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).