Journalartikel

Jahr der Veröffentlichung: 2021

Seiten: 1933-1944

Zeitschrift: Clinical Oral Investigations

Bandnummer: 25

Heftnummer: 4

ISSN: 1432-6981

eISSN: 1436-3771

Open Access Status: Hybrid

DOI Link: https://doi.org/10.1007/s00784-020-03501-3

Verlag: Springer

Abstract: 
Objectives Juvenile obesity is a complex clinical condition that is present more and more frequently in the daily orthodontic practice. Over-weighted patients have an impaired bone metabolism, due in part to their increased levels of circulating adipokines. Particularly, leptin has been reported to play a key role in bone physiology. Leptin is ubiquitously present in the body, including blood, saliva, and crevicular fluid. If, and to what extent, it could influence the reaction of cementoblasts during orthodontic-induced forces is yet unknown. Material and methods OCCM-30 cementoblasts were cultivated under compressive forces using different concentrations of leptin. The expression ofObR,Runx-2,Osteocalcin,Rank-L,Sost,Caspase 3,8, and9were analyzed by RT-PCR. Western blots were employed for protein analysis. The ERK1/2 antagonist FR180204 (Calbiochem) was used and cPLA2 activation, PGE2, and cytochrome C release were further evaluated. Results In vitro, when compressive forces are applied, leptin promotes ERK1/2 phosphorylation, as well as upregulates PGE2 and caspase 3 and caspase 9 on OCCM cells. Blockade of ERK1/2 impairs leptin-induced PGE2 secretion and reduced caspase 3 and caspase 9 expression. Conclusions Leptin influences the physiological effect of compressive forces on cementoblasts, exerting in vitro a pro-inflammatory and pro-apoptotic effect.

Harvard-Zitierstil: Ruiz-Heiland, G., Yong, J., von Bremen, J. and Ruf, S. (2021) Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment, Clinical Oral Investigations, 25(4), pp. 1933-1944. https://doi.org/10.1007/s00784-020-03501-3

APA-Zitierstil: Ruiz-Heiland, G., Yong, J., von Bremen, J., & Ruf, S. (2021). Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment. Clinical Oral Investigations. 25(4), 1933-1944. https://doi.org/10.1007/s00784-020-03501-3