兰克尔
牙龈卟啉单胞菌
化学
骨保护素
牙周炎
趋化因子
医学
炎症
脂多糖
内科学
CCL5
激活剂(遗传学)
肿瘤坏死因子α
受体
细胞毒性T细胞
生物化学
体外
白细胞介素2受体
作者
Takanori Shuto,Takanori Wachi,Yoshinori Shinohara,Hiroki Nikawa,Seicho Makihira
标识
DOI:10.1016/j.jds.2015.10.005
摘要
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).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.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.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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