Background: Emdogain (EMD) is made from enamel matrix proteins (EMPs) from the tooth germ of swine and propylene glycol alginate (PGA) as a matrix. The function of EMD is known to differentiate cells of the dental follicle into cementoblasts. However, little is known about the effect of EMD on mesenchymal cells in other tissue.
Objective: The purpose of this study was to investigate whether EMD has the ability to induce hard tissue when applied with or without demineralized dentin matrix.
Methods: Half of the dentin tubes prepared from rat incisors were demineralized by treatment with 0.6 N hydrochloric acid for 3 h. EMD or PGA was injected into the demineralized or non-demineralized dentin tubes, which were then transplanted into rectus abdominis muscles. Untreated dentin tubes were also transplanted as a control. Animals were killed at 7, 14 and 21 days after the implantation.
Results: Non-demineralized dentin tubes with or without EMD or PGA did not form any hard tissue. In the demineralized group, chondrogenesis in the PGA groups occurred earlier than in the EMD groups. The expression of vascular endothelial growth factor (VEGF) mRNA in the demineralized group with PGA at day 14 was the highest. The expression of osteopontin and osteocalcin mRNAs was higher in all groups at 21 days compared with 7 or 14 days.
Conclusion: These results suggest that neither EMD nor PGA has the ability to induce hard tissue and that EMPs contained within EMD might aggregate on the dentin surface and inhibit the effect of the demineralized dentin matrix.