Melito, Christine Marie MacLellan2019-05-162019-05-1620072007(OCoLC)184837987(OCoLC)184837987b27542919https://hdl.handle.net/2144/35618Thesis (MSD)--Boston University, Goldman School of Dental Medicine, 2007 (Endodontics).Includes bibliographical references: leaves 77-92.BACKGROUND Advanced glycosylation end products (AGEs) have been implicated in multi-organ diabetic complications including artherosclerosis, nephropathy, neuropathy, retinopathy, and decreased wound healing. AG Es aggregate as a result of increased glycation modifications, which occur during chronic hyperglycemic states such as diabetes. Accumulation of these by-products consequently allows for the formation of free radicals, which is believed to contribute to apoptotic events that lead to tissue destruction and thus systemic complications seen in diabetic patients. The goal of this study was to investigate signaling pathways by which AGE induced fibroblast apoptosis occurs and the proposed association with type II diabetes mellitus wound healing complications. [TRUNCATED]en-USThis work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author.ApoptosisDiabetes mellitus, type 2Glycosylation end products, advancedThesis/Dissertation