BMC oral health · 2025
CH02 peptide-stimulated periodontal ligament cells enhance periodontal defect repair in rats.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Wang Huijuan, He Huiying, Cheng Xin, Feng Qi, Yang Xuesong, Chen Xiaojia, Huang Yue
Аннотация
OBJECTIVES: Periodontal ligament cells (PDLCs) are considered ideal seed cells for periodontal tissue engineering and regeneration, and optimizing their efficacy is a pressing challenge. Although basic fibroblast growth factor (bFGF) has been extensively studied for promoting periodontal regeneration, its instability limits its application. This study introduces a smaller, less degradable peptide, CH02, to address this issue. Therefore, this study aims to explore the promoting effect of the CH02 peptide on the osteogenic differentiation of PDLCs, providing new support for periodontal regeneration.
METHODS: Extracted PDLCs from human premolars; used bFGF as a positive control to analyze the effects of CH02 on the proliferation, toxicity, migration, osteogenic differentiation, and calcification ability of PDLCs; RT-qPCR analysis of osteogenesis-related gene expression; Construct a rat periodontal bone defect model, deliver PDLCs encapsulated in Matrigel to the defect site, and intervene with CH02 for 2 and 4 weeks. Subsequently, evaluate bone regeneration through Micro-CT, HE staining, Masson staining, and immunohistochemical analysis.
RESULTS: PDLCs were successfully extracted. In vitro experiments showed that CH02 was comparable to bFGF in promoting PDLCs proliferation, but CH02 was more effective in promoting cell migration and osteogenic differentiation. CH02 enhanced the expression of osteogenic-related genes (such as RUNX2, OCN, and COL-1) in PDLCs. In vivo experiments demonstrated that CH02 could promote PDLCs to repair rat periodontal bone defects.
CONCLUSION: CH02 promotes osteogenic differentiation of PDLCs in vitro more effectively than bFGF; in vivo, CH02 effectively promotes PDLCs to repair rat periodontal bone defects.
METHODS: Extracted PDLCs from human premolars; used bFGF as a positive control to analyze the effects of CH02 on the proliferation, toxicity, migration, osteogenic differentiation, and calcification ability of PDLCs; RT-qPCR analysis of osteogenesis-related gene expression; Construct a rat periodontal bone defect model, deliver PDLCs encapsulated in Matrigel to the defect site, and intervene with CH02 for 2 and 4 weeks. Subsequently, evaluate bone regeneration through Micro-CT, HE staining, Masson staining, and immunohistochemical analysis.
RESULTS: PDLCs were successfully extracted. In vitro experiments showed that CH02 was comparable to bFGF in promoting PDLCs proliferation, but CH02 was more effective in promoting cell migration and osteogenic differentiation. CH02 enhanced the expression of osteogenic-related genes (such as RUNX2, OCN, and COL-1) in PDLCs. In vivo experiments demonstrated that CH02 could promote PDLCs to repair rat periodontal bone defects.
CONCLUSION: CH02 promotes osteogenic differentiation of PDLCs in vitro more effectively than bFGF; in vivo, CH02 effectively promotes PDLCs to repair rat periodontal bone defects.