Yoneda Mitsuhiro, Ideguchi Hidetaka, Nakamura Shin, Arias Zulema, Ono Mitsuaki, Omori Kazuhiro, Yamamoto Tadashi, Takashiba Shogo
Department of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital, Japan.
Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan.
Heliyon. 2024 Jul 6;10(13):e34206. doi: 10.1016/j.heliyon.2024.e34206. eCollection 2024 Jul 15.
Vital pulp therapy (VPT) is performed to preserve dental pulp. However, the biocompatibility of the existing materials is of concern. Therefore, novel materials that can induce pulp healing without adverse effects need to be developed. Resolvin D2 (RvD2), one of specialized pro-resolving mediators, can resolve inflammation and promote the healing of periapical lesions. Therefore, RvD2 may be suitable for use in VPT. In the present study, we evaluated the efficacy of RvD2 against VPT using and models.
First molars of eight-week-old male Sprague-Dawley rats were used for pulpotomy. They were then divided into three treatment groups: RvD2, phosphate-buffered saline, and calcium hydroxide groups. Treatment results were assessed using radiological, histological, and immunohistochemical (GPR18, TNF-α, Ki67, VEGF, TGF-β, CD44, CD90, and TRPA1) analyses. Dental pulp-derived cells were treated with RvD2 and analyzed using cell-proliferation and cell-migration assays, real-time PCR (, , , , , , and ), ELISA (VEGF and TGF-β), immunocytochemistry (TRPA1), and flow cytometry (dental pulp stem cells: DPSCs).
The formation of calcified tissue in the pulp was observed in the RvD2 and calcium hydroxide groups. RvD2 inhibited inflammation in dental pulp cells. RvD2 promoted cell proliferation and migration and the expression of TGF-β and VEGF and . RvD2 increased the number of DPSCs. In addition, RvD2 suppressed TRPA1 expression as a pain receptor.
RvD2 induced the formation of reparative dentin, anti-inflammatory effects, and decreased pain, along with the proliferation of DPSCs via the expression of VEGF and TGF-β, on the pulp surface in pulpotomy models.
进行活髓治疗（VPT）是为了保留牙髓。然而，现有材料的生物相容性令人担忧。因此，需要开发能够诱导牙髓愈合且无不良影响的新型材料。消退素D2（RvD2）是一种特殊的促消退介质，可减轻炎症并促进根尖周病变的愈合。因此，RvD2可能适用于活髓治疗。在本研究中，我们使用[具体模型1]和[具体模型2]模型评估了RvD2对活髓治疗的疗效。
使用八周龄雄性Sprague-Dawley大鼠的第一磨牙进行牙髓切断术。然后将它们分为三个治疗组：RvD2组、磷酸盐缓冲盐水组和氢氧化钙组。使用放射学、组织学和免疫组织化学（GPR18、TNF-α、Ki67、VEGF、TGF-β、CD44、CD90和TRPA1）分析评估治疗结果。用RvD2处理牙髓来源的细胞，并使用细胞增殖和细胞迁移测定、实时PCR（[具体基因1]、[具体基因2]、[具体基因3]、[具体基因4]、[具体基因5]、[具体基因6]和[具体基因7]）、酶联免疫吸附测定（ELISA）（VEGF和TGF-β）、免疫细胞化学（TRPA1）和流式细胞术（牙髓干细胞：DPSCs）进行分析。
在RvD2组和氢氧化钙组中观察到牙髓中钙化组织的形成。RvD2抑制牙髓细胞中的炎症。RvD2促进细胞增殖和迁移以及TGF-β和VEGF[具体基因1]和[具体基因2]的表达。RvD2增加了DPSC的数量。此外，RvD2抑制作为疼痛受体的TRPA1的表达。
在牙髓切断术模型中，RvD2通过VEGF和TGF-β的表达诱导修复性牙本质的形成、抗炎作用并减轻疼痛，同时促进牙髓表面DPSC的增殖。
