Association between Periodontitis and Alzheimer’s Disease

Association between Periodontitis and Alzheimer’s Disease

Abbayya, K., Puthanakar, N. Y., Naduwinmani, S., & Chidambar, Y. S. (2015). Association between Periodontitis and Alzheimer’s Disease. North American journal of medical sciences, 7(6), 241–246. https://doi.org/10.4103/1947-2714.159325

As suggested by the title, this article explores the linkage between Periodontitis and Alzheimer’s Disease. There are four key concepts that the author uses in assessing the connection between the two main concepts. The first term is Alzheimer’s Disease (AD) which is defined as an age-related disease the is a result of swelling or inflammation of the central nervous system. In this case, inflammation which is the second term use does not only refer to swelling but also bacterial destruction caused by the oral bacteria periodontitis. Periodontitis has been described in the article as an anaerobic bacteria that causes swelling and destruction of the mouth tissue that holds the teeth. The author also used Proinflammatory cytokines to refer to signalling molecules produced by the immune and are released into the body system, causing the inflammation. The author explores the pathogenesis of AD and the mechanism of spread to the brain and hence establishes the link between periodontitis bacteria and AD.

The article explains that Alzheimer’s Disease is a result of the formation of extracellular amyloids and intraneuronal neurofibrillary tangles which eventually causes loss of neuronal synapse. These changes are triggered by the inflammation of the nervous system induced by the proinflammatory cytokines. The disease is most prevalent among the aged. Other factors that may influence the vulnerability include family history, hypertension, high fat diet, diabetes, and history of head trauma. The disease exists in two categories; early or late-onset. The article holds that early-onset is genetic, while late-onset is a combination of both genetic and environmental factors.

When it comes to the pathogenesis of AD, the process starts by inflammation of the amyloid 1-42 peptide in the senile plaques. This, in turn, triggers multiplication of microglial cells whose role is to protect the nervous system through maintaining homeostasis in the brain. The disease is related to age because microglial cells lose their protective capability, leading to a persistent inflammatory response. The brain responds to inducing the production of the neurotoxic substance. This response plays a role in the pathogenesis of AD because the microglial cells start to secret antigens which in turn result in uncontrolled expressions of proinflammatory factors. The manifestation of the uncontrolled expression in an AD patient leads to neurodegeneration, and hence the problem of AD develops and progresses further. To this end, the article finds microglial cells to be pivotal in the development of AD. It is described as a “double-edged sword since it protects under normal circumstances and destroys when AD chips in.

The article further explores how the inflammation spreads to the brain. Two mechanisms are identified. One is through systemic circulation in which the inflammatory molecules get into the brain through blood in areas where no blood-brain barrier. Also, it can be facilitated by fenestrated capillaries of the BBB, increased permeability of BBB or through cytokine transporters. The second mechanism is through neural pathways in which peripheral cytokines triggers peripheral nerve fibres leading to high levels of brain cytokines. The connection

To establish the link between Periodontitis and Ad, the author looks at Periodontitis as a systemic disease. In his analysis, the author declares that since Periodontitis is inflammation of the gum, it induces immune reaction. Periodontitis induced reaction leads to inflammation which extends from the gum to the deeper tissues, affecting the epithelium and hence severe inflammation. The inflammation extends further and affects the entire nervous system. Therefore, the article identifies two ways of linkage between Periodontitis and AD. One is the increase of proinflammatory cytokines as a result of responses to periodontopathic microorganisms, which lead to a series of inflammations let out through the systemic circulation. This goes on to affect the microglial cells and hence neuronal damage. The second way is by microorganisms from the dental plague invading the brain either through blood circulation or peripheral stimulation. The inversion induces inflammation which affects the nervous system. To this end, the article concludes that Periodontitis plays a significant role in the development of Alzheimer’s Disease.