Inflammation and Alzheimer's disease: possible role of periodontal diseases.
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.
Article: Ageing, dementia and oral health.[Show abstract] [Hide abstract]
ABSTRACT: Neurocognitive decline and delirium, frailty, incontinence, falls, hearing and vision impairment, medication compliance and pharmacokinetics, skin breakdown, impaired sleep and rest are regarded as geriatric giants by gerontologists, geriatricians and nursing home staff. As these are all interrelated in the elderly, failure to act on one can impact on the others. However, the implications of poor oral health have for too long been ignored and deserve equal status. Mouth pain can be devastating for the elderly, compound psychosocial problems, frustrate carers and nursing home staff and disrupt family dynamics. As appearance, function and comfort suffer, so may a person's self-esteem and confidence. The contributing factors for poor oral health such as rapid dental decay, acute and chronic periodontal infections and compromised systemic health on a background of a dry mouth, coupled with xerostomia-inducing medications, reduced fine motor function, declining cognition and motivation will not only lead to an increase in both morbidity and mortality but also impact on quality of life. © 2015 Australian Dental Association.
[Show abstract] [Hide abstract]
ABSTRACT: Despite the outbreak in dental science, oral and dental complications in Alzheimer are of the unsolved problems. It is assumed that tumor necrosis factor-α, which is a key factor in Alzheimer, has a relation with periodontal complications in patients with Alzheimer disease. The present study evaluated the effect of chronic periodontitis on serum levels of tumor necrosis factor-α in Alzheimer disease. This case-control study was performed on 80 patients with Alzheimer disease seeking medical care at Nour Hospital, Isfahan, Iran. Eighty patients with Alzheimer disease between 40 and 70 years old attended this study. Forty had chronic periodontitis (case group), and 40 patients had healthy periodontium (control group). Blood sample was taken, and serum levels of tumor necrosis factor-α were measured by means of an ELISA Reader device. Independent T-Test was used to analyze data, and P < 0.05 was considered significant. The mean of tumor necrosis factor-α was 749.1 ng/μL in case group and 286.8 ng/μL in control group. Independent t-test showed that the mean of tumor necrosis factor-α in patients with Alzheimer and periodontitis was approximately three folds higher than the patients only with Alzheimer, and this difference was statistically significant (P < 0.001). According to the results of this study, it seems that there is a difference between serum levels of tumor necrosis factor-α in patient with Alzheimer and chronic periodontitis and patients with Alzheimer disease and healthy periodontium. Tumor necrosis factor-α level in serum may act as a diagnostic marker of periodontal disease in patients with Alzheimer disease.
[Show abstract] [Hide abstract]
ABSTRACT: Alzheimer's disease (AD) is the world's most common dementing illness, affecting over 150 million patients. Classically AD has been viewed as a neurodegenerative disease of the elderly, characterized by the extracellular deposition of misfolded amyloid-β (Aβ) peptide and the intracellular formation of neurofibrillary tangles. Only recently has neuroinflammation emerged as an important component of AD pathology. Experimental, genetic and epidemiological data now indicate a crucial role for activation of the innate immune system as a disease-promoting factor. The sustained formation and deposition of Aβ aggregates causes chronic activation of the immune system and disturbance of microglial clearance functions. Here we review advances in the molecular understanding of the inflammatory response in AD that point to novel therapeutic approaches for the treatment of this devastating disease.Nature Immunology 02/2015; 16(3):229-236. DOI:10.1038/ni.3102 · 24.97 Impact Factor