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Publication:
The Chinese Journal of Dental Research

Year 2004
Volume 7 , Issue 2

Back
Pages: 24 - 32

Soluble Receptor Against Tumor Necrosis Factor Inhibits Root Resorption by a Mechanism Independent of the RANKL/RANK Interaction

Dongliang Zhang, DDS, MS Orth, PhD/Jie Ouyang, DDS/Lingli Wang, DDS, MS Orth, PhD/Goetz Werner, DDS, MS Orth, PhD/Andreas Jaeger, DDS, MS Orth, PhD

Objectives: To understand the role of tumor necrosis factor-alpha (TNFa) and interleukin-1 (IL-1) in root resorption process. To gain an understanding of the relationship between double mechanism RANKL/RANK and interaction with cytokine inflammatory regulation system. Methods: Eighteen 4-week-old male Wistar rats were divided into three groups, with 6 animals in each group. On the seventh day of the experiment, all animals were sacrificed by perfusion through the left heart ventricle. ED1 cells were stained using immunohistochemistry. In situ hybridization was employed to identify RANKL, RANK mRNA expression differences in the three groups. Results: Odontoclast showed strong immunoreactivity to ED1. No significant differences were found between the control group and IL-1 group. The RANKL mRNA positive signals could be detected in the odontoblast, endosteal cells, stromal cells, spindle-shaped fibroblast near root resorption lacuna. High levels of expression of RANK mRNA were detected in relatively small cells and in large cells of the endosteum. No significant difference was found in the RANKL mRNA and RANK mRNA expression levels among the three groups. Discussion: IL-1, TNFa and RANKL independently stimulate osteoclast differentiation through RANK mediated signals. Osteoclast differentiation induction by TNFa occurs via TNFR1 and TNFR2 receptors expressed by osteoclast precursors. As for root resorption, the differentiation stage of odontoclast/osteoclast precursors play more critical role than the activation of odontoclast/osteoclast.

 

 

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