2014
DOI: 10.1016/j.joen.2014.07.002
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Iloprost Induces Tertiary Dentin Formation

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Cited by 16 publications
(10 citation statements)
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“…Local neovascularization around the site of injury during the early inflammatory phase is required for prevention of pulp tissue necrosis (29). In agreement with our previous findings (8,9), iloprost was able to increase HDPC proliferation and VEGF expression. The prolonged release of iloprost in vitro for up to 72 h might help to extend the healing of the dental pulp and further promote angiogenesis.…”
Section: Discussionsupporting
confidence: 91%
See 1 more Smart Citation
“…Local neovascularization around the site of injury during the early inflammatory phase is required for prevention of pulp tissue necrosis (29). In agreement with our previous findings (8,9), iloprost was able to increase HDPC proliferation and VEGF expression. The prolonged release of iloprost in vitro for up to 72 h might help to extend the healing of the dental pulp and further promote angiogenesis.…”
Section: Discussionsupporting
confidence: 91%
“…Iloprost, a PGI 2 analog, has been used in animal models and in patients with syndromes involving vascular deficiency in order to promote revascularization and increase blood flow (6,7). Previous studies have shown that iloprost increases the expression of VEGF and proliferative growth factors in human dental pulp cells in vitro, as well as increasing dental pulp blood flow and tertiary dentin formation in vivo (8,9). A recent study has also demonstrated that iloprost can increase the expression of VEGF in periodontal ligament cells, which are another type of mesenchymal stem cell that could be employed to achieve dentin and hard tissue formation as well as tooth revascularization (10).…”
Section: Originalmentioning
confidence: 99%
“…During pulp inflammation, AA metabolism generates prostaglandin E 2 (PGE 2 ) (5) and this lipid mediator produced by stem cells shows such a potent immunomodulator with anti-inflammatory effects through regulation of cell maturation and activation (6). PGE 2 have demonstrate a dual role in proliferation and cell differentiation, because inhibit osteogenic differentiation of mesenchymal stem cells (7), but also has anabolic effects on osteogenic and odontogenic markers in vitro, enhances tertiary dentin formation in vivo (8). These findings shed light on this mediator as a potential therapeutical agent to accelerate pulp repair.…”
Section: Introductionmentioning
confidence: 99%
“…On the other hand, studies have shown that PGE 2 inhibits the osteogenic differentiation of mesenchymal stem cells (Ern et al, 2017). In addition, PGE 2 induces the expression of genes associated with mineralization by undifferentiated cells of the dental pulp (Lorencetti‐Silva et al, 2019), improving the formation of tertiary dentine (Limjeerajarus et al, 2014). Various studies carried out on human dental pulps have reported that, during pulp inflammation, the concentration of PGE 2 in dental pulps with pulpitis (Nakanishi et al, 1995) significantly increases, both reversible (Cohen et al, 1985; Petrini et al, 2012) and irreversible (Cohen et al, 1985), compared to healthy dental pulps.…”
Section: Discussionmentioning
confidence: 99%