How inflammatory mediators produced in periodontitis can be a
risk for developing AD
The host response is crucial in eliciting systemic consequences in
periodontal infection because it releases an array of inflammatory
mediators, including cytokines, to combat periodontal bacteria that
penetrate the systemic circulation.Periodontal infections and their
products trigger an inflammatory response in the Brain. It is well known
and validated by evidence that the presence of inflammation in the Brain
causes cognitive impairment, including that exhibited in AD. This
inflammatory dysfunction is induced by cytokine-mediated interactions
between neurons and glial cells (27, 28).
Periodontitis may lead to the development of AD as a consequence of the
host’s response to periodontal infections, which produces a rise in the
production of proinflammatory cytokines. This triggers a cascade of
cytokine and pro-inflammatory substances to be produced into the
circulatory system, leading in a systemic inflammation load and an
episode of systemically/peripheral inflammation. These pro-inflammatory
chemicals have a propensity to permeate the BBB and reach brain regions.
These results in the priming/activation of cells called microglial cells
and the deleterious implications of neuronal injury. “TNFα, TGF-, and
chemokines (monocyte chemotactic protein, IL-8, macrophage migration
inhibitory variable, and monokine generated by -interferon)” were
additionally reported as serum and plasma indicators for the cause of AD
(29).
The synthesis of cytokines, particularly TNFα, during inflammation plays
a crucial influence in neurodegenerative disorders. Gliosis,
demyelination, BBB degradation, and cell death are triggered by TNFα’s
amplification of the inflammatory process. In light of this, TNFα is
critical to the neurodegenerative process (28).