In the expansion of odontogenic cyst, degradation of extracellular matrix and resorp디on of bone are accompa띠ed ， but its mechanism is under debate. The degrees of inflammation and fibrosis were graded in 39 cases of odontogenic cysts. Cytoplasrnic expressions in various cell types according to them were analyzed using immunohistochemis띠， for MMPs and πMPs. In epithelial cells, MMP-2 expression was increased with marked fibrosis(p=O.018) and in stromal cells, MMP-2,-9 and TIMP-2 expressions were slightly higher in cases with mild inflammation and marked fibrosis. Tendencies of positive correlation were found between MMP-2,-9 and TIMP-2 expressions in epithelial cells and between MMP-l and MMP-9 expressions in stromal cells. These results suggest that MMP-l ,-2 ,-9 and TIMP-2 expression might be related to the expansion of odontogenic cysts, and the expression rate of them was different according to cell types and the degree of inflammation and fibrosis.

Human adult stem cells have widely been examined for their clinical application including their wound healing effect in vivo. To function as therapeutic cells, however, cells must represent the ability of directed migration in response to signals. This study aimed to investigate the mechanism of platelet-derived growth factor (PDGF)-induced migration of the human abdominal adipose-derived stem cells (hADSCs) in vitro. A general matrix metalloproteinase (MMP) inhibitor or a MMP2 inhibitor significantly inhibited the PDGF-induced migration. PDGF treatment exhibited greater mRNA level and denser protein level of MMP1. The conditioned medium of PDGF-treated cells showed a caseinolytic activity of MMP1. Transfection of cells with siRNA against MMP1 significantly inhibited MMP1 expression, its caseinolytic activity, and cell migration following PDGF treatment. Phosphatidylinositol 3-kinase (PI3K) inhibitor reduced the migration by about 50% without affecting ERK and MLC proteins. Rho-associated protein kinase inhibitor mostly abolished the migration and MLC proteins. The results suggest that PDGF might signal hADSCs through PI3K, and MMP1 activity could play an important role in this PDGF-induced migration in vitro.