“…On the other hand, despite the clean mechanical pulp exposure model, the bioactive aFGF investigated did not appear to produce hard tissue repair of similar quality to that capped with aqueous calcium hydroxide paste. This seemed to substantiate the previous in vitro observation that aFGF alone could merely promote cell polarization but not odontoblastic differentiation (25) although it enhances fibroblast proliferation (26) and angiogenesis in the early phase of wound healing (27). It has been suggested that the previously formed irregular extracellular osteo‐dentin‐like hard tissue matrix at 6 week might have served as a reservoir for cytokines such as Transforming Growth Factor‐β (TGF‐ β ) (28).…”
Acidic fibroblast growth factor (aFGF) has been shown to facilitate wound healing by stimulating fibroblast proliferation and angiogenesis. It has also been reported to possess a powerful anti-apoptotic function This study compared the histological pulp responses to aFGF on collagen carrier and Ca(OH)(2) placed on the mechanically exposed dental pulp in monkeys at two observation periods. Thirty-six teeth with pulp exposures were distributed into three groups according to the capping agents used prior to application of the coronal seal: collagen-based matrix carrier (group 1), aFGF on the collagen-based matrix carrier (group 2) and aqueous calcium hydroxide [Ca(OH)(2)] paste (group 3). Specimens were harvested at 6 and 13 weeks postoperatively and prepared for hematoxylin and eosin, and Gram staining. Histological qualitative evaluation of pulp responses were performed under the light microscope following criteria modified from Cox et al. (17) and Hu et al. (18). Semi-quantitative analysis was also carried out using Kruskal-Wallis and Mann-Whitney U-tests. There was neither negligible inflammatory infiltrates with no bacteria present in the three groups at both timings, nor was there any significant difference in the soft tissue organization among the three groups at or between the 6- and 13-week observation periods. At 6 weeks, the hard tissue barrier produced by Ca(OH)(2) group (1.040 +/- 0.089) was significantly more superior than aFGF/collagen carrier group (1.930 +/- 0.825) (P = 0.030) as well as collagen carrier group (3.142 +/- 1.069, P = 0.018). At 13 weeks, both aFGF/collagen carrier group (1.214 +/- 0.485) and the collagen carrier group (1.457 +/- 0.814) produced significantly better hard tissue barrier (P = 0.040 and P = 0.017, respectively) than earlier timing. However, these two groups did not induce significantly improved hard tissue barrier compared to that produced by aqueous Ca(OH)(2) paste which stimulated matrix secretion in a polar tubular dentin-like pattern.
“…On the other hand, despite the clean mechanical pulp exposure model, the bioactive aFGF investigated did not appear to produce hard tissue repair of similar quality to that capped with aqueous calcium hydroxide paste. This seemed to substantiate the previous in vitro observation that aFGF alone could merely promote cell polarization but not odontoblastic differentiation (25) although it enhances fibroblast proliferation (26) and angiogenesis in the early phase of wound healing (27). It has been suggested that the previously formed irregular extracellular osteo‐dentin‐like hard tissue matrix at 6 week might have served as a reservoir for cytokines such as Transforming Growth Factor‐β (TGF‐ β ) (28).…”
Acidic fibroblast growth factor (aFGF) has been shown to facilitate wound healing by stimulating fibroblast proliferation and angiogenesis. It has also been reported to possess a powerful anti-apoptotic function This study compared the histological pulp responses to aFGF on collagen carrier and Ca(OH)(2) placed on the mechanically exposed dental pulp in monkeys at two observation periods. Thirty-six teeth with pulp exposures were distributed into three groups according to the capping agents used prior to application of the coronal seal: collagen-based matrix carrier (group 1), aFGF on the collagen-based matrix carrier (group 2) and aqueous calcium hydroxide [Ca(OH)(2)] paste (group 3). Specimens were harvested at 6 and 13 weeks postoperatively and prepared for hematoxylin and eosin, and Gram staining. Histological qualitative evaluation of pulp responses were performed under the light microscope following criteria modified from Cox et al. (17) and Hu et al. (18). Semi-quantitative analysis was also carried out using Kruskal-Wallis and Mann-Whitney U-tests. There was neither negligible inflammatory infiltrates with no bacteria present in the three groups at both timings, nor was there any significant difference in the soft tissue organization among the three groups at or between the 6- and 13-week observation periods. At 6 weeks, the hard tissue barrier produced by Ca(OH)(2) group (1.040 +/- 0.089) was significantly more superior than aFGF/collagen carrier group (1.930 +/- 0.825) (P = 0.030) as well as collagen carrier group (3.142 +/- 1.069, P = 0.018). At 13 weeks, both aFGF/collagen carrier group (1.214 +/- 0.485) and the collagen carrier group (1.457 +/- 0.814) produced significantly better hard tissue barrier (P = 0.040 and P = 0.017, respectively) than earlier timing. However, these two groups did not induce significantly improved hard tissue barrier compared to that produced by aqueous Ca(OH)(2) paste which stimulated matrix secretion in a polar tubular dentin-like pattern.
“…This result indicates that the FGF-2-protective effect of γ-PGA-S72 was greater than that of other heparinoids. Based on this comparison, sulfonation is thought to be necessary for FGF-2 protective effects. , 4 Comparison of the FGF-2-protective effect of heparin, γ-PGA, and γ-PGA-S72 under various temperature conditions (37 °C (○), 60 °C (▵), and 90 °C (□)). The polymer concentrations were 10 μg/mL, and the FGF-2 concentration was 10 ng/mL.…”
Section: Resultsmentioning
confidence: 99%
“…Based on this comparison, sulfonation is thought to be necessary for FGF-2 protective effects. 24,26 Coltrini et al reported the capacity of different GAGs to protect FGF-2 from proteolysis. 25 The protect effect from proteolysis decreases in the following order: heparin > heparan sulfate > dermatan sulfate ) chondroitin sulfates A and C > hyaluronic acid.…”
Section: Figure 2 Comparison Of Fgf-2 Activity Of γ-Pga-s72mentioning
confidence: 99%
“…FGF-2 was reported to stably interact with heparin or HSPG by electrostatic interaction. − Gospodarpwocz et al reported heparin, HSPG, and synthetic heparinoids have protective effect of FGFs. , In interactions between sulfated polysaccharides and FGFs, sulfate groups appeared to predominantly bind to basic amino acid residues in FGFs. Polyanions such as dextran sulfate, nucleotides, sulfated β-cyclodextrin, glycosaminoglycnas (GAG), and synthetic (1 → 6)-α- d -mannopyranan sulfate having sulfate groups strongly interact with FGFs and mimic heparin effects on the biological activities of FGFs . These days, however, Kunou et al reported that carboxyl groups in polysaccharides complement sulfate groups to significantly contribute to interactions between sulfated polysaccharide and FGFs …”
Basic fibroblast growth factor (FGF-2) mitogenic activities of sulfonated poly(gamma-glutamic acid) (gamma-PGA-S) were investigated with chlorate-treated L929 fibroblast culture tests. When 72% of the carboxyl groups in gamma-PGA were sulfonated (gamma-PGA-S72), cell numbers reached a maximum. The activity of gamma-PGA-S72 was higher than that of gamma-PGA and synthetic heparinoids and was almost comparable to that of heparin. Cytotoxicity of gamma-PGA-S72 was not observed, regardless of the degree of sulfonation. FGF-2-protective effects of gamma-PGA-S72 against acid and thermal inactivation were also evaluated, and gamma-PGA-S72 showed higher FGF-2-protective effects in comparison to nonsulfonated gamma-PGA. The steric structures of various sulfonated gamma-PGA-Ss were analyzed by molecular modeling (molecular orbital method (MOPAC)) and indicated that gamma-PGA-Ss are helical in vacuo. Results from MOPAC and the molecular mechanics method (MM2) demonstrated that electrostatic interactions can take place between sulfonic and carboxyl groups of gamma-PGA-S and basic amino acid residues in FGF-2. gamma-PGA-S72 can interact with FGF-2 strongly.
“…It can therefore be presumed that the content of sulfate groups is more important for the mitogenic activity on 3T3 fibroblasts in the presence of FGF-2 than carboxyl groups. Similar conclusions have been drawn from a strong increase of the effect of FGF-2 at lower concentrations with other highly sulfated compounds (Kunou & Hatanaka, 1995). Possibly, a higher DS COO of COCS might be required to show a substantial mitogenic activity.…”
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