Thermally induced osteocyte damage initiates pro-osteoclastogenic gene expression in vivo

Eimear B. Dolan, David Tallon, Wing Yee Cheung, Mitchell B. Schaffler, Oran D. Kennedy, Laoise M. McNamara

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Bone is often subject to harsh temperatures during orthopaedic procedures resulting in thermally induced bone damage, which may affect the healing response. Postsurgical healing of bone is essential to the success of surgery, therefore, an understanding of the thermally induced responses of bone cells to clinically relevant temperatures in vivo is required. Osteocytes have been shown to be integrally involved in the bone remodelling cascade, via apoptosis, in micro-damage systems. However, it is unknown whether this relationship is similar following thermal damage. Sprague-Dawley rat tibia were exposed to clinically relevant temperatures (47°C or 60°C) to investigate the role of osteocytes in modulating remodelling related factors. Immunohistochemistry was used to quantify osteocyte thermal damage (activated caspase-3). Thermally induced pro-osteoclastogenic genes (Rankl, Opg and M-csf), in addition to genes known to mediate osteoblast and osteoclast differentiation via prostaglandin production (Cox2), vascularization (Vegf) and inflammatory (Il1a) responses, were investigated using gene expression analysis. The results demonstrate that heat-treatment induced significant bone tissue and cellular damage. Pro-osteoclastogenic genes were upregulated depending on the amount of temperature elevation compared with the control. Taken together, the results of this study demonstrate the in vivo effect of thermally induced osteocyte damage on the gene expression profile.

Original languageEnglish
Article number20160337
JournalJournal of the Royal Society Interface
Volume13
Issue number119
DOIs
StatePublished - 1 Jun 2016
Externally publishedYes

Keywords

  • Apoptosis
  • Osteocyte
  • Remodelling
  • Thermal damage

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