Possible mechanism of 15D-PGJ2 in promoting periodontal tissue regeneration in patients with mandibular defects

• 作者: Zi-Juan Liu Bing-Yi Chen Rui Zhang Zhou Zhou Si-Ying Ye Jia-Cong Wu Hui-Ling Xia Jing-Yuan Ma Mei-Xiu Tang
• 来源期刊: 海南医科大学学报（英文版）
• 年，卷（期）: 2021,（3）
• 所属期刊栏目: Original article
• 页码范围: 17-22
• 页数: 6页
• 语种: 英文

摘要

Objective: To explore the main physiological mechanism of 15d-PGJ2 promoting periodontal tissue regeneration in patients with jaw defects caused by periodontal disease. Methods: From February 2016 to July 2019,a controlled study was conducted on 73 healthy residents (healthy group) and 73 patients (case group) with periodontal disease combined with jaw defects in Changsha medical university. T test was used to compare the growth factors of gingival crevicular fluid between the two groups. Peripheral blood cells;Cement-specific protein; Peripheral blood enzyme;Statistical differences in bone metabolites. The t test method compared the content of each index before and after treatment(15d-PGJ2 was treated at a dose of 200 mu /kg for 14 days). The method of factor analysis explores the internal correlation of each index. Result: RANKL,ICAM-1,TGF-β1,Th17,Treg, PDLSCs,SOST,CAP,HMGB1,CTSK,5-LOX,COX-2,NTX were higher in the case group than in the healthy group. In the case group, RANKL,ICAM-1,TGF-β1, Th17,Treg,PDLSCs,SOST,CAP,HMGB1,CTSK,5-LOX,COX-2,NTX were lower than those in the healthy group. The differences between the groups were statistically significant (P<0.05). Compared with before treatment, IL-1β, IL-17, Bfgf, YKL-40, BMP-2, ICTP, PICP, CTX were significantly decreased after treatment. RANKL, ICAM-1, TGF-β1, Th17, Treg, PDLSCs, SOST, CAP, HMGB1, CTSK, 5-LOX, COX-2, NTX were significantly increased. The differences were statistically significant(P<0.05). Factor analysis shows that four common factors can be extracted from 21 indicators, and the cumulative contribution rate is 96.993％. Conclusions: The treatment of 15d-PGJ2 in patients with periodontal disease with maxillary defects can significantly affect the expression of multiple characteristic indicators, which may involve four mechanisms: dysregulation of cell differentiation or migration, local inflammation or immune imbalance, destruction of alveolar bone microstructure, load or stimulation, and remodeling. The specific pathway related to this is still to be further explored.