title: Progression of periodontal destruction and the roles of advanced glycation end products in experimental diabetes.
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.
authors.affiliation: Faculty of Dentistry, National University of Singapore, Singapore, Singapore. changpc@ntu.edu.tw
authors.forename: Po-Chun
authors.initials: PC
authors.lastname: Chang
authors.forename: Li-Ying
authors.initials: LY
authors.lastname: Chien
authors.forename: Jin Fei
authors.initials: JF
authors.lastname: Yeo
authors.forename: Yi-Ping
authors.initials: YP
authors.lastname: Wang
authors.forename: Min-Chun
authors.initials: MC
authors.lastname: Chung
authors.forename: Li Yen
authors.initials: LY
authors.lastname: Chong
authors.forename: Mark Yen-Ping
authors.initials: MY
authors.lastname: Kuo
authors.forename: Chun-Hao
authors.initials: CH
authors.lastname: Chen
authors.forename: Huan-Ching
authors.initials: HC
authors.lastname: Chiang
authors.forename: Benjamin N
authors.initials: BN
authors.lastname: Ng
authors.forename: Qi Qi
authors.initials: QQ
authors.lastname: Lee
authors.forename: Yong Kang
authors.initials: YK
authors.lastname: Phay
authors.forename: Jeffery R
authors.initials: JR
authors.lastname: Ng
authors.forename: Kok Yong
authors.initials: KY
authors.lastname: Erk
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D016301:Alveolar Bone Loss / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D003094:Collagen / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism*; D018450:Disease Progression; D017127:Glycation End Products, Advanced / Q000502:physiology*; D007527:Isoenzymes / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D010518:Periodontitis / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism*; D016966:Porphyromonas gingivalis; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000096:biosynthesis; D000071681:Tartrate-Resistant Acid Phosphatase; D055114:X-Ray Microtomography
chemical_list: D017127:Glycation End Products, Advanced; D007527:Isoenzymes; D008070:Lipopolysaccharides; D018809:Proliferating Cell Nuclear Antigen; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D003094:Collagen; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase