Progression of Periodontal Destruction and the Roles of Advanced Glycation End Products in Experimental Diabetes

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 lipopoly...

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Published in:Journal of periodontology (1970) 2013-03, Vol.84 (3), p.379-388
Main Authors: Chang, Po‐Chun, Chien, Li‐Ying, Yeo, Jin Fei, Wang, Yi‐Ping, Chung, Min‐Chun, Chong, Li Yen, Kuo, Mark Yen‐Ping, Chen, Chun‐Hao, Chiang, Huan‐Ching, Ng, Benjamin N., Lee, Qi Qi, Phay, Yong Kang, Ng, Jeffery R., Erk, Kok Yong
Format: Article
Language:English
Subjects:
Acid Phosphatase - metabolism
Advanced glycosylation end‐product receptor
Alveolar Bone Loss - diagnostic imaging
Alveolar Bone Loss - metabolism
Alveolar Bone Loss - pathology
Animals
Collagen - metabolism
Dentistry
diabetes mellitus
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - metabolism
Disease Progression
Glycation End Products, Advanced - physiology
immunohistochemistry
inflammation
Isoenzymes - metabolism
Lipopolysaccharides
Male
periodontitis
Periodontitis - complications
Periodontitis - diagnostic imaging
Periodontitis - metabolism
Porphyromonas gingivalis
Proliferating Cell Nuclear Antigen - metabolism
Random Allocation
Rats
Rats, Sprague-Dawley
Receptor for Advanced Glycation End Products
Receptors, Immunologic - biosynthesis
Tartrate-Resistant Acid Phosphatase
X-Ray Microtomography
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Summary: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.
ISSN:0022-3492
1943-3670
DOI:10.1902/jop.2012.120076