Gingivitis as a risk factor in periodontal disease

doi:10.1038/sj.bdj.2009.818

Cited by 1 publication

(1 citation statement)

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“…Chronic Periodontitis (CP) is an oral chronic infection/inflammatory disease that affects a considerable worldwide population (López and Baelum, 2015). CP comprises both gingivitis and periodontitis; for the latter, inflammation is localized in the gingival tissues or the inflammatory process reaches deeper connective and bone tissue, causing bone and attachment loss that may ultimately lead to tooth loss (Lang et al, 2009). This local inflammatory process may induce a systemic inflammatory state via mechanisms including dissemination of pro-inflammatory cytokines or bacteria or both from oral to extra-oral sites or even to blood circulation, which may contribute to the exacerbation of several diseases (Martins et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Chronic Periodontitis and Alzheimer Disease: A Putative Link of Serum Proteins Identification by 2D-DIGE Proteomics

Rong

Xiang

et al. 2020

Front. Aging Neurosci.

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Increasing evidence indicates Chronic Periodontitis (CP) is a comorbidity of Alzheimer's disease (AD), which is the most common form of age-related dementia, and for the latter, effective diagnostic and treatment strategies are lacking. Although inflammation is present in both diseases, the exact mechanisms and cross-links between CP and AD are poorly understood; and a direct association between the two has not been reported. This study aimed to identify a direct serum proteins link between AD and CP. Two-dimensional differential in-gel electrophoresis was employed to analyze serum samples from 12 CP patients and 12 age-matched controls. Furthermore, to determine the molecular link between CP and AD, neuroblastoma SK-N-SH APPwt cells were treated with 1 µg/ml of lipopolysaccharide from Porphyromonas gingivalis (P.g-LPS). Ten differentially expressed proteins were identified in CP patients. Among them, nine proteins were up-regulated, and one protein was down-regulated. Of the 10 differentially expressed proteins, five proteins were reportedly involved in the pathology of AD: Cofilin-2, Cathepsin B, Clusterin, Triosephosphate isomerase, and inter-alpha-trypsin inhibitor heavy chain H4 (ITI-H4). Western blotting indicated significantly higher expression of Cofilin-2, Cathepsin B, and Clusterin and lower expression of ITI-H4 in the CP group than in the Control group. The serum concentration of Cathepsin B has a good correlation with MMSE scores. Moreover, the protein level of Cathepsin B (but not that of ADAM10 and BACE1) increased significantly along with a prominent increase in Aβ 1-40 and Aβ 1-42 in the cell lysates of P.g-LPS-treated SK-N-SH APPwt cells. Cathepsin B inhibition resulted in a sharp decrease in Aβ 1-40 and Aβ 1-42 in the cell lysates. Furthermore, TNF-α was one of the most important inflammatory cytokines for the P.g-LPS-induced Cathepsin B upregulation in SK-N-SH APPwt cells. These results show that CP and AD share an association, while Cathepsin B could be a key link between the two diseases. The discovery of the identical serum proteins provides a potential mechanism underlying the increased risk of AD in CP patients, which could be critical for elucidating the pathophysiology of AD.

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Section: Introductionmentioning

confidence: 99%