ABSTRACT
Abstract
Inflammation-related
immune responses and
bone metabolism lead to extensive
tooth loss in
periodontitis.
Objective:
This study aims to investigate the effect of
peroxisome proliferator-activated receptor (
PPAR) alpha agonist anti-inflammatory
treatment in vitro and in
ligature-induced experimental
periodontitis in vivo .
Methodology:
Splenocytes were isolated from C57BL/6J
mice and cultured for 48 hours under the following conditions control, P. gingivalis
lipopolysaccharide (LPS) (1 µg/ml); experimental, LPS (1 µg/ml) +
PPARα agonist (
fenofibrate) at 1, 10, 50, 100 µM.
MRNA and secreted
protein levels of TNF-α expression were detected by RT-qPCR and
ELISA, respectively.
Silk ligatures (7-0) were tied around maxillary second
molars of C57BL/6J
mice for two weeks. Optimized doses of
fenofibrate (50 µM) and vehicle control were injected into the contralateral side of the palatal
gingiva on days three, six, and nine. At day 14,
bone resorption,
osteoclastogenesis, and gingival
mRNA expression levels of TNF-α,
IL-1β,
IL-6, and RANKL/OPG were measured by micro-computed
tomography,
Tartrate-resistant acid phosphatase (TRAP)
staining, and Real-
time quantitative
PCR, respectively.
Results:
TNF-α expression in cultured
spleen cells were significantly increased in the presence of LPS, when compared with the
control group, and significantly reduced by
fenofibrate treatment in a
dose-dependent manner from 1-100 µM (p<0.05). Gingival
mRNA levels of TNF-α,
IL-1β,
IL-6, and the ratio of RANKL/OPG, were significantly decreased after
injection of
fenofibrate, when compared to the control side (p<0.05).
Periodontal bone loss and TRAP positive
cell formation were significantly decreased on the side with an
injection of
fenofibrate, as compared to the control side (p<0.05).
Conclusions:
An anti-inflammatory
treatment,
PPARα agonist, inhibited
inflammation and
periodontal bone loss in
ligature-induced experimental
periodontitis.