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Tumor necrosis factor-α antagonist diminishes osteocytic RANKL and sclerostin expression in diabetes rats with periodontitis.

Abstract Type 1 diabetes with periodontitis shows elevated TNF-α expression. Tumor necrosis factor (TNF)-α stimulates the expression of receptor activator of nuclear factor-κB ligand (RANKL) and sclerostin. The objective of this study was to determine the effect of TNF-α expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis using infliximab (IFX), a TNF-α antagonist. Rats were divided into two timepoint groups: day 3 and day 20. Each timepoint group was then divided into four subgroups: 1) control (C, n = 6 for each time point); 2) periodontitis (P, n = 6 for each time point); 3) diabetes with periodontitis (DP, n = 8 for each time point); and 4) diabetes with periodontitis treated with IFX (DP+IFX, n = 8 for each time point). To induce type 1 diabetes, rats were injected with streptozotocin (50 mg/kg dissolved in 0.1 M citrate buffer). Periodontitis was then induced by ligature of the mandibular first molars at day 7 after STZ injection (day 0). IFX was administered once for the 3 day group (on day 0) and twice for the 20 day group (on days 7 and 14). The DP group showed greater alveolar bone loss than the P group on day 20 (P = 0.020). On day 3, higher osteoclast formation and RANKL-positive osteocytes in P group (P = 0.000 and P = 0.011, respectively) and DP group (P = 0.006 and P = 0.017, respectively) than those in C group were observed. However, there was no significant difference in osteoclast formation or RANKL-positive osteocytes between P and DP groups. The DP+IFX group exhibited lower alveolar bone loss (P = 0.041), osteoclast formation (P = 0.019), and RANKL-positive osteocytes (P = 0.009) than that of the DP group. On day 20, DP group showed a lower osteoid area (P = 0.001) and more sclerostin-positive osteocytes (P = 0.000) than P group. On days 3 and 20, the DP+IFX group showed more osteoid area (P = 0.048 and 0.040, respectively) but lower sclerostin-positive osteocytes (both P = 0.000) than DP group. Taken together, these results suggest that TNF-α antagonist can diminish osteocytic RANKL/sclerostin expression and osteoclast formation, eventually recovering osteoid formation. Therefore, TNF-α might mediate alveolar bone loss via inducing expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis.
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PMID- 29240821
OWN - NLM
STAT- In-Process
LR  - 20171224
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - Tumor necrosis factor-alpha antagonist diminishes osteocytic RANKL and sclerostin
      expression in diabetes rats with periodontitis.
PG  - e0189702
LID - 10.1371/journal.pone.0189702 [doi]
AB  - Type 1 diabetes with periodontitis shows elevated TNF-alpha expression. Tumor
      necrosis factor (TNF)-alpha stimulates the expression of receptor activator of
      nuclear factor-kappaB ligand (RANKL) and sclerostin. The objective of this study 
      was to determine the effect of TNF-alpha expression of osteocytic RANKL and
      sclerostin in type 1 diabetes rats with periodontitis using infliximab (IFX), a
      TNF-alpha antagonist. Rats were divided into two timepoint groups: day 3 and day 
      20. Each timepoint group was then divided into four subgroups: 1) control (C, n =
      6 for each time point); 2) periodontitis (P, n = 6 for each time point); 3)
      diabetes with periodontitis (DP, n = 8 for each time point); and 4) diabetes with
      periodontitis treated with IFX (DP+IFX, n = 8 for each time point). To induce
      type 1 diabetes, rats were injected with streptozotocin (50 mg/kg dissolved in
      0.1 M citrate buffer). Periodontitis was then induced by ligature of the
      mandibular first molars at day 7 after STZ injection (day 0). IFX was
      administered once for the 3 day group (on day 0) and twice for the 20 day group
      (on days 7 and 14). The DP group showed greater alveolar bone loss than the P
      group on day 20 (P = 0.020). On day 3, higher osteoclast formation and
      RANKL-positive osteocytes in P group (P = 0.000 and P = 0.011, respectively) and 
      DP group (P = 0.006 and P = 0.017, respectively) than those in C group were
      observed. However, there was no significant difference in osteoclast formation or
      RANKL-positive osteocytes between P and DP groups. The DP+IFX group exhibited
      lower alveolar bone loss (P = 0.041), osteoclast formation (P = 0.019), and
      RANKL-positive osteocytes (P = 0.009) than that of the DP group. On day 20, DP
      group showed a lower osteoid area (P = 0.001) and more sclerostin-positive
      osteocytes (P = 0.000) than P group. On days 3 and 20, the DP+IFX group showed
      more osteoid area (P = 0.048 and 0.040, respectively) but lower
      sclerostin-positive osteocytes (both P = 0.000) than DP group. Taken together,
      these results suggest that TNF-alpha antagonist can diminish osteocytic
      RANKL/sclerostin expression and osteoclast formation, eventually recovering
      osteoid formation. Therefore, TNF-alpha might mediate alveolar bone loss via
      inducing expression of osteocytic RANKL and sclerostin in type 1 diabetes rats
      with periodontitis.
FAU - Kim, Ji-Hye
AU  - Kim JH
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
FAU - Kim, Ae Ri
AU  - Kim AR
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
AD  - Department of Applied Life Science, The Graduate School, Yonsei University,
      Seoul, Republic of Korea.
AD  - BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Republic of
      Korea.
FAU - Choi, Yun Hui
AU  - Choi YH
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
FAU - Jang, Sungil
AU  - Jang S
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
FAU - Woo, Gye-Hyeong
AU  - Woo GH
AD  - Department of Clinical Laboratory Science, Semyung University, Jecheon, Republic 
      of Korea.
FAU - Cha, Jeong-Heon
AU  - Cha JH
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
AD  - Department of Applied Life Science, The Graduate School, Yonsei University,
      Seoul, Republic of Korea.
AD  - BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Republic of
      Korea.
FAU - Bak, Eun-Jung
AU  - Bak EJ
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
FAU - Yoo, Yun-Jung
AU  - Yoo YJ
AUID- ORCID: http://orcid.org/0000-0002-0045-9597
AD  - Department of Oral Biology, Yonsei University College of Dentistry, Seoul,
      Republic of Korea.
AD  - Department of Applied Life Science, The Graduate School, Yonsei University,
      Seoul, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20171214
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC5730195
EDAT- 2017/12/15 06:00
MHDA- 2017/12/15 06:00
CRDT- 2017/12/15 06:00
PHST- 2017/08/30 00:00 [received]
PHST- 2017/11/30 00:00 [accepted]
PHST- 2017/12/15 06:00 [entrez]
PHST- 2017/12/15 06:00 [pubmed]
PHST- 2017/12/15 06:00 [medline]
AID - 10.1371/journal.pone.0189702 [doi]
AID - PONE-D-17-31801 [pii]
PST - epublish
SO  - PLoS One. 2017 Dec 14;12(12):e0189702. doi: 10.1371/journal.pone.0189702.
      eCollection 2017.