Increase in receptor activator of nuclear factor κb ligand/osteoprotegerin ratio in peri-implant gingiva exposed to Porphyromonas gingivalis lipopolysaccharide

Takahiro Shuto, Takanori Wachi, Yoshinori Shinohara, Hiroki Nikawa, Seicho Makihira

Research output: Contribution to journalArticle

Abstract

Background/purpose The prevalence of peri-implant diseases, including peri-implant mucositis and peri-implantitis, is increasing. The aim of this study was to elucidate the pathological mechanisms of inflammation and alveolar bone resorption in peri-implant tissues. To do this, we fabricated inflamed gingiva around mini-implants in the palatine processes of rats using lipopolysaccharide derived from Porphyromonas gingivalis (P.g-LPS). Materials and methods Pure titanium mini-implants were implanted into the palatine processes of rats, and then intermittent injections of P.g-LPS were made into the gingival tissues surrounding the mini-implants. The expression patterns of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, receptor activator of nuclear factor κB ligand (RANKL), and osteoprotegerin (OPG) in the tissues were examined using real-time reverse transcriptase polymerase chain reaction or enzyme-linked immunosorbent assays. Immunohistochemical analysis was also performed to compare the T and B cells expressing RANKL. Results P.g-LPS increased the expressions of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, and RANKL in the gingival tissues surrounding the mini-implants. In contrast, the expression of OPG in the P.g-LPS samples was decreased. Consequently, the RANKL/OPG ratio was significantly increased. Moreover, cells stained positively for both anti-CD3 and anti-RANKL antibodies were only found in the samples treated with P.g-LPS. Conclusion These data revealed that P.g-LPS injections increased the RANKL/OPG ratio in the gingival tissues surrounding mini-implants in the rat model. In addition, the CD3-positive cells in the gingival tissues injected with P.g-LPS expressed RANKL. This suggests that the activated T cells capable of infiltrating gingival tissues affected by P.g-LPS may be one of the sources of RANKL and may also be involved in the disease progression from peri-implant mucositis to peri-implantitis.

Original languageEnglish
Pages (from-to)8-16
Number of pages9
JournalJournal of Dental Sciences
Volume11
Issue number1
DOIs
Publication statusPublished - Mar 1 2016

Fingerprint

RANK Ligand
Porphyromonas gingivalis
Gingiva
Cytoplasmic and Nuclear Receptors
Lipopolysaccharides
Osteoprotegerin
Peri-Implantitis
Mucositis
Chemokine CCL2
Interleukin-1
Tumor Necrosis Factor-alpha
Alveolar Bone Loss
T-Lymphocytes
Injections
Bone Resorption
Titanium
Reverse Transcriptase Polymerase Chain Reaction
Disease Progression
Real-Time Polymerase Chain Reaction
Anti-Idiotypic Antibodies

All Science Journal Classification (ASJC) codes

  • Dentistry(all)

Cite this

Increase in receptor activator of nuclear factor κb ligand/osteoprotegerin ratio in peri-implant gingiva exposed to Porphyromonas gingivalis lipopolysaccharide. / Shuto, Takahiro; Wachi, Takanori; Shinohara, Yoshinori; Nikawa, Hiroki; Makihira, Seicho.

In: Journal of Dental Sciences, Vol. 11, No. 1, 01.03.2016, p. 8-16.

Research output: Contribution to journalArticle

@article{0e1233db72ad43e6a8a0ec91a438108d,
title = "Increase in receptor activator of nuclear factor κb ligand/osteoprotegerin ratio in peri-implant gingiva exposed to Porphyromonas gingivalis lipopolysaccharide",
abstract = "Background/purpose The prevalence of peri-implant diseases, including peri-implant mucositis and peri-implantitis, is increasing. The aim of this study was to elucidate the pathological mechanisms of inflammation and alveolar bone resorption in peri-implant tissues. To do this, we fabricated inflamed gingiva around mini-implants in the palatine processes of rats using lipopolysaccharide derived from Porphyromonas gingivalis (P.g-LPS). Materials and methods Pure titanium mini-implants were implanted into the palatine processes of rats, and then intermittent injections of P.g-LPS were made into the gingival tissues surrounding the mini-implants. The expression patterns of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, receptor activator of nuclear factor κB ligand (RANKL), and osteoprotegerin (OPG) in the tissues were examined using real-time reverse transcriptase polymerase chain reaction or enzyme-linked immunosorbent assays. Immunohistochemical analysis was also performed to compare the T and B cells expressing RANKL. Results P.g-LPS increased the expressions of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, and RANKL in the gingival tissues surrounding the mini-implants. In contrast, the expression of OPG in the P.g-LPS samples was decreased. Consequently, the RANKL/OPG ratio was significantly increased. Moreover, cells stained positively for both anti-CD3 and anti-RANKL antibodies were only found in the samples treated with P.g-LPS. Conclusion These data revealed that P.g-LPS injections increased the RANKL/OPG ratio in the gingival tissues surrounding mini-implants in the rat model. In addition, the CD3-positive cells in the gingival tissues injected with P.g-LPS expressed RANKL. This suggests that the activated T cells capable of infiltrating gingival tissues affected by P.g-LPS may be one of the sources of RANKL and may also be involved in the disease progression from peri-implant mucositis to peri-implantitis.",
author = "Takahiro Shuto and Takanori Wachi and Yoshinori Shinohara and Hiroki Nikawa and Seicho Makihira",
year = "2016",
month = "3",
day = "1",
doi = "10.1016/j.jds.2015.10.005",
language = "English",
volume = "11",
pages = "8--16",
journal = "Journal of Dental Sciences",
issn = "1991-7902",
publisher = "Association for Dental Sciences of the Republic of China",
number = "1",

