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Glycated matrix up‐regulates inflammatory signaling similarly to P orphyromonas gingivalis lipopolysaccharide
Author(s) -
Chang PC.,
Chien LY.,
Chong L. Y.,
Kuo YP.,
Hsiao JK.
Publication year - 2013
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2012.01519.x
Subject(s) - glycation , porphyromonas gingivalis , chemistry , rage (emotion) , endocrinology , receptor , inflammation , medicine , osteoprotegerin , periodontitis , oxidative stress , lipopolysaccharide , mesenchymal stem cell , microbiology and biotechnology , biology , biochemistry , activator (genetics) , neuroscience
Background and Objective Hyperglycemia and advanced glycation end‐products ( AGE s) have been hypothesized as the etiologic factors of diabetic periodontitis. The aim of this study was to clarify in greater detail the patterns of AGE ‐mediated periodontal inflammation under various physiological conditions. Material and Methods The deposition of AGE s and expression of the receptor for AGE s ( RAGE ) were identified by immunohistochemistry in S prague– D awley rats with experimentally induced periodontitis or diabetes. Human periodontal ligament cells ( PDLC s) and mesenchymal stem cells ( MSC s) were cultured under simulated conditions of hyperglycemia, P orphyromonas gingivalis lipopolysaccharide ( LPS ) stimulation and matrix glycation. Cell viability and expression of toll‐like receptors ( T LRs ), R age , an inflammatory signaling initiator (nuclear factor kappa light chain enhancer of activator β cells), an oxidative stressor (heme oxygenase‐1) and collagen synthesis (type I and type IV ) genes were evaluated. Results The deposition of AGE s and the expression of R age were evident in the inflamed periodontal tissues in all rats and appeared to be enhanced in rats with diabetes. Matrix glycation augmented cytotoxicity, up‐regulated RAGE and TLR s in both PDLC s and MSC s, and significantly activated downstream inflammatory signaling in MSC s. Oxidative stress was significantly increased under matrix glycation in both PDLC s and MSC s and was significantly increased at a high‐glucose concentration in MSC s. A consistent decrease in expression of type I and type IV collagens was observed in MSC s, but a delayed reduction was noted in PDLC s. Conclusions Matrix glycation modulated cell behavior to induce inflammation equivalent to that produced by incubation with P . gingivalis LPS . Periodontal inflammation also led to matrix glycation, thus demonstrating a definite interaction between diabetes and periodontitis.