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Title: Effects of the periodontal pathogens Porphyromonas gingivalis and Tannerella forsythia on platelets
Author: Andrews, Alexander
ISNI:       0000 0004 7960 6055
Awarding Body: Sheffield Hallam University
Current Institution: Sheffield Hallam University
Date of Award: 2019
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Cardiovascular disease (CVD) accounts for ~17.7 million deaths annually, worldwide. Although several key risk factors including smoking, diet and obesity have been identified, these account for only 40-50% of all cases. Historically, poor oral hygiene and the chronic oral condition, periodontitis, characterised by gum bleeding and tooth loss has been implicated in the aggravation of CVD. It has been postulated that in cases of periodontitis, oral bacterial pathogens including Porphyromonas gingivalis and Tannerella forsythia can access the vascular system during gum bleeding and inflammatory responses within the periodontal pocket and subsequently contribute to atherosclerosis though interactions with platelets. This study aims to determine how periodonto-pathogens interact with platelets and contribute to CVD, specifically atherosclerosis. Here it is demonstrated that the CHRF-288-11 megakaryocytic-like cells can be utilised through a series of methodologies to study the pathogenic effects of periodontal pathogens on platelets and megakaryocytic cells. In vitro P. gingivalis, but not T. forsythia, is able to interact with platelets by inducing both platelet activation and aggregation. P. gingivalis is able to initiate platelet activation though intracellular calcium mobilisation that leads to the release of both alpha and dense granules, independent of bacterial outer membrane protein OMPA. P. gingivalis NCTC 11834, but not ATCC W50, actively associates and interacts with integrin α2β1 inducing strain dependant platelet aggregation and could suggest a role for bacterial fimbriae within platelet interactions. Taken collectively, this data suggests that P. gingivalis could contribute to CVD and atherosclerosis through interactions with platelets following invasion of the vasculature. Interestingly, direct interactions between bacterial cells and platelets, as well as bacterial genetics and virulence, appear key to the extent of platelet response and could highlight novel risk factors for future patient treatments.
Supervisor: Stafford, Prachi Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available