title: Study of TNF-α, IL-1β and LPS levels in the gingival crevicular fluid of a rat model of diabetes mellitus and periodontitis.
abstract: OBJECTIVE
  In this study, we sought to investigate the dynamic changes in the levels of TNF-α, IL-1β and LPS in the gingival crevicular fluid (GCF) in a rat model of diabetes mellitus (DM) and periodontitis (PD). Additionally, we evaluated alveolar bone loss and the histopathological response associated with experimental diabetes mellitus and experimental periodontitis.
  
  
  METHODS
  DM and PD were induced together in 15 rats (group 1) by streptozotocin injection and ligature induction. Periodontitis alone was produced by ligature induction in 15 rats (group 2), diabetes alone was produced by streptozotocin injection in 15 rats (group 3), and fifteen systemically and periodontally healthy rats were used as controls (group 4). The gingival TNF-α, IL-1β and LPS levels were measured by using ELISA method. Periodontal destruction was assessed by measuring the alveolar bone loss. Periodontal inflammation was quantified by histopathological grading in H&E stained samples.
  
  
  RESULTS
  Higher levels of TNF-α, IL1-β and LPS, increased alveolar bone loss and more serve histopathology were found in group 1 compared with group 2, group 3 and group 4 (p< 0.05). The quantities of TNF-α, IL1-β and LPS, the amount of alveolar bone loss and the severity of the histopathological finding were greater in group 2 than group 3 and group 4 (p< 0.05). Group 3 demonstrated higher levels of TNF-α, IL1-β and LPS, increased alveolar bone loss and more serve histopathology than group 4 (p< 0.05). Statistically significant differences were noted between all of the groups.
  
  
  CONCLUSIONS
  These data indicate that DM may lead to enhanced TNF-α, IL1-β and LPS production in the periodontal tissues. The resorption values of alveolar bone and the histological inflammation were more severe in rats with periodontitis and diabetes mellitus than in those with periodontitis alone, diabetes mellitus alone and control rats. Our findings are consistent with the hypothesis that hyperglycemia contributes to the heightened inflammatory response associated with periodontitis.
authors.affiliation: Department of Implantology, the 2nd Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: Zhu-Ling
authors.initials: ZL
authors.lastname: Jiang
authors.forename: Yu-Qiong
authors.initials: YQ
authors.lastname: Cui
authors.forename: Rui
authors.initials: R
authors.lastname: Gao
authors.forename: Ying
authors.initials: Y
authors.lastname: Li
authors.forename: Zhao-Chen
authors.initials: ZC
authors.lastname: Fu
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.forename: Cheng-Chao
authors.initials: CC
authors.lastname: Guan
mesh_terms: D016301:Alveolar Bone Loss / Q000473:pathology; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D005883:Gingival Crevicular Fluid / Q000737:chemistry*; D053583:Interleukin-1beta / Q000032:analysis*; D008070:Lipopolysaccharides / Q000032:analysis*; D008297:Male; D010518:Periodontitis / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha