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 language | English |
|---|---|
| Pages (from-to) | 8-16 |
| Number of pages | 9 |
| Journal | Journal of Dental Sciences |
| Volume | 11 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Mar 1 2016 |
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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 journal › Article
}
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.
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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 -