TITLE:
Increased Expression of 11β-Hydroxysteroid Dehydrogenase Type 1 in Experimental Periodontitis Induced by Lipopolysaccharide from Porphyromonas gingivalis
AUTHORS:
Atsuko Fujita, Takaya Nakata, Makoto Umeda, Hiroaki Masuzaki, Hirofumi Sawai
KEYWORDS:
Chronic Periodontitis, 11β-Hydroxysteroid Dehydrogenase Type 1, Lipopolysaccharide, Porphyromonas gingivalis
JOURNAL NAME:
Open Journal of Stomatology,
Vol.7 No.10,
September
30,
2017
ABSTRACT: It has been proposed that 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1),
which activates glucocorticoids, plays a role in chronic inflammatory diseases
including metabolic diseases, rheumatoid arthritis, and ulcerative colitis. We
have recently reported that the expression of 11β-HSD1 is increased in the gingiva of patients with chronic
periodontitis and in that of rats with ligature-induced periodontitis. In this
study, to further demonstrate the involvement of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in another rat
model of experimental periodontitis induced by intragingival injection of
lipopolysaccharide from Porphyromonas
gingivalis (LPS-PG). Alveolar bone loss was observed two weeks after
intragingival injection of LPS-PG. The level of 11β-HSD1 mRNA assessed by real-time reverse transcriptase-polymerase chain reaction was significantly elevated
in LPS-PG-induced periodontitis compared with controls. The expression of 11β-hydroxysteroid dehydrogenase type 2
(11β-HSD2), which inactivates glucocorticoids, was not significantly different
between control and LPS-PG-induced
periodontitis. The expression of 11β-HSD1
was significantly correlated with that of TNF in LPS-PG-induced periodontitis.
The increased expression of 11β-HSD1
protein in LPS-PG-induced periodontitis was confirmed by immunohistochemistry
using anti-11β-HSD1 antibody. These
results further suggest a role for 11β-HSD1
in the pathogenesis of chronic periodontitis.