzheimer's Disease (AD). Periodontitis is a chronic inflammatory disease of the oral cavity that is common among the elderly, especially for those who have decline in cognitive functions. While epidemiological findings support the association of chronic periodontitis and cognitive decline, whether they have causal relationship remains unclear. Nonetheless, the possibility that periodontopathogens, systemic immune cells and inflammatory cytokines could reach the CNS should not be overlooked. The impacts of periodontitis on CNS homeostasis and inflammation as a pathophysiological factor concerning the association between periodontitis and AD will be discussed in this review. Future work should elucidate the pathological pathways involved in periodontitis-induced cerebral infections and inflammation, and define the role of the latter in AD progression.

Keywords: Alzheimer’s disease; BBB permeability; Cognitive dysfunctions; Neuroinflammation; Periodontitis; Systemic inflammation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aged
  • Alzheimer Disease / metabolism
  • Blood-Brain Barrier / immunology
  • Chronic Disease
  • Chronic Periodontitis / immunology*
  • Chronic Periodontitis / physiopathology
  • Cognition / physiology
  • Cognitive Dysfunction / complications
  • Cognitive Dysfunction / etiology*
  • Cognitive Dysfunction / immunology*
  • Cytokines / immunology
  • Disease Progression
  • Humans
  • Inflammation / complications
  • Neuroimmunomodulation / immunology
  • Risk Factors

Substances

  • Cytokines