title: The expression of 11β-hydroxysteroid dehydrogenase type 1 is increased in experimental periodontitis in rats.
abstract: BACKGROUND
  The involvement of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts inactive glucocorticoids into active glucocorticoids intracellularly, in metabolic diseases and chronic inflammatory diseases has been elucidated. We recently reported that an increase in 11β-HSD1 expression was associated with chronic periodontitis in humans irrespective of obesity. To further clarify the role of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in experimental periodontitis model in rats.
  
  
  METHODS
  Experimental periodontitis was induced by silk ligature of left maxillary second molars of 7-week-old male Wistar rats, and periodontal tissues were collected at day 3. The expression of 11β-HSD1, 11β-HSD2, and TNFα mRNA was examined using real time reverse transcription-polymerase chain reaction. The expression of TNFα was used as an indicator of inflammation. Thus, the rats in which the levels of TNFα mRNA were increased in the ligature-induced periodontitis compared with the control were analysed.
  
  
  RESULTS
  The findings demonstrated that the expression of 11β-HSD1 mRNA was significantly increased in experimental periodontitis compared with the control. The increase in the levels of 11β-HSD1 mRNA in the ligature-induced periodontitis compared with the control was positively correlated with that of TNFα mRNA. On the other hand, the expression of 11β-HSD2 mRNA, which inactivates glucocorticoids, was slightly decreased in experimental periodontitis. Therefore, the ratio of 11β-HSD1 versus 11β-HSD2 mRNA was significantly higher in experimental periodontitis than in the control.
  
  
  CONCLUSIONS
  These results suggest that the increased expression of 11β-HSD1, which would result in the increased levels of intracellular glucocorticoids, may play a role in the pathophysiology of experimental periodontitis.
authors.affiliation: Department of Periodontology, Graduate School of Dentistry, Osaka Dental University, Hirakata, Osaka, Japan.
authors.forename: Takaya
authors.initials: T
authors.lastname: Nakata
authors.affiliation: Department of Periodontology, Osaka Dental University, Hirakata, Osaka, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Umeda
authors.affiliation: Division of Endocrinology, Diabetes and Metabolism, Hematology, Rheumatology, Graduate School of Internal Medicine, University of the Ryukyus, Nakagami-gun, Okinawa, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Masuzaki
authors.affiliation: Department of Internal Medicine, Osaka Dental University, Hirakata, Osaka, Japan. sawai@cc.osaka-dent.ac.jp.
authors.forename: Hirofumi
authors.identifier: http://orcid.org/0000-0002-8328-0049
authors.initials: H
authors.lastname: Sawai
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000378:metabolism*; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism*; D000818:Animals; D005938:Glucocorticoids; D008297:Male; D010518:Periodontitis / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005938:Glucocorticoids; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2
keywords: 11β-Hydroxysteroid dehydrogenase type 1; Chronic periodontitis; Experimental periodontitis; Glucocorticoids; Inflammation