}

TY - JOUR

T1 - Increase in receptor activator of nuclear factor κb ligand/osteoprotegerin ratio in peri-implant gingiva exposed to Porphyromonas gingivalis lipopolysaccharide

AU - Shuto, Takahiro

AU - Wachi, Takanori

AU - Shinohara, Yoshinori

AU - Nikawa, Hiroki

AU - Makihira, Seicho

PY - 2016/3/1

Y1 - 2016/3/1

N2 - Background/purpose The prevalence of peri-implant diseases, including peri-implant mucositis and peri-implantitis, is increasing. The aim of this study was to elucidate the pathological mechanisms of inflammation and alveolar bone resorption in peri-implant tissues. To do this, we fabricated inflamed gingiva around mini-implants in the palatine processes of rats using lipopolysaccharide derived from Porphyromonas gingivalis (P.g-LPS). Materials and methods Pure titanium mini-implants were implanted into the palatine processes of rats, and then intermittent injections of P.g-LPS were made into the gingival tissues surrounding the mini-implants. The expression patterns of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, receptor activator of nuclear factor κB ligand (RANKL), and osteoprotegerin (OPG) in the tissues were examined using real-time reverse transcriptase polymerase chain reaction or enzyme-linked immunosorbent assays. Immunohistochemical analysis was also performed to compare the T and B cells expressing RANKL. Results P.g-LPS increased the expressions of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, and RANKL in the gingival tissues surrounding the mini-implants. In contrast, the expression of OPG in the P.g-LPS samples was decreased. Consequently, the RANKL/OPG ratio was significantly increased. Moreover, cells stained positively for both anti-CD3 and anti-RANKL antibodies were only found in the samples treated with P.g-LPS. Conclusion These data revealed that P.g-LPS injections increased the RANKL/OPG ratio in the gingival tissues surrounding mini-implants in the rat model. In addition, the CD3-positive cells in the gingival tissues injected with P.g-LPS expressed RANKL. This suggests that the activated T cells capable of infiltrating gingival tissues affected by P.g-LPS may be one of the sources of RANKL and may also be involved in the disease progression from peri-implant mucositis to peri-implantitis.

AB - Background/purpose The prevalence of peri-implant diseases, including peri-implant mucositis and peri-implantitis, is increasing. The aim of this study was to elucidate the pathological mechanisms of inflammation and alveolar bone resorption in peri-implant tissues. To do this, we fabricated inflamed gingiva around mini-implants in the palatine processes of rats using lipopolysaccharide derived from Porphyromonas gingivalis (P.g-LPS). Materials and methods Pure titanium mini-implants were implanted into the palatine processes of rats, and then intermittent injections of P.g-LPS were made into the gingival tissues surrounding the mini-implants. The expression patterns of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, receptor activator of nuclear factor κB ligand (RANKL), and osteoprotegerin (OPG) in the tissues were examined using real-time reverse transcriptase polymerase chain reaction or enzyme-linked immunosorbent assays. Immunohistochemical analysis was also performed to compare the T and B cells expressing RANKL. Results P.g-LPS increased the expressions of tumor necrosis factor-α, interleukin-1β, chemokine (C-C motif) ligand 2, and RANKL in the gingival tissues surrounding the mini-implants. In contrast, the expression of OPG in the P.g-LPS samples was decreased. Consequently, the RANKL/OPG ratio was significantly increased. Moreover, cells stained positively for both anti-CD3 and anti-RANKL antibodies were only found in the samples treated with P.g-LPS. Conclusion These data revealed that P.g-LPS injections increased the RANKL/OPG ratio in the gingival tissues surrounding mini-implants in the rat model. In addition, the CD3-positive cells in the gingival tissues injected with P.g-LPS expressed RANKL. This suggests that the activated T cells capable of infiltrating gingival tissues affected by P.g-LPS may be one of the sources of RANKL and may also be involved in the disease progression from peri-implant mucositis to peri-implantitis.

UR - http://www.scopus.com/inward/record.url?scp=84959450971&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84959450971&partnerID=8YFLogxK

U2 - 10.1016/j.jds.2015.10.005

DO - 10.1016/j.jds.2015.10.005

M3 - Article

VL - 11

SP - 8

EP - 16

JO - Journal of Dental Sciences

JF - Journal of Dental Sciences

SN - 1991-7902

IS - 1

ER -