Background
Alzheimer’s disease (AD) is a fatal brain condition that predominantly affects older people and is a major global health concern for people in their senior years. Alzheimer’s disease prevalence increases sharply with aging, reaching about 50% in persons over the age of 85 (1).
Periodontitis is more common in elderly people due to its chronic and cumulative nature, with two-thirds (68%) of those over the age of 65 suffering from chronic periodontitis. Also, individuals aged 70 to 81 years old had a considerably greater frequency of periodontitis than those aged 50 to 59 years old (2,3). Worldwide, around 11% of people suffer from severe periodontitis (4).
Unless an important medical improvement, the incidence of AD will probably double by the middle of this century, finally leading to a worldwide incidence of roughly 131.5 million (5,6). Great deals of fresh cases of AD are random and late-onset illnesses.
In the next 50 years, it’s predicted that AD and periodontal disease would impact about 14 million individuals (1,7) as the population at large ages and their lifespan rises. Switching to newer treatment techniques that can be efficient towards possible contributing factors for both conditions can help lower the incidence of AD and periodontal diseases (1).
Both AD and periodontitis may contain an early or late start. Early-onset AD and periodontitis are assumed to be inheritable, whereas late-onset AD and periodontal disease, which effects a lot of people, appears to be the result of an interplay of genetic and extrinsic factors. Age, type 2 diabetes, and teaching are all connected with risk for both disorders. In addition, periodontitis is regarded as being one of the potential risk variables for AD (1,7).
The ”chicken or egg first” argument may be made from a significant portion of cross-sectional and longitudinal correlation studies. Is the association between AD and periodontal disease entirely due to Alzheimer’s Disease patients‘ failure to sufficiently eliminate a dysbiotic biofilm using a regular plaque control program? Or, can the infiltration of inflammation-causing cytokines into the cerebral cortex as a result of the host’s contact with pathogenic microbiota have a function in the commencement and progression of AD? (8,9)
There is emerging confirmation that periodontitis can damage all parts of the body and is an independent risk factor for AD. Hence, here may be a link between the mediators of inflammation generated by the contact of oral infections with the host’s cells and AD. This would be especially noteworthy given the age-related frequency of chronic periodontitis and AD (10).
The continual growth in an internal pro-inflammatory status with age maintains the level of susceptibility to periodontitis and AD (11).