EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

RANKL-associated suppression of particle-induced osteolysis in an aged model of Calcitonin and α-CGRP deficiency



RANKL-associated suppression of particle-induced osteolysis in an aged model of Calcitonin and α-CGRP deficiency



Biomaterials 34(12): 2911-2919



An aging population with higher bone turnover intensifies the need for joint replacement surgery. However, particle-induced osteolysis (PIO) remains a major cause of early implant loosening. Differences in bone remodeling between young and aged Calcitonin (CT)- and α-CGRP (Calcitonin gene-related peptide)-deficient mice (Calca(-/-)) might modify our previous findings regarding CT/α-CGRP in PIO. This may have important implications for PIO in an aging population. Four groups of twelve-month-old wild-type and Calca(-/-) mice underwent either SHAM surgery with and without CT, or polyethylene-particle implantation with related treatment. Morphometric changes were detected using μ-CT, histomorphometric analysis and by counting TRAP(+) cells (osteoclast-staining). Bone remodeling was assessed using serum and urinary markers. There was no osteolysis in aged particle-treated Calca(-/-) animals and the effect of CT on PIO was reduced compared to wild-type mice. However, there were significantly higher numbers of TRAP(+) cells in Calca(-/-) animals, and bone remodeling markers revealed a significant increase in OPG/OCN and a significant reduction in RANKL compared to aged wild-type mice. CT/α-CGRP modulates bone cell activity in PIO in aged mice in a way that is distinct from young animals. This may have implications for the treatment of PIO in the periprosthetic surface of joint replacements in an aging population.

(PDF emailed within 0-6 h: $19.90)

Accession: 055333201

Download citation: RISBibTeXText

PMID: 23357366

DOI: 10.1016/j.biomaterials.2013.01.034



Related references

Calcitonin substitution in calcitonin deficiency reduces particle-induced osteolysis. Bmc Musculoskeletal Disorders 12: 186-186, 2012

Inhibition of RANKL-induced osteoclastogenesis through the suppression of the ERK signaling pathway by astragaloside IV and attenuation of titanium-particle-induced osteolysis. International Journal of Molecular Medicine 36(5): 1335-1344, 2016

The inhibition of RANKL-induced osteoclastogenesis through the suppression of p38 signaling pathway by naringenin and attenuation of titanium-particle-induced osteolysis. International Journal of Molecular Sciences 15(12): 21913-21934, 2015

Scutellarin inhibits RANKL-mediated osteoclastogenesis and titanium particle-induced osteolysis via suppression of NF-κB and MAPK signaling pathway. International Immunopharmacology 40(): 458-465, 2016

Geraniin suppresses RANKL-induced osteoclastogenesis in vitro and ameliorates wear particle-induced osteolysis in mouse model. Experimental Cell Research 330(1): 91-101, 2015

Triptolide inhibits osteoclast formation, bone resorption, RANKL-mediated NF-қB activation and titanium particle-induced osteolysis in a mouse model. Molecular and Cellular Endocrinology 399: 346-353, 2015

Pyrroloquinoline quinine inhibits RANKL-mediated expression of NFATc1 in part via suppression of c-Fos in mouse bone marrow cells and inhibits wear particle-induced osteolysis in mice. Plos One 8(4): E61013-E61013, 2013

MMP-9 inhibition suppresses wear debris-induced inflammatory osteolysis through downregulation of RANK/RANKL in a murine osteolysis model. International Journal of Molecular Medicine 30(6): 1417-1423, 2013

Myricetin prevents titanium particle-induced osteolysis in vivo and inhibits RANKL-induced osteoclastogenesis in vitro. Biochemical Pharmacology 93(1): 59-71, 2015

The fibroblast expression of RANKL in CoCrMo-particle-induced osteolysis is mediated by ER stress and XBP1s. Acta Biomaterialia 24(): 352-360, 2016

Protective effects of COX-2 inhibitor on titanium-particle-induced inflammatory osteolysis via the down-regulation of RANK/RANKL. Acta Biomaterialia 7(8): 3216-3221, 2011

ER Stress Mediates TiAl6V4 Particle-Induced Peri-Implant Osteolysis by Promoting RANKL Expression in Fibroblasts. Plos One 10(9): E0137774-E0137774, 2016

Schisantherin A suppresses osteoclast formation and wear particle-induced osteolysis via modulating RANKL signaling pathways. Biochemical and Biophysical Research Communications 449(3): 344-350, 2014

Inhibition of osteolysis and increase of bone formation after local administration of siRNA-targeting RANK in a polyethylene particle-induced osteolysis model. Acta Biomaterialia 13: 150-158, 2015

The role of calcitonin receptor signalling in polyethylene particle-induced osteolysis. Acta Biomaterialia 14: 125-132, 2015