Abstract
Diabetics have an increased prevalence of periodontitis, and diabetes is one of the causative factors of severe periodontitis. Apoptosis is thought to be involved in this pathogenic relationship. The aim of this study was to investigate apoptosis in human periodontal ligament (PDL) fibroblasts induced by advanced glycation end products (AGEs) and their receptor (RAGE). We examined the roles of apoptosis, AGEs, and RAGE during periodontitis in diabetes mellitus using cultured PDL fibroblasts that were treated by AGE-modified bovine serum albumin (AGE-BSA), bovine serum albumin (BSA) alone, or given no treatment (control). Microscopy and real-time quantitative PCR indicated that PDL fibroblasts treated with AGE-BSA were deformed and expressed higher levels of RAGE and caspase 3. Cell viability assays and flow cytometry indicated that AGE-BSA reduced cell viability (69.80±5.50%, P<0.01) and increased apoptosis (11.31±1.73%, P<0.05). Hoechst 33258 staining and terminal-deoxynucleotidyl transferase-mediated nick-end labeling revealed that AGE-BSA significantly increased apoptosis of PDL fibroblasts. The results showed that the changes in PDL fibroblasts induced by AGE-BSA may explain how AGE-RAGE participates in and exacerbates periodontium destruction.
Highlights
Periodontal disease is a common complication of diabetes [1], but the underlying pathogenesis and internal relationship of the two diseases is not yet clear [2]
We examined the roles of apoptosis, advanced glycation end products (AGEs), and receptor for advanced glycation end products (RAGE) during periodontitis in diabetes mellitus using cultured periodontal ligament (PDL) fibroblasts that were treated by AGE-modified bovine serum albumin (AGE-BSA), bovine serum albumin (BSA) alone, or given no treatment
To determine the extent of RAGE expression after AGE-BSA treatment, human PDL fibroblasts were subjected to AGE-BSA, BSA, or given no treatment
Summary
Periodontal disease is a common complication of diabetes [1], but the underlying pathogenesis and internal relationship of the two diseases is not yet clear [2]. Previous studies suggest that advanced glycation end products (AGEs) and the receptor for advanced glycation end products (RAGE), which form during chronic hyperglycemia, play roles in the pathogenesis of diverse diseases [3,4], and may play a key role in periodontitis in the diabetic patient [5]. There has been considerable interest in the role RAGE plays in periodontitis. RAGE is a member of the immunoglobulin receptor superfamily and is expressed by diverse cells, including endothelial and smooth muscle cells, lymphocytes, monocytes, and neurons [8]. The accumulation of RAGE ligands in diseased tissues leads to sustained receptor expression through positive feedback; this prolongs cell activation and plays a significant role in diverse chronic disorders [9]
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