There are several factors that can promote Alzheimer’s disease, including genetics, diet, exercise, head trauma and exposure to neurotoxins. However, researchers have provided the strongest evidence to date that a bacterium involved in periodontitis contributes to the development of Alzheimer’s disease.
Alzheimer’s disease is characterized by the salient inflammatory features, microglial activation, and increased levels of proinflammatory cytokines which contribute to the inflammatory status of the central nervous system (CNS). Whereas, periodontitis is a common oral infection associated with the gram negative anaerobic bacteria. Periodontitis can be marked as a “low-grade systemic disease” by release of pro-inflammatory cytokines into systemic circulation and elevation of C-reactive protein (CRP). Inflammation is known to play a pivotal role in both the disease process serving as a connecting link between periodontitis and AD.
As the pro-inflammatory molecules enter the brain, it leads to increase in the local pro-inflammatory cytokine pool or stimulation of glial cells to synthesize additional pro-inflammatory cytokines. Alternative pathway through which the cytokines derived from peripheral inflammatory sources might affect the brain is through neuronal pathway. Peripheral cytokines have the capability to stimulate afferent fibers of peripheral nerves, resulting in increased levels of brain cytokines; similarly they can also utilize channels or compartments associated with peripheral nerves to enter the brain.
Periodontal disease (PD) is a condition that causes inflammation and destruction of the gingiva (gums), alveolar bone, and other structures that support the teeth. The etiology of PD is complex involving the presence of pathogenic bacteria found in dental plaque evoking host immune response. PD is a common source of chronic systemic inflammation and immune reactions that result in loss of bone and soft tissue that supports teeth in the jaws.
Periodontitis which is primarily a result of plaque exists in the form of biofilm and consists of numerous microorganisms. The inflammatory process in periodontitis extends from the gingiva (gums) into deeper connective tissues.
Periodontitis is basically a result of inflammation caused due to wide array of pathogenic microorganisms. Periodontopathic microorganisms and the host response cause an increase in the levels of pro-inflammatory cytokines. This results in an array of cytokines and pro-inflammatory agents that are spurted out in systemic circulation leading to systemic inflammatory burden resulting in a state of systemic/peripheral inflammation. These pro-inflammatory molecules are capable of compromising the BBB and entering the cerebral regions. This leads to priming/activation of microglial cells and the adverse repercussions leading to neuronal damage.
Secondly, the microorganisms in the dental plaque can enter brain either through blood stream or via peripheral nerves. These microorganisms and their products elicit an inflammatory mechanism within the central nervous system (CNS). It is generally accepted with appreciable evidence that presence of inflammation in the CNS results in cognitive impairment, such as that seen in AD. Cytokines released during inflammation play a major role in neurodegenerative disease.
Therefore, periodontitis is considered to be one of the probable risk factors for AD. It is a chronic inflammation of the tissue surrounding teeth, which is due to complex bacterial interaction and infection around the teeth. The present review highlights the link between AD and periodontitis, showcasing the pathophysiology and possible implications of the association.
P. gingivalis (gingivatis) generally starts to infiltrate gums during the teenage years and low levels of the bacteria are present in the gums of around one-fifth of people aged under 30. The bacterium is not usually harmful, unless it proliferates to the point that it triggers inflammation and causes redness, swelling, bleeding and erosion of the gums.
For the study, the team compared brain samples taken from deceased individuals with and without Alzheimer’s disease who had died at approximately the same age.
Potempa and colleagues report that P. gingivalis was more commonly found in the samples taken from people with Alzheimer’s disease, as evidenced by the bacterium’s DNA signature and the presence of toxic enzymes called gingipains that it exudes. They also present evidence that the bacterium is involved in rheumatoid arthritis and aspiration pneumonia.
In a mouse model, the team demonstrated that the bacterium can move from the oral cavity to the brain and that certain chemicals can interact with gingipains to block this migration. One drug that inhibits gingipains is currently being tested in phase 1 trials of Alzheimer’s disease and Pontempa says her team are also investigating other inhibitors of the enzymes P. gingivalis needs to “exert its devilish tasks.”
Potempa and team think these enzymes could serve as potential targets for therapeutic interventions to combat various different diseases.
“The beauty of such approaches in comparison to antibiotics is that such interventions are aimed only at key pathogens, leaving alone good bacteria, which we need,” says Potempa, who adds that the best way to ensure P. gingivalis does not grow out of control is to maintain oral hygiene by brushing and flossing and visiting the dentist at least once a year.
Unfortunately, Alzheimer’s disease is proving to be an infectious disease—a prion disease, also known as transmissible spongiform encephalopathy (TSE). Prions also are in the bodily fluids of those who have Alzheimer’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. Prions are impossible to neutralize during sterilization of medical and dental equipment. As such, a visit to the dentist to prevent Alzheimer’s disease might actually increase your overall risk.
Secondly, the above study did not determine if poor oral health was a result of Alzheimer’s disease. It’s also important to point out that dental implants also increase your risk for prion disease. The procedure requires a bone fragment inserted into your jaw. The bones come from cadavers. They don’t/can’t screen them for prion disease. Proceed with caution.
Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy. The operative word is “transmissible.” Even the global surge in autism appears to be related.