scholarly journals Effects of extracellular matrix components on the biological activities of human periodontal ligament cells.

Ensho ◽  
1993 ◽  
Vol 13 (4) ◽  
pp. 365-368
Author(s):  
Kazuhiko Ikezawa ◽  
Yasuo Miki ◽  
Hiroshi Okada
1988 ◽  
Vol 2 (2) ◽  
pp. 215-222 ◽  
Author(s):  
V.P. Terranova ◽  
U.M.E. Wikesjo

Directed migration of many different cell types is necessary for uneventful wound healing to occur. From clinical periodontal regeneration procedures, it is commonly believed that periodontal ligament cells will be of critical importance in obtaining a new connective tissue attachment. Here we present data which indicate that extracellular matrix components (fibronectin) and polypeptide growth factors (FGF, TGF-a, and TGF-β) modulate the ability of periodontal ligament cells to express directed migration. These data indicate a potential role for matrix components and growth factors in clinical periodontal regenerative procedures.


2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Yoshitaka Hosokawa ◽  
Ikuko Hosokawa ◽  
Kazumi Ozaki ◽  
Takashi Matsuo

Sudachitin, which is a polymethoxylated flavonoid found in the peel of Citrus sudachi, has some biological activities. However, the effect of sudachitin on periodontal resident cells is still uncertain. The aim of this study was to examine if sudachitin could decrease the expression of inflammatory mediators such as cytokines, chemokines, or matrix metalloproteinase (MMP) in interleukin- (IL-) 1β-stimulated human periodontal ligament cells (HPDLC). Sudachitin inhibited IL-1β-induced IL-6, IL-8, CXC chemokine ligand (CXCL)10, CC chemokine ligand (CCL)2, MMP-1, and MMP-3 production in HPDLC. On the other hand, tissue inhibitor of metalloproteinase- (TIMP-) 1 expression was increased by sudachitin treatment. Moreover, we found that the nuclear factor- (NF-) κB and protein kinase B (Akt) pathways in the IL-1β-stimulated HPDLC were inhibited by sudachitin treatment. These findings indicate that sudachitin is able to reduce inflammatory mediator production in IL-1β-stimulated HPDLC by inhibiting NF-κB and Akt pathways.


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