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Inflammation and Alzheimer's disease: Possible role of periodontal diseases

Department of Periodontology and Implant Dentistry, College of Dentistry, New York University, New York, NY, USA.
Alzheimer's & dementia: the journal of the Alzheimer's Association (Impact Factor: 17.47). 07/2008; 4(4):242-50. DOI: 10.1016/j.jalz.2007.08.004
Source: PubMed

ABSTRACT The molecular and cellular mechanisms responsible for the etiology and pathogenesis of Alzheimer's disease (AD) have not been defined; however, inflammation within the brain is thought to play a pivotal role. Studies suggest that peripheral infection/inflammation might affect the inflammatory state of the central nervous system. Chronic periodontitis is a prevalent peripheral infection that is associated with gram-negative anaerobic bacteria and the elevation of serum inflammatory markers including C-reactive protein. Recently, chronic periodontitis has been associated with several systemic diseases including AD. In this article we review the pathogenesis of chronic periodontitis and the role of inflammation in AD. In addition, we propose several potential mechanisms through which chronic periodontitis can possibly contribute to the clinical onset and progression of AD. Because chronic periodontitis is a treatable infection, it might be a readily modifiable risk factor for AD.

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    • "Systemic inflammation and infections could worsen a number of CNS disorders [26] [43]. Among the common chronic inflammatory disorders in adults, much attention has been paid to the periodontitis as the pathogenesis of CNS disorders, including AD [13] [15] [44]. The increase in macrophage-derived TNF-í µí»¼ and IL-1í µí»½ in the circulation during periodontitis [39] [40] also supports the idea that chronic periodontitis is involved in the pathogenesis of systemic inflammatory diseases, including atherosclerosis, cardiovascular disease, and diabetes [10] [11] [12]. "
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    • "Lastly, associations between periodontal disease and other diseases in living populations can exist because the body responds to the presence of bacteria and bacterial antigens in the oral cavity and in the bloodstream through the production of proinflammatory immune cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-a), which can have systemic or distant effects (Loos, 2005; Moutsopoulos and Madianos, 2006; Spahr et al., 2006). These effects include causing or accelerating atherogenesis (the formation of plaques within arteries) and thus contributing to cardiovascular disease (Amabile et al., 2008; Kamer et al., 2008; Watts et al., 2008), affecting cell growth control and leading to carcinogenesis (Meyer et al., 2008), or priming microglial cells and other factors associated with Alzheimer's disease pathology (Watts et al., 2008). "
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    • "The interaction between periodontopathic bacteria and the host response may result in significant systemic inflammation characterized by production of inflammatory molecules including IL-1β, IL-6, and TNF-α (D'Aiuto et al., 2004). Therefore, periodontal bacteria and systemic inflammatory molecules may contribute to brain inflammation that characterizes AD and affects its expression (Kamer et al., 2008a). Support for this hypothesis comes from earlier studies that used dark field microscopy, molecular and immunological techniques to identify spirochetes including Treponema species (periodontal pathogens) with higher frequency in the brains of AD patients compared to non-AD subjects (Miklossy, 1993; Riviere et al., 2002). "
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