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Leptin effects on the regenerative capacity of human periodontal cells.

Nokhbehsaim M, Keser S, Nogueira AV, Jäger A, Jepsen S, Cirelli JA, Bourauel C, Eick S, Deschner J - Int J Endocrinol (2014)

Bottom Line: Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels.Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing.Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link.

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
Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGFβ1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.

No MeSH data available.


Related in: MedlinePlus

Effect of EMD on the nuclear translocation of SMAD1/5/8 in the presence and absence of leptin (3 ng/mL), as determined by immunofluorescence ((a)–(f)). Experiments were performed in triplicate and repeated twice. Untreated cells served as control. Images from one representative donor are shown.
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fig3: Effect of EMD on the nuclear translocation of SMAD1/5/8 in the presence and absence of leptin (3 ng/mL), as determined by immunofluorescence ((a)–(f)). Experiments were performed in triplicate and repeated twice. Untreated cells served as control. Images from one representative donor are shown.

Mentions: EMD induced a nuclear translocation of SMAD1/5/8, which was most pronounced at 60 min. However, in the presence of leptin, the EMD-stimulated SMAD1/5/8 nuclear translocation was almost completely blocked, as shown in Figures 3(a)–3(f).


Leptin effects on the regenerative capacity of human periodontal cells.

Nokhbehsaim M, Keser S, Nogueira AV, Jäger A, Jepsen S, Cirelli JA, Bourauel C, Eick S, Deschner J - Int J Endocrinol (2014)

Effect of EMD on the nuclear translocation of SMAD1/5/8 in the presence and absence of leptin (3 ng/mL), as determined by immunofluorescence ((a)–(f)). Experiments were performed in triplicate and repeated twice. Untreated cells served as control. Images from one representative donor are shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4129942&req=5

fig3: Effect of EMD on the nuclear translocation of SMAD1/5/8 in the presence and absence of leptin (3 ng/mL), as determined by immunofluorescence ((a)–(f)). Experiments were performed in triplicate and repeated twice. Untreated cells served as control. Images from one representative donor are shown.
Mentions: EMD induced a nuclear translocation of SMAD1/5/8, which was most pronounced at 60 min. However, in the presence of leptin, the EMD-stimulated SMAD1/5/8 nuclear translocation was almost completely blocked, as shown in Figures 3(a)–3(f).

Bottom Line: Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels.Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing.Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link.

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
Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGFβ1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.

No MeSH data available.


Related in: MedlinePlus