Fogorvosi szemle, 2007 (100. évfolyam, 1-6. szám)

2007-10-01 / 5. szám

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FOGORVOSI SZEMLE ■ 100. évf. 5. sz. 2007.

gingival fibroblasts. Other experimental investigations have shown that the application of EMD can regulate the expression of the genes associated with cementoblasts which in turn affects crucially the mineralization process [25]. tnoue et at. [26] showed that EMD can alter the phenotype of PDL cells when cultured on different dental materials (i.e. Gutta percha, amalgam etc.). On the other hand, it has to be mentioned that some studies have failed to show any influence of EMD upon the proliferation of mouse fibroblasts and marrow stromal cells [27], Very recent data have suggested that EMP aggregate on the dentin surface and inhibit the effect of the demineralized dentin matrix [28], A study investigating clot adhesion to protein conditioned human dentin blocks indicated that EDTA was less efficacious than citric acid (CA) in removing smear layer and in exposing dentin tubules and collagen. Fibrin clot adhesion was best supported by the CA-treated dentin surface. The results have also indicated that BSA- or EMD-treated surfaces poorly retained the fibrin clot and produce a surface morphology similar to that of the smear layer [29].

Kawase et al. [30] examined the effect of EMD on the proliferation of oral epithelium cells (SCC25). After 3 days of treatment with EMD, cell division was prevented and at the same time the cell cycle was stopped in the G1 phase and EMD limited significantly the expression of Cytokeratin-18 (CK18). Authors concluded that EMD does not possess a cytostatic but rather, a cytotoxic effect on epithelial cells [30]. In an in vitro study the combination of 4 mg EMD and active demineralized freeze-dried allogenic bone (DFDBA) showed an increased bone induction with osteopromotive characteristics [31]. Schwarz et al. [32] have shown that EMD stimulates the early stages of the osteoblast maturation by increasing cell proliferation and later promotes cell differentiation on mature cell lines. A stimulatory role of EMD on mineralized tissue formation by modulating regulatory molecules critical to bone metabolism at the RNA level has also been reported [33].

Schwarz et al. [34] indicated that EMD enhanced cell proliferation and viability of human SaOs(2) osteoblasts on SLA titanium implants in a concentration-dependent manner. Treatment of osteoblasts with EMD significantly stimulated cell proliferation and fibroblast growth factor (FGF)-2 expression, but decreased alkaline phosphatase expression [35]. It was also suggested that EMD might elicit its mitogenic signal through an EMD-specific receptor [36]. It seems that EMD treatment may enhance cellular activities of osteoblasts and of osteoclasts which in turn might support the regeneration of periodontal bony defects [37], Since soluble peptides released from EMD may contribute to the stimulating effects on cell proliferation, a direct contact between EMD and osteoblasts might not be required to induce cell proliferation [38]. Shimizu et al. [39] have examined the ability of EMD to regulate bone sialoprotein (BSP) gene transcription in osteoblast-like cells.

The findings have identified EMD response elements in the rat BSP gene promoter that might mediate the effects of EMD on BSP gene transcription.

A very recent study has evaluated the effect of a combination of a bioactive glass and EMD upon the proliferation and differentiation of the mouse preosteoblastic cell line MC3T3-E1 [40]. The results have indicated that both BG alone or coated with EMD have the ability to support the growth of osteoblast-like cells in vitro and to promote osteoblast differentiation by stimulating the expression of major phenotypic markers. The bioactive granules coated with EMD revealed, however, significantly higher protein production than the bioactive granules alone.

Parkar and Tonetti [41] have evaluated the selective effects of EMD on the activities of 268 cytokine, growth factor, and receptor genes in PDL. The results have indicated that 46% (125 of 268) of the tested genes were found to be expressed by the PDL cells. Of these 125 genes, 38 were differentially expressed by PDL cells which had been cultured in the presence of EMD. Among the 38, 12 were found to be down-regulated, notably mostly inflammatory genes, whereas 26 genes demonstrated upregulation, many of these coding for growth factors and growth factor receptors. It was concluded that EMD down-regulates the expression of genes involved in the early inflammatory phases of wound healing while simultaneously upregulating genes encoding growth and repair-promoting molecules.

It is important to note that certain antibacterial effects and disturbances of bacterial adherence were also found to be influenced by EMD [42-47], It was concluded that the antibacterial effect of EMD is mainly due to the effect of the PGA carrier. These findings were later confirmed demonstrating a direct influence of EMD on the vitality of supragingival dental plaque in vivo [43]. In a further investigation it was demonstrated that EMD inhibits the growth of the periodontal pathogenic bacteria Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia. 24 hours following the application of EMD no living colonies of these pathogenic bacteria could be observed. Moreover, EMD demonstrated no negative effect on gram positive bacteria [44], The inhibiting effect of EMD on periodontal pathogenic bacteria was also confirmed by others [45, 46]. Recent data also suggest that Porphyromonas gingivalis diminishes the effect of EMD on PDL cells in vitro through a cooperative action of gingipains [47], Rincon et al. [48] have evaluated the influence of EMD on cultured gingival fibroblasts, periodontal ligament fibroblasts and dermal fibroblasts, using an in vitro model of wound healing. The results have demonstrated that cells in vitro fill an empty space by a combination of proliferation and cell migration thus indicating that EMD may exert an influence on cells involved in wound healing. In a study Mirastschijski et al. [49] examined the in vit-