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Diabetic periodontitis: a model for activated innate immunity and impaired resolution of inflammation
Author(s) -
Nassar Hamdy,
Kantarci Alpdogan,
Van Dyke Thomas E.
Publication year - 2007
Publication title -
periodontology 2000
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.725
H-Index - 122
eISSN - 1600-0757
pISSN - 0906-6713
DOI - 10.1111/j.1600-0757.2006.00168.x
Subject(s) - medicine , periodontitis , citation , inflammation , periodontology , innate immune system , correct name , immunology , library science , dentistry , computer science , immune system , paleontology , biology
Diabetes mellitus comprises a heterogeneous group of disorders characterized by altered glucose tolerance, and impaired lipid and carbohydrate metabolism. It is associated with a number of complications directly resulting from hyperglycemia (115). Most of these complications are vascular in nature such that macrovascular changes in diabetes lead to increased risk of myocardial infarction and stroke as a result of atherosclerosis (64), while diabetic microvascular pathology includes retinopathy, end-stage renal disease, a variety of debilitating neuropathies, poor wound healing, enhanced risk of infection, and periodontal disease (5,6,23,63,106). The hyperglycemic state is also associated with activated innate immunity, which is characterized by higher levels of inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6 (17,21,27,32,125). Moreover, specific inflammatory immune cell phenotypes are characterized by enhanced monocyte/ polymorphonuclear leukocyte adhesion to endothelial cells, and expression of adhesion molecules (endothelial cell leukocyte adhesion molecule-1, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1) on endothelial cells and leukocytes (46,82). An abundance of information accumulated from studies on the complications of diabetes and periodontal disease has revealed that a hyperactive innate immune response may be the