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Beneficial effects of adiponectin on periodontal ligament cells under normal and regenerative conditions.

Nokhbehsaim M, Keser S, Nogueira AV, Cirelli JA, Jepsen S, Jäger A, Eick S, Deschner J - J Diabetes Res (2014)

Bottom Line: The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link.Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression.In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

View Article: PubMed Central - PubMed

Affiliation: Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany ; Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany.

ABSTRACT
Type 2 diabetes and obesity are increasing worldwide and linked to periodontitis, a chronic disease which is characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium. The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link. The aim of this in vitro study was to examine the effects of adiponectin on periodontal ligament (PDL) cells under normal and regenerative conditions, and to study the regulation of adiponectin and its receptors in these cells. Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression. The beneficial actions of enamel matrix derivative on a number of PDL cell functions critical for periodontal regeneration were partially enhanced by adiponectin. The periodontopathogen Porphyromonas gingivalis inhibited the adiponectin expression and stimulated the expression of its receptors. In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

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Effects of EMD and/or adiponectin (3 μg/mL) on wound closure over 4 d (a). Untreated cells were used as control. Mean ± SEM (n = 12); ∗significantly (P < 0.05) different from cells treated with EMD, either alone or with adiponectin; #significantly (P < 0.05) different from all other groups. Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of Ki67 at 1 d and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of EMD on SMAD1/5/8 nuclear translocation in the presence and absence of adiponectin (1 μg/mL) at 60 min, as analyzed by immunofluorescence (c–f). Untreated cells served as control. Experiments were performed in triplicate and repeated twice. Images from one representative donor are shown.
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fig2: Effects of EMD and/or adiponectin (3 μg/mL) on wound closure over 4 d (a). Untreated cells were used as control. Mean ± SEM (n = 12); ∗significantly (P < 0.05) different from cells treated with EMD, either alone or with adiponectin; #significantly (P < 0.05) different from all other groups. Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of Ki67 at 1 d and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of EMD on SMAD1/5/8 nuclear translocation in the presence and absence of adiponectin (1 μg/mL) at 60 min, as analyzed by immunofluorescence (c–f). Untreated cells served as control. Experiments were performed in triplicate and repeated twice. Images from one representative donor are shown.

Mentions: Next we examined the effects of adiponectin on the in vitro wound fill rate. In the absence of EMD, adiponectin accelerated significantly the wound closure by 13.37 ± 8.63% and 23.96 ± 3.78, at 2 d and 3 d, respectively. However, no regulatory effects of adiponectin on the wound closure were observed in the presence of EMD (Figure 2(a)). Since the wound fill rate depends on cell proliferation, we then analyzed the actions of adiponectin on Ki67, a marker of proliferation, in the presence and absence of EMD. As shown in Figure 2(b), EMD increased significantly the Ki67 mRNA expression at 1 d and 3 d. In the absence of EMD, adiponectin also caused a significant Ki67 upregulation at 3 d. However, no significant effects of adiponectin on the Ki67 mRNA expression were observed in the presence of EMD at 1 d and 3 d (Figure 2(b)).


Beneficial effects of adiponectin on periodontal ligament cells under normal and regenerative conditions.

Nokhbehsaim M, Keser S, Nogueira AV, Cirelli JA, Jepsen S, Jäger A, Eick S, Deschner J - J Diabetes Res (2014)

Effects of EMD and/or adiponectin (3 μg/mL) on wound closure over 4 d (a). Untreated cells were used as control. Mean ± SEM (n = 12); ∗significantly (P < 0.05) different from cells treated with EMD, either alone or with adiponectin; #significantly (P < 0.05) different from all other groups. Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of Ki67 at 1 d and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of EMD on SMAD1/5/8 nuclear translocation in the presence and absence of adiponectin (1 μg/mL) at 60 min, as analyzed by immunofluorescence (c–f). Untreated cells served as control. Experiments were performed in triplicate and repeated twice. Images from one representative donor are shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4120919&req=5

fig2: Effects of EMD and/or adiponectin (3 μg/mL) on wound closure over 4 d (a). Untreated cells were used as control. Mean ± SEM (n = 12); ∗significantly (P < 0.05) different from cells treated with EMD, either alone or with adiponectin; #significantly (P < 0.05) different from all other groups. Effects of EMD and/or adiponectin (1 μg/mL) on the mRNA expression of Ki67 at 1 d and 3 d (b). Untreated cells were used as control. Mean ± SEM (n = 18); ∗significant (P < 0.05) difference between groups. Effects of EMD on SMAD1/5/8 nuclear translocation in the presence and absence of adiponectin (1 μg/mL) at 60 min, as analyzed by immunofluorescence (c–f). Untreated cells served as control. Experiments were performed in triplicate and repeated twice. Images from one representative donor are shown.
Mentions: Next we examined the effects of adiponectin on the in vitro wound fill rate. In the absence of EMD, adiponectin accelerated significantly the wound closure by 13.37 ± 8.63% and 23.96 ± 3.78, at 2 d and 3 d, respectively. However, no regulatory effects of adiponectin on the wound closure were observed in the presence of EMD (Figure 2(a)). Since the wound fill rate depends on cell proliferation, we then analyzed the actions of adiponectin on Ki67, a marker of proliferation, in the presence and absence of EMD. As shown in Figure 2(b), EMD increased significantly the Ki67 mRNA expression at 1 d and 3 d. In the absence of EMD, adiponectin also caused a significant Ki67 upregulation at 3 d. However, no significant effects of adiponectin on the Ki67 mRNA expression were observed in the presence of EMD at 1 d and 3 d (Figure 2(b)).

Bottom Line: The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link.Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression.In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

View Article: PubMed Central - PubMed

Affiliation: Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany ; Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany.

ABSTRACT
Type 2 diabetes and obesity are increasing worldwide and linked to periodontitis, a chronic disease which is characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium. The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link. The aim of this in vitro study was to examine the effects of adiponectin on periodontal ligament (PDL) cells under normal and regenerative conditions, and to study the regulation of adiponectin and its receptors in these cells. Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression. The beneficial actions of enamel matrix derivative on a number of PDL cell functions critical for periodontal regeneration were partially enhanced by adiponectin. The periodontopathogen Porphyromonas gingivalis inhibited the adiponectin expression and stimulated the expression of its receptors. In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.

Show MeSH
Related in: MedlinePlus