Common Pathways of Immune Response and Inflammatory State
Chronic inflammation is correlated with the onset and progression of Alzheimer’s Disease, and it has been postulated that chronic inflammation and neuronal aging induces stress and neuropathological changes.76 In this model, chronic inflammation primes the microglia and induces a hyperreactive state, which then results in a failure to clear misfolded or damaged neuronal proteins and enhances the aggregation of neuronal proteins associated with dementia, such as Aß1-42.77,78 Similarly, periodontal tissue breakdown seen in periodontitis is a result of host inflammatory response to bacterial stimuli. Periodontal tissue breakdown is mediated by pro-inflammatory cytokines and mediators such as interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), receptor activator of nuclear factor kapp B ligand (RANKL), and matrix metalloproteinases (MMPs). These pro-inflammatory mediators interact with bacteria and the surrounding tissues. The heterogeneity among individuals in this response can influence disease susceptibility and severity.79 Additionally, periodontal disease severity is correlated to increased levels of pro-inflammatory mediators systemically.80-82 Because inflammation may influence the progression of disease in both periodontitis and dementia, one mechanism of interaction between periodontitis and dementia may include increased levels of inflammation and their influence on neuronal function.