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).