Yaita Naomichi, Maruyama Kosuke, Hiroyasu Kazuhiko, Sato Soh
Field of Advanced Conservative Dentistry and Periodontology, Periodontology, Course of Clinical Science, The Nippon Dental University Graduate School Life Dentistry at Niigata, 1-8 Hamaura-cho, Chuo-ku, Niigata, 951-8580, Japan.
Department of Periodontology, The Nippon Dental University School of Life Dentistry at Niigata, 1-8 Hamaura-cho, Chuo-ku, Niigata, 951-8580, Japan.
Odontology. 2025 Jan;113(1):180-190. doi: 10.1007/s10266-024-00959-5. Epub 2024 Jun 5.
Early peri-implant disease detection remains difficult. Enamel matrix derivative (EMD), which is used for periodontal tissue regeneration, promotes leukocyte chemotactic factor and adhesion molecule expression in vascular endothelial cells. We hypothesized that stimulating vascular endothelial cells with EMD would induce an inflammatory response in the peri-implant mucosa, enabling early peri-implant infection detection. To verify this hypothesis, we assessed the intercellular adhesion between human alveolar ridge mucosa-derived vascular endothelial cells (ARMEC) stimulated with lipopolysaccharide (LPS) and EMD and human periodontal ligament-derived vascular endothelial cells (PDLEC). Leukocyte chemotactic factors and cell adhesion molecules were investigated and we established an experimental model of peri-implant disease by stimulating ARMEC (representing the peri-implant mucosa) with Porphyromonas gingivalis-derived LPS. ARMEC and PDLEC were obtained from patients (n = 6) who visited the Nippon Dental University Niigata Hospital. The cells were divided into four subcategories, each cultured with: LPS (1 µg/mL), EMD (100 µg/mL), LPS + EMD, and pure medium. Cell viability, leukocyte chemotactic factor (interleukin-8: IL-8), adhesion molecules (intercellular adhesion molecule-1: ICAM-1), tight junction protein gene expression (zonula occludens-1: ZO-1 and Occludin), and transendothelial electrical resistance (TEER) was then determined. LPS reduced ARMEC viability, whereas simultaneous stimulation with EMD improved it. LPS and EMD stimulation enhanced IL-8 and ICAM-1 gene expression, suppressed TEER, and decreased ZO-1 and Occludin expression levels compared to that with stimulation with LPS alone. EMD stimulates leukocyte migration, increase vascular permeability, and trigger an immune response in the peri-implant mucosa, thus facilitating the early detection and treatment of peri-implant disease.
早期种植体周围疾病的检测仍然困难。用于牙周组织再生的釉基质衍生物（EMD）可促进血管内皮细胞中白细胞趋化因子和黏附分子的表达。我们假设用EMD刺激血管内皮细胞会在种植体周围黏膜中引发炎症反应，从而实现种植体周围感染的早期检测。为了验证这一假设，我们评估了用脂多糖（LPS）和EMD刺激的人牙槽嵴黏膜来源的血管内皮细胞（ARMEC）与牙周膜来源的血管内皮细胞（PDLEC）之间的细胞间黏附。研究了白细胞趋化因子和细胞黏附分子，并通过用牙龈卟啉单胞菌来源的LPS刺激ARMEC（代表种植体周围黏膜）建立了种植体周围疾病的实验模型。ARMEC和PDLEC取自访问日本新潟齿科大学医院的患者（n = 6）。细胞分为四个亚组，每组分别用以下物质培养：LPS（1μg/mL）、EMD（100μg/mL）、LPS + EMD和纯培养基。然后测定细胞活力、白细胞趋化因子（白细胞介素-8：IL-8）、黏附分子（细胞间黏附分子-1：ICAM-1）、紧密连接蛋白基因表达（闭合蛋白-1：ZO-1和闭合蛋白）以及跨内皮电阻（TEER）。LPS降低了ARMEC的活力，而同时用EMD刺激则提高了活力。与单独用LPS刺激相比，LPS和EMD刺激增强了IL-8和ICAM-1基因表达，抑制了TEER，并降低了ZO-1和闭合蛋白的表达水平。EMD刺激白细胞迁移，增加血管通透性，并在种植体周围黏膜中引发免疫反应，从而有助于种植体周围疾病的早期检测和治疗。
