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: 12.41). 07/2008; 4(4):242-50. DOI: 10.1016/j.jalz.2007.08.004
Source: PubMed


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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    • "It has been established that bacterial pathogens and their products play an essential role in the initiation of the chronic inflammatory process causing damage to periodontal tissues. The host response appears to play a key role in pathogenesis of periodontitis by amplifying the destructive inflammatory process initiated by the bacterial insult [3]. The complex pathogenesis of this disease is further complicated by the coexistence of systemic diseases, such as diabetes, which has the potential to aggravate the manifestations of periodontitis [4]. "
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    ABSTRACT: The association between diabetes mellitus and chronic periodontal disease has long been established. Most of the researches linking these two very common chronic diseases were based on type 2 diabetes mellitus and chronic periodontal disease. However, this study was conducted to investigate the association between type 1 diabetes and chronic periodontal disease in Malaysian subjects. Forty-one Malaysian subjects, of which 20 subjects were type 1 diabetics and with chronic periodontal disease (test group) and 21 subjects with only chronic periodontal disease (control group), were included in the study. Periodontal parameters and plaque samples for microbiological evaluation were done at baseline, 2 and 3 months after nonsurgical periodontal therapy. Blood samples were taken from only the test group and evaluated for HbA1c at baseline and 3 months after periodontal therapy. There were no statistically significant difference in periodontal parameters between groups ( P>0.05 ) and no significant improvement in the level of HbA1c in the test group. Microbiological studies indicated that there were significant reductions in the levels of the tested pathogens in both groups. The results of our study were similar to the findings of several other studies that had been done previously.
    The Scientific World Journal 07/2014; Volume 2014 (2014), Article ID 232535, 7 pages(3):7. DOI:10.1155/2014/232535 · 1.73 Impact Factor
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    • "An estimated 5–20% of the world's population suffers from generalized periodontitis; it is among the most common chronic infections in humans [3]. Periodontitis is now recognized as a risk and contributing factor to systemic diseases, including atherosclerotic vascular disease [4], [5], diabetes [6], rheumatoid arthritis [7], Alzheimer's disease [8], [9], and respiratory disease [10]. A chronic immune and inflammatory response triggered by periodontal bacteria, Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia, which are strongly associated with periodontal disease in humans and are together known as the “red complex”, results in severe destruction of the periodontium [1], [2]. "
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    ABSTRACT: Periodontal diseases are multifactorial, caused by polymicrobial subgingival pathogens, including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Chronic periodontal infection results in inflammation, destruction of connective tissues, periodontal ligament, and alveolar bone resorption, and ultimately tooth loss. Enoxacin and a bisphosphonate derivative of enoxacin (bis-enoxacin) inhibit osteoclast formation and bone resorption and also contain antibiotic properties. Our study proposes that enoxacin and/or bis-enoxacin may be useful in reducing alveolar bone resorption and possibly bacterial colonization. Rats were infected with 109 cells of polymicrobial inoculum consisting of P. gingivalis, T. denticola, and T. forsythia, as an oral lavage every other week for twelve weeks. Daily subcutaneous injections of enoxacin (5 mg/kg/day), bis-enoxacin (5, 25 mg/kg/day), alendronate (1, 10 mg/kg/day), or doxycycline (5 mg/day) were administered after 6 weeks of polymicrobial infection. Periodontal disease parameters, including bacterial colonization/infection, immune response, inflammation, alveolar bone resorption, and systemic spread, were assessed post-euthanasia. All three periodontal pathogens colonized the rat oral cavity during polymicrobial infection. Polymicrobial infection induced an increase in total alveolar bone resorption, intrabony defects, and gingival inflammation. Treatment with bis-enoxacin significantly decreased alveolar bone resorption more effectively than either alendronate or doxycycline. Histologic examination revealed that treatment with bis-enoxacin and enoxacin reduced gingival inflammation and decreased apical migration of junctional epithelium. These data support the hypothesis that bis-enoxacin and enoxacin may be useful for the treatment of periodontal disease.
    PLoS ONE 03/2014; 9(3):e92119. DOI:10.1371/journal.pone.0092119 · 3.23 Impact Factor
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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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    ABSTRACT: We report here that the leptomeningeal cells transduce inflammatory signals from peripheral macrophages to brain-resident microglia in response to Porphyromonas gingivalis (P.g.) LPS. The expression of Toll-like receptor 2 (TLR2), TLR4, TNF- α , and inducible NO synthase was mainly detected in the gingival macrophages of chronic periodontitis patients. In in vitro studies, P.g. LPS induced the secretion of TNF- α and IL-1 β from THP-1 human monocyte-like cell line and RAW264.7 mouse macrophages. Surprisingly, the mean mRNA levels of TNF- α and IL-1 β in leptomeningeal cells after treatment with the conditioned medium from P.g. LPS-stimulated RAW264.7 macrophages were significantly higher than those after treatment with P.g. LPS alone. Furthermore, the mean mRNA levels of TNF- α and IL-1 β in microglia after treatment with the conditioned medium from P.g. LPS-stimulated leptomeningeal cells were significantly higher than those after P.g. LPS alone. These observations suggest that leptomeninges serve as an important route for transducing inflammatory signals from macrophages to microglia by secretion of proinflammatory mediators during chronic periodontitis. Moreover, propolis significantly reduced the P.g. LPS-induced TNF- α and IL-1 β production by leptomeningeal cells through inhibiting the nuclear factor- κ B signaling pathway. Together with the inhibitory effect on microglial activation, propolis may be beneficial in preventing neuroinflammation during chronic periodontitis.
    Mediators of Inflammation 12/2013; 2013(4):407562. DOI:10.1155/2013/407562 · 3.24 Impact Factor
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