Periodontal innate immune mechanisms relevant to atherosclerosis

被引:27
|
作者
Amar, S. [1 ]
Engelke, M. [1 ]
机构
[1] Boston Univ, Sch Dent Med, Ctr Antiinflammatory Therapeut, Boston, MA 02118 USA
基金
美国国家卫生研究院;
关键词
atherosclerosis; innate immunity; nucleotide-binding oligomerization domain 2; Porphyromonas gingivalis; toll-like receptors; TOLL-LIKE RECEPTORS; GINGIVAL CREVICULAR FLUID; CORONARY-HEART-DISEASE; C-REACTIVE PROTEIN; NF-KAPPA-B; NECROSIS-FACTOR-ALPHA; PORPHYROMONAS-GINGIVALIS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; PATHOGEN-RECOGNITION; VIRULENCE FACTORS;
D O I
10.1111/omi.12087
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Atherosclerosis is a common cardiovascular disease in the USA where it is a leading cause of illness and death. Atherosclerosis is the most common cause for heart attack and stroke. Most commonly, people develop atherosclerosis as a result of diabetes, genetic risk factors, high blood pressure, a high-fat diet, obesity, high blood cholesterol levels, and smoking. However, a sizable number of patients suffering from atherosclerosis do not harbor the classical risk factors. Ongoing infections have been suggested to play a role in this process. Periodontal disease is perhaps the most common chronic infection in adults with a wide range of clinical variability and severity. Research in the past decade has shed substantial light on both the initiating infectious agents and host immunological responses in periodontal disease. Up to 46% of the general population harbors the microorganism(s) associated with periodontal disease, although many are able to limit the progression of periodontal disease or even clear the organism(s) if infected. In the last decade, several epidemiological studies have found an association between periodontal infection and atherosclerosis. This review focuses on exploring the molecular consequences of infection by pathogens that exacerbate atherosclerosis, with the focus on infections by the periodontal bacterium Porphyromonas gingivalis as a running example.
引用
收藏
页码:171 / 185
页数:15
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