Please use this identifier to cite or link to this item: https://doi.org/10.1902/jop.2012.120076
Title: Progression of periodontal destruction and the roles of advanced glycation end products in experimental diabetes
Authors: Chang, P.-C. 
Chien, L.-Y.
Yeo, J.F.
Wang, Y.-P.
Chung, M.-C.
Chong, L.Y.
Kuo, M.Y.-P.
Chen, C.-H.
Chiang, H.-C.
Ng, B.N.
Lee, Q.Q.
Phay, Y.K.
Ng, J.R.
Erk, K.Y.
Keywords: Advanced glycosylation end-product receptor
Diabetes mellitus
Immunohistochemistry
Inflammation
Periodontitis
X-ray microtomography
Issue Date: 2013
Source: Chang, P.-C., Chien, L.-Y., Yeo, J.F., Wang, Y.-P., Chung, M.-C., Chong, L.Y., Kuo, M.Y.-P., Chen, C.-H., Chiang, H.-C., Ng, B.N., Lee, Q.Q., Phay, Y.K., Ng, J.R., Erk, K.Y. (2013). Progression of periodontal destruction and the roles of advanced glycation end products in experimental diabetes. Journal of Periodontology 84 (3) : 379-388. ScholarBank@NUS Repository. https://doi.org/10.1902/jop.2012.120076
Abstract: 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.
Source Title: Journal of Periodontology
URI: http://scholarbank.nus.edu.sg/handle/10635/47158
ISSN: 00223492
DOI: 10.1902/jop.2012.120076
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