Programmed cell death of periodontal ligament cells

被引:8
作者
He, Wei [1 ,2 ,3 ]
Fu, Yu [1 ,2 ,3 ]
Yao, Song [1 ,2 ,3 ]
Huang, Lan [1 ,2 ,3 ,4 ]
机构
[1] Chongqing Med Univ, Coll Stomatol, Dept Orthodont, Chongqing, Peoples R China
[2] Chongqing Key Lab Oral Dis & Biomed Sci, Chongqing, Peoples R China
[3] Chongqing Municipal Key Lab Oral Biomed Engn Highe, Chongqing, Peoples R China
[4] Chongqing Med Univ, 426,North Songshi Rd,Yubei Dist, Chongqing 401147, Peoples R China
基金
中国国家自然科学基金;
关键词
apoptosis; autophagy; cementoblasts; diabetes; hypoxia; periodontal ligament fibroblasts; GLYCATION END-PRODUCTS; INDUCED APOPTOSIS; HIGH GLUCOSE; STEM-CELLS; OSTEOBLAST DIFFERENTIATION; DEPENDENT APOPTOSIS; INHIBITS RANKL; TNF-ALPHA; AUTOPHAGY; HYPOXIA;
D O I
10.1002/jcp.31091
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The periodontal ligament is a crucial tissue that provides support to the periodontium. Situated between the alveolar bone and the tooth root, it consists primarily of fibroblasts, cementoblasts, osteoblasts, osteoclasts, periodontal ligament stem cells (PDLSCs), and epithelial cell rests of Malassez. Fibroblasts, cementoblasts, osteoblasts, and osteoclasts are functionally differentiated cells, whereas PDLSCs are undifferentiated mesenchymal stem cells. The dynamic development of these cells is intricately linked to periodontal changes and homeostasis. Notably, the regulation of programmed cell death facilitates the clearance of necrotic tissue and plays a pivotal role in immune response. However, it also potentially contributes to the loss of periodontal supporting tissues and root resorption. These findings have significant implications for understanding the occurrence and progression of periodontitis, as well as the mechanisms underlying orthodontic root resorption. Further, the regulation of periodontal ligament cell (PDLC) death is influenced by both systemic and local factors. This comprehensive review focuses on recent studies reporting the mechanisms of PDLC death and related factors.
引用
收藏
页码:1768 / 1787
页数:20
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