https://scholars.lib.ntu.edu.tw/handle/123456789/569158
標題: | Progression of periodontal destruction and the roles of advanced glycation end products in experimental diabetes | 作者: | PO-CHUN CHANG Chien L.-Y. Yeo J.F. YI-PING WANG Chung M.-C. Chong L.Y. YEN-PING KUO Chen C.-H. Chiang H.-C. Ng B.N. Lee Q.Q. Phay Y.K. Ng J.R. Erk K.Y. |
公開日期: | 2013 | 卷: | 84 | 期: | 3 | 起(迄)頁: | 379-388 | 來源出版物: | Journal of Periodontology | 摘要: | Background: Progression of diabetes-associated periodontal destruction and the roles of advanced glycation end products (AGEs) are investigated. Methods: Diabetes was induced by streptozocotin injection, and periodontitis was induced via silk ligature placement with Porphyromonas gingivalis lipopolysaccharide injection in 64 Sprague-Dawley rats for 7 to 21 days. The quality of alveolar bone and attachment loss (AL) were measured by microcomputed tomography and histology. Destruction profiles were evaluated by histology, histochemistry, immunohistochemistry, and quantitative assessments of inflammatory cells, expression of receptors for AGEs (RAGE), tartrate-resistant acid phosphatase, and proliferating cell nuclear antigen. Results: Without periodontitis induction, there was no obvious morphologic change in the periodontium, although slight elevations of AGEs and RAGE levels were noted in animals with diabetes. In the group with experimental periodontitis, significant periodontal bone loss was noted in animals both with and without diabetes from day 7, with more progressive bone loss in animals with diabetes during days 14 to 21. Histologically, the disruption of attachment and inflammation were observed from day 7, but subsequently subsided in animals without diabetes. A stronger and more prolonged response with significant AL was observed in animals with diabetes. Stronger inflammation, attenuated and persistent resorptive activity, and weaker proliferating potential were demonstrated by animals with diabetes. AGE deposition and RAGE expression were noted in animals without diabetes but with periodontitis, although levels were considerably elevated in the later stages in animals with diabetes. Conclusions: Diabetes augments periodontal destruction by reducing the proliferating capability and activating resorptive activities. Presence of the AGE-RAGE axis without diabetes implies that it is involved in the regulation of inflammation. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84874585214&doi=10.1902%2fjop.2012.120076&partnerID=40&md5=9b437fccbb19756de7b363cfefb4d5d3 https://scholars.lib.ntu.edu.tw/handle/123456789/569158 |
ISSN: | 0022-3492 | DOI: | 10.1902/jop.2012.120076 | SDG/關鍵字: | acid phosphatase; acid phosphatase tartrate resistant isoenzyme; advanced glycation end product; advanced glycosylation end product receptor; advanced glycosylation end-product receptor; collagen; cycline; immunoglobulin receptor; isoenzyme; lipopolysaccharide; tartrate-resistant acid phosphatase; alveolar bone loss; animal; article; biosynthesis; disease course; experimental diabetes mellitus; male; metabolism; micro-computed tomography; pathology; periodontitis; physiology; Porphyromonas gingivalis; radiography; randomization; rat; Sprague Dawley rat; Acid Phosphatase; Alveolar Bone Loss; Animals; Collagen; Diabetes Mellitus, Experimental; Disease Progression; Glycosylation End Products, Advanced; Isoenzymes; Lipopolysaccharides; Male; Periodontitis; Porphyromonas gingivalis; Proliferating Cell Nuclear Antigen; Random Allocation; Rats; Rats, Sprague-Dawley; Receptors, Immunologic; X-Ray Microtomography |
顯示於: | 牙醫學系 |
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