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

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
出处
期刊:Journal of Dental Sciences [Elsevier]
卷期号:11 (1): 8-16 被引量:4
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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