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Diabetes‐enhanced inflammation and apoptosis – impact on periodontal pathosis
Author(s) -
Graves Dana T.,
Liu Rongkun,
Oates Thomas W.
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.1600-0757.2007.00219.x
Subject(s) - medicine , diabetes mellitus , inflammation , apoptosis , citation , endocrinology , bioinformatics , library science , genetics , computer science , biology
Diabetes, particularly type 2 diabetes, is a looming health issue with many ramifications. Because diabetes alters the cellular microenvironment in many different types of tissues, it causes myriad untoward effects, collectively referred to as 'diabetic complications'. Two cellular processes affected by diabetes are inflammation and apoptosis. This review discusses how diabetes-enhanced inflammation and apoptosis may affect the oral environment. In particular, dysregulation of tumor necrosis factor and the formation of advanced glycation products, both of which occur at higher levels in diabetic humans and animal models, potentiate inflammatory responses and induce apoptosis of matrix-producing cells. The enhanced loss of fibroblasts and osteoblasts through apoptosis in diabetics could contribute to limited repair of injured tissue, particularly when combined with other known deficits in diabetic wound-healing. These findings may shed light on diabetes-enhanced risk of periodontal diseases.