Gum Disease Now Linked to Dementia:
All countries are experiencing an increase in the number of people over the age of 65 with Alzheimer’s. Alzheimer’s disease is the leading cause of dementia in the US population. Current studies demonstrate a definitive link between the presence of periodontal pathogens and the inflammatory burden and oxidative stress observed in the brain’s of individuals with Alzheimer’s.
A study of dementia led by University of South California researchers revealed that missing teeth and chronic inflammation of the mouth at an early age quadruples the risk of developing Alzheimer’s disease. The study, which was presented at the first Alzheimer’s Association International Conference on Prevention of Dementia, looked at the records of over a hundred pairs of identical twins. Each pair consisted of one twin who had developed dementia, and one who had not. Acting on the principle that identical twins share the same genetic blueprint, the study looked into external factors that could have led to the mental demise of the demented twin.
Dementia is an umbrella term that includes Alzheimer’s disease, and once correctly diagnosed in the twins examined, researchers looked into several potentially modifiable risk factors that could have brought it on. Among these were: periodontal disease before age 35, the experience of a stroke before the onset of dementia, physical exercise between ages 25-50 and years of education.
Titled Potentially Modifiable Risk Factors From Dementia: Evidence from Identical Twins, the study found that a stroke could increase the risk of dementia six-fold in later years, while periodontal disease in early years quadruples that risk.
Effective periodontal treatment is now considered a modifiable risk factor for Alzheimer’s – new information about periodontal pathogens and Alzheimer’s:
Rev Assoc Med Bras. 2014 Mar-Apr;60(2):173-80.
Alzheimer’s disease and periodontitis–an elusive link.
Alzheimer’s disease is the preeminent cause and commonest form of dementia. It is clinically characterized by a progressive descent in the cognitive function, which commences with deterioration in memory. The exact etiology and pathophysiologic mechanism of Alzheimer’s disease is still not fully understood. However it is hypothesized that, neuroinflammation plays a critical role in the pathogenesis of Alzheimer’s disease. Alzheimer’s disease is marked by salient inflammatory features, characterized by microglial activation and escalation in the levels of pro-inflammatory cytokines in the affected regions. Studies have suggested a probable role of systemic infection conducing to inflammatory status of the central nervous system. Periodontitis is common oral infection affiliated with gram negative, anaerobic bacteria, capable of orchestrating localized and systemic infections in the subject. Periodontitis is known to elicit a “low grade systemic inflammation” by release of pro-inflammatory cytokines into systemic circulation. This review elucidates the possible role of periodontitis in exacerbating Alzheimer’s disease. Periodontitis may bear the potential to affect the onset and progression of Alzheimer’s disease. Periodontitis shares the two important features of Alzheimer’s disease namely oxidative damage and inflammation, which are exhibited in the brain pathology of Alzheimer’s disease. Periodontitis can be treated and hence it is a modifiable risk factor for Alzheimer’s disease.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712346/ – Serum Antibodies to Periodontal Pathogens are a Risk Factor for Alzheimer’s Disease
this is an excellent study from the above link, read a poignant clip of it below:
In the current study, both the AD and MCI subjects demonstrated significant elevations in antibody to P. intermedia and F. nucleatum at baseline, prior to diagnosis of the neurological changes. Additionally, the AD subjects expressed significantly elevated antibody to T. denticola, and P. gingivalis at baseline. These sera were obtained years prior to the clinical diagnosis of AD or MCI, while subjects were still cognitively normal. Therefore these elevations cannot be attributed to secondary effects of the AD disease process, such as poor nutrition or other dementia-related neglect. While it could be suggested that the antibody to these oral pathogens may have been cross-reactive with antigens from other sources, the literature is replete with studies supporting the specificity of these antibodies for oral infections [20–21, 43–46], and that successful treatment and maintenance of periodontitis significantly lowers these antibody levels . Comparison of these antibody levels to those described in numerous populations show levels in the AD and MCI subjects in the current study to be similar to chronic periodontitis patients [45–49]. Interestingly, the control group also showed antibody levels higher than healthy values for four of the seven bacteria (A. actinomycetemcomitans, C. rectus, T. forsythia and P gingivalis) with three of the four at levels consistent with chronic periodontal disease. This may be because the study population was older, with a mean age at baseline of 70–74 years of age and periodontal disease occurs more frequently in elder adults. Regardless, the levels of antibodies in the control group were significantly less than the levels of those who converted to AD at baseline for five of the seven bacteria studied.
For more information about Alzheimer’s:
Definitive treatment for periodontal disease involves a multi-faceted approach to control chronic inflammation. Putting periodontal disease into remission and ending the chronic inflammation associated with it is not achieved by merely removing tartar, the repetitive use of antibiotics (either locally or systemically), or cutting out pockets with a laser or traditional periodontal surgery. Chronic hyper-inflammation is a host response problem and may require the addition of safe and effective anti-inflammatory medications. Definitive treatment should also include Oral DNA salivary pathogen testing not only to target more effective treatment strategies but also to definitively determine if the therapy has been effective in eliminating periodontal pathogens.