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J Periodontal Res ; 43(2): 179-85, 2008 Apr.
Article in English | MEDLINE | ID: mdl-18302620

ABSTRACT

BACKGROUND AND OBJECTIVE: The effect of enamel matrix derivative (EMD) on bone differentiation remains unclear. Transforming growth factor beta1 (TGF-beta1) is reported to be contained in EMD. The aim of this study was to clarify the effect of EMD on osteoblastic cell differentiation and the possible role of TGF-beta1. MATERIAL AND METHODS: Fetal rat carvarial cells were treated with 10, 50 or 100 microg/ml EMD for 5-17 days. Alkaline phosphatase (ALP) activity and bone nodule formation were measured, and mRNA expressions of bone matrix proteins and core binding factor were analysed. RESULTS: Enamel matrix derivative inhibited ALP activity from the early stage of culture (29-44% inhibition) on days 5 and 10 and decreased bone nodule formation by 37-67% on day 17. These effects of EMD were concentration dependent. Enamel matrix derivative inhibited mRNA expression of osteocalcin and core binding factor. A high level of the active form of TGF-beta1 protein was detected in the conditioned medium treated with 100 microg/ml EMD. Treatment with TGF-beta1 antibody partly restored the inhibitory effect of EMD on ALP activity. CONCLUSION: Enamel matrix derivative inhibited the osteoblastic differentiation of rat carvarial cells and this was partly mediated by an increase in the activated form of TGF-beta1, suggesting that EMD may function initially to inhibit osteoblastic differentiation to allow a predominant formation of other periodontal tissues.


Subject(s)
Dental Enamel Proteins/pharmacology , Osteoblasts/drug effects , Transforming Growth Factor beta1/physiology , Alkaline Phosphatase/antagonists & inhibitors , Animals , Blotting, Northern , Cell Differentiation/drug effects , Cells, Cultured , Core Binding Factors/antagonists & inhibitors , Osteocalcin/antagonists & inhibitors , Rats , Rats, Wistar , Recombinant Proteins/pharmacology , Reverse Transcriptase Polymerase Chain Reaction , Skull/surgery , Transforming Growth Factor beta1/pharmacology
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