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Progression of Periodontal Destruction and the Roles of Advanced Glycation End Products in Experimental Diabetes
Author(s) -
Chang PoChun,
Chien LiYing,
Yeo Jin Fei,
Wang YiPing,
Chung MinChun,
Chong Li Yen,
Kuo Mark YenPing,
Chen ChunHao,
Chiang HuanChing,
Ng Benjamin N.,
Lee Qi Qi,
Phay Yong Kang,
Ng Jeffery R.,
Erk Kok Yong
Publication year - 2013
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2012.120076
Subject(s) - periodontitis , diabetes mellitus , glycation , porphyromonas gingivalis , medicine , periodontium , rage (emotion) , inflammation , dental alveolus , advanced glycation end product , endocrinology , dentistry , biology , neuroscience
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.