Abstract
Enamel matrix derivative (EMD) has been found to induce reactive dentin formation; however the molecular mechanisms involved are unclear. The effect of EMD (5–50 μg/mL) on primary human pulp cells were compared to untreated cells and cells incubated with 10−8 M dexamethasone (DEX) for 1, 2, 3, 7, and 14 days in culture. Expression analysis using Affymetrix microchips demonstrated that 10 μg/mL EMD regulated several hundred genes and stimulated the gene expression of proteins involved in mesenchymal proliferation and differentiation. Both EMD and DEX enhanced the expression of amelogenin (amel), and the dentinogenic markers dentin sialophosphoprotein (DSSP) and dentin matrix acidic phosphoprotein 1 (DMP1), as well as the osteogenic markers osteocalcin (OC, BGLAP) and collagen type 1 (COL1A1). Whereas, only EMD had effect on alkaline phosphatase (ALP) mRNA expression, the stimulatory effect were verified by enhanced secretion of OC and COL1A from EMD treated cells, and increased ALP activity in cell culture medium after EMD treatment. Increased levels of interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant proteins (MCP-1) in the cell culture medium were also found. Consequently, the suggested effect of EMD is to promote differentiation of pulp cells and increases the potential for pulpal mineralization to favor reactive dentine formation.
Highlights
Dental pulp cells have the potential to differentiate into odontoblasts that forms dentin both during odontogenesis and reparative/reactive dentin after completion of root formation. [1]
Positive effects were found on molecules regulating anti-apoptosis concomitant with down-regulation of molecules that stimulates apoptosis and phagocytosis indicating decreased programmed cell death (PCD) and atrophy
Affymetrix microarray expression analysis has previously shown that enamel matrix derivative (EMD) activate the expression of a high number of genes in the primary human osteoblasts [26], and we found the similar pattern in pulp cells
Summary
Dental pulp cells have the potential to differentiate into odontoblasts that forms dentin both during odontogenesis and reparative/reactive dentin after completion of root formation. [1]. Deposition of protective reactive dentin by the induction of hard-tissue deposition is essential to maintain pulpal health and prevent hypersensitivity or necrosis after injury or conservative therapy. This effect is currently obtained by applications of calcium hydroxide in endodontic and dental traumatology [2]. EMD is reported to stimulate a process mimicking normal odontogenesis where epithelial derived and mesenchymal tissue reciprocally interact [5], and can thereby serve as a biologically active pulp-dressing agent that induces pulpal wound healing and hard-tissue formation without negatively affecting the healthy pulp [6,7]. Previous studies have shown that both pulpal stem cells from late and early developmental stages are able to differentiate toward cells of the osteo-/odontoblastic lineage, induce alkaline-phosphatase-activity and produce calcified matrix, this ability was gradually lost during culturing [9]
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