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https://doi.org/10.1302/2046-3758.911.BJR-2020-0001.R2
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dc.title | The effect of TNF-? on osteoblasts in metal wear-induced periprosthetic bone loss | |
dc.contributor.author | Hameister, R. | |
dc.contributor.author | Dheen, Shaikali Thameem | |
dc.contributor.author | Kaur, Charanjit | |
dc.contributor.author | Lohmann, C.H. | |
dc.contributor.author | Singh, G. | |
dc.date.accessioned | 2021-08-16T02:22:07Z | |
dc.date.available | 2021-08-16T02:22:07Z | |
dc.date.issued | 2020 | |
dc.identifier.citation | Hameister, R., Dheen, Shaikali Thameem, Kaur, Charanjit, Lohmann, C.H., Singh, G. (2020). The effect of TNF-? on osteoblasts in metal wear-induced periprosthetic bone loss. Bone and Joint Research 9 (11) : 827-839. ScholarBank@NUS Repository. https://doi.org/10.1302/2046-3758.911.BJR-2020-0001.R2 | |
dc.identifier.issn | 20463758 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/196962 | |
dc.description.abstract | Aims This study aimed to examine the effects of tumour necrosis factor-alpha (TNF-?) on osteoblasts in metal wear-induced bone loss. Methods TNF-? immunoexpression was examined in periprosthetic tissues of patients with failed metal-on-metal hip arthroplasties and also in myeloid MM6 cells after treatment with cobalt ions. Viability and function of human osteoblast-like SaOs-2 cells treated with recombinant TNF-? were studied by immunofluorescence, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assay, western blotting, and enzyme-linked immunosorbent assay (ELISA). Results Macrophages, lymphocytes, and endothelial cells displayed strong TNF-? immunoexpression in periprosthetic tissues containing metal wear debris. Colocalization of TNF-? with the macrophage marker CD68 and the pan-T cell marker CD3 confirmed TNF-? expression in these cells. Cobalt-treated MM6 cells secreted more TNF-? than control cells, reflecting the role of metal wear products in activating the TNF-? pathway in the myeloid cells. While TNF-? did not alter the immunoexpression of the TNF-receptor 1 (TNF-R1) in SaOs-2 cells, it increased the release of the soluble TNF-receptor 1 (sTNF-R1). There was also evidence for TNF-?-induced apoptosis. TNF-? further elicited the expression of the endoplasmic reticulum stress markers inositol-requiring enzyme (IRE)-1?, binding-immunoglobulin protein (BiP), and endoplasmic oxidoreductin1 (Ero1)-L?. In addition, TNF-? decreased pro-collagen I ? 1 secretion without diminishing its synthesis. TNF-? also induced an inflammatory response in SaOs-2 cells, as evidenced by the release of reactive oxygen and nitrogen species and the proinflammatory cytokine vascular endothelial growth factor. Conclusion The results suggest a novel osteoblastic mechanism, which could be mediated by TNF-? and may be involved in metal wear debris-induced periprosthetic bone loss. © 2020 Author(s) et al. This is an open-access article distributed under the terms ofthe Creative Commons Attribution Non-Commercial No Derivatives (CC BY-NC-ND 4.0) licence, which permits the copying and redistribution of the work only, and providedthe original author and source are credited. See https://creativecommons.org/licenses/by-nc-nd/4.0/. | |
dc.publisher | British Editorial Society of Bone and Joint Surgery | |
dc.rights | Attribution-NonCommercial 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by-nc/4.0/ | |
dc.source | Scopus OA2020 | |
dc.subject | Bone loss | |
dc.subject | Endoplasmic reticulum stress | |
dc.subject | Implant loosening | |
dc.subject | Osteoblast | |
dc.subject | Tumour necrosis factor-alpha | |
dc.type | Article | |
dc.contributor.department | ANATOMY | |
dc.description.doi | 10.1302/2046-3758.911.BJR-2020-0001.R2 | |
dc.description.sourcetitle | Bone and Joint Research | |
dc.description.volume | 9 | |
dc.description.issue | 11 | |
dc.description.page | 827-839 | |
Appears in Collections: | Staff Publications Elements |
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