Oral infection, hyperglycemia, and endothelial dysfunction

被引:63
作者
Janket, Sok-Ja [1 ]
Jones, Judith A. [1 ]
Meurman, Jukka H. [2 ]
Baird, Alison E. [3 ]
Van Dyke, Thomas E. [4 ]
机构
[1] Boston Univ, Sch Dent Med, Dept Gen Dent, Boston, MA 02118 USA
[2] Univ Helsinki, Cent Hosp, Inst Dent, Helsinki, Finland
[3] Natl Inst Neurol Disorders & Stroke, Stroke Div, NIH, Bethesda, MD USA
[4] Boston Univ, Sch Dent Med, Dept Periodontol & Oral Biol, Boston, MA 02118 USA
来源
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTOLOGY | 2008年 / 105卷 / 02期
关键词
D O I
10.1016/j.tripleo.2007.06.027
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Metabolic syndrome and type 2 diabetes ( T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease ( CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products ( AGE), which are postulated to stimulate interleukin-6 ( IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha ( TNF-alpha) and C-reactive protein ( CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia ( i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.
引用
收藏
页码:173 / 179
页数:7
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