TY - JOUR
T1 - Calcium hydroxide suppresses Porphyromonas endodontalis lipopolysaccharide-induced bone destruction
AU - Guo, J.
AU - Yang, D.
AU - Okamura, H.
AU - Teramachi, J.
AU - Ochiai, K.
AU - Qiu, L.
AU - Haneji, T.
N1 - Funding Information:
This study was supported by grants from the Science and Technology Foundation of Liaoning Province ( 2011225020 ), the Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan ( 21592330 and 23592703 ), the Ichiro Kanehara Foundation, and Takeda Science Foundation.
PY - 2014/5
Y1 - 2014/5
N2 - Porphyromonas endodontalis and its main virulence factor, lipopolysaccharide (LPS), are associated with the development of periapical diseases and alveolar bone loss. Calcium hydroxide is commonly used for endodontic therapy. However, the effects of calcium hydroxide on the virulence of P. endodontalis LPS and the mechanism of P. endodontalis LPS-induced bone destruction are not clear. Calcium hydroxide rescued the P. endodontalis LPS-suppressed viability of MC3T3-E1 cells and activity of nuclear factor-κB (NF-κB) in these cells, resulting in the reduced expression of interleukin-6 and tumor necrosis factor-α. In addition, calcium hydroxide inhibited P. endodontalis LPS-induced osteoclastogenesis by decreasing the activities of NF-κB, p38, and ERK1/2 and the expression of nuclear factor of activated T-cell cytoplasmic 1 in RAW264.7 cells. Calcium hydroxide also rescued the P. endodontalis LPS-induced osteoclastogenesis and bone destruction in mouse calvaria. Taken together, our present results indicate that calcium hydroxide suppressed bone destruction by attenuating the virulence of P. endodontalis LPS on bone cells.
AB - Porphyromonas endodontalis and its main virulence factor, lipopolysaccharide (LPS), are associated with the development of periapical diseases and alveolar bone loss. Calcium hydroxide is commonly used for endodontic therapy. However, the effects of calcium hydroxide on the virulence of P. endodontalis LPS and the mechanism of P. endodontalis LPS-induced bone destruction are not clear. Calcium hydroxide rescued the P. endodontalis LPS-suppressed viability of MC3T3-E1 cells and activity of nuclear factor-κB (NF-κB) in these cells, resulting in the reduced expression of interleukin-6 and tumor necrosis factor-α. In addition, calcium hydroxide inhibited P. endodontalis LPS-induced osteoclastogenesis by decreasing the activities of NF-κB, p38, and ERK1/2 and the expression of nuclear factor of activated T-cell cytoplasmic 1 in RAW264.7 cells. Calcium hydroxide also rescued the P. endodontalis LPS-induced osteoclastogenesis and bone destruction in mouse calvaria. Taken together, our present results indicate that calcium hydroxide suppressed bone destruction by attenuating the virulence of P. endodontalis LPS on bone cells.
KW - bone resorption
KW - interleukin-6
KW - nuclear factor of activated T-cell cytoplasmic 1
KW - osteoblasts
KW - osteoclasts
KW - tumor necrosis factor-α
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U2 - 10.1177/0022034514526886
DO - 10.1177/0022034514526886
M3 - Article
C2 - 24603641
AN - SCOPUS:84898968069
SN - 0022-0345
VL - 93
SP - 508
EP - 513
JO - Journal of Dental Research
JF - Journal of Dental Research
IS - 5
ER -