| pubmed-article:21523210 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21523210 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:21523210 | lifeskim:mentions | umls-concept:C0442027 | lld:lifeskim |
| pubmed-article:21523210 | lifeskim:mentions | umls-concept:C0087086 | lld:lifeskim |
| pubmed-article:21523210 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
| pubmed-article:21523210 | pubmed:dateCreated | 2011-4-27 | lld:pubmed |
| pubmed-article:21523210 | pubmed:abstractText | In recent times the concept of infectious agents playing a role in cardiovascular disease has attracted much attention. Chronic oral disease such as periodontitis, provides a plausible route for entry of bacteria to the circulation. Upon entry to the circulation, the oral bacteria interact with platelets. It has been proposed that their ability to induce platelet aggregation and support platelet adhesion is a critical step in the pathogenesis of the infection process. Many published studies have demonstrated multiple mechanisms through which oral bacteria are able to bind to and activate platelets. This paper will review the various mechanisms oral bacteria use to interact with platelets. | lld:pubmed |
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