Naruto Research Institute, Research and Development Center, Otsuka Pharmaceutical Factory, Inc, Takuya Nii, 115 Kuguhara, Tateiwa, Muya-cho, Naruto, Tokushima, 772-8601, Japan.
Department of Periodontology and Endodontology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
BMC Oral Health. 2019 Nov 8;19(1):239. doi: 10.1186/s12903-019-0932-0.
Periodontitis is a biofilm-induced chronic inflammatory condition of the periodontium. Chemokines produced by the innate and acquired immune responses play a significant role in disease progression. Reducing biofilm formation and inflammatory response caused by chemokines is vital for preventing and treating periodontitis. Previously, we observed that treatment with 0.1% olanexidine gluconate (OLG) inhibited biofilm formation on saliva-coated hydroxyapatite. This study aimed to evaluate the anti-inflammatory effect of OLG on oral epithelial cells.
We examined if OLG could inhibit the inflammatory responses caused by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS) and heat-killed P. gingivalis in immortalized human oral keratinocytes (RT7).
Treatment of RT7 with non-cytotoxic OLG concentrations significantly inhibited the production of inflammatory chemokines such as interleukin 8 (IL-8), C-C motif ligand 20 (CCL20), and growth-related oncogene protein-α (GRO-α), which are stimulated by P. gingivalis LPS in a concentration-dependent manner. Moreover, the inhibitory effects were observed regardless of the treatment time with P. gingivalis LPS (6, 12, or 24 h). OLG also significantly inhibited chemokine production stimulated by heat-killed P. gingivalis.
The findings of this study suggest that treatment with OLG inhibits chronic inflammatory reactions in oral mucosal cells, such as periodontitis, caused by oral bacteria.
牙周炎是一种由生物膜引起的牙周组织慢性炎症。先天和获得性免疫反应产生的趋化因子在疾病进展中起重要作用。减少生物膜的形成和趋化因子引起的炎症反应对于预防和治疗牙周炎至关重要。先前,我们观察到 0.1%葡萄糖酸奥替尼啶(OLG)的治疗抑制了唾液包被羟磷灰石上的生物膜形成。本研究旨在评估 OLG 对口腔上皮细胞的抗炎作用。
我们研究了 OLG 是否可以抑制牙龈卟啉单胞菌(P. gingivalis)脂多糖(LPS)和热灭活 P. gingivalis 对永生化人口腔角质细胞(RT7)引起的炎症反应。
用非细胞毒性 OLG 浓度处理 RT7 可显著抑制炎症趋化因子的产生,如白细胞介素 8(IL-8)、C-C 基序趋化因子配体 20(CCL20)和生长相关癌基因蛋白-α(GRO-α),这些趋化因子受牙龈卟啉单胞菌 LPS 刺激呈浓度依赖性。此外,无论用牙龈卟啉单胞菌 LPS(6、12 或 24 小时)处理时间如何,抑制作用都很明显。OLG 还显著抑制了热灭活的 P. gingivalis 刺激的趋化因子的产生。
本研究结果表明,OLG 治疗可抑制由口腔细菌引起的牙周炎等口腔黏膜细胞的慢性炎症反应。