4.6 Article

Heat-shock-induced cellular responses to temperature elevations occurring during orthopaedic cutting

Journal

JOURNAL OF THE ROYAL SOCIETY INTERFACE
Volume 9, Issue 77, Pages 3503-3513

Publisher

ROYAL SOC
DOI: 10.1098/rsif.2012.0520

Keywords

thermal necrosis; apoptosis; heat-shock; bone; surgical cutting; mineralization

Funding

  1. National University of Ireland Galway Fellowship Scheme
  2. National University of Ireland Travelling Scholarships in Engineering
  3. European Research Council (ERC) [258992]

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Severe heat-shock to bone cells caused during orthopaedic procedures