Conclusion
Regarding the importance of peripheral factors that are inflammation in
commencing neuroimmune reactions and affecting cognitive capacities, the
process linking cytokine immune systems generated by the tissues of
periodontal disease to the brain system remained unexplained.
The present evidence clearly supports proinflammatory cytokines as a
significant component in the etiology of periodontal disease and AD. A
plausible idea is that lowering proinflammatory cytokines might be a
potential technique for interfering with the illness process. Since the
existence of proinflammatory cytokines is an established cause for AD,
proper PD therapy or prevention may help to postpone the onset of the
chronic condition. As a result, additional rigorous and higher-level
research, such as RCTs, will be needed to back up these
conclusions.
The recovery of microbiome/host balance by specific pro-resolving lipid
mediator treatment shows that microbiome dysbiosis, the host
hyperinflammatory phenotype, and periodontitis may all be restored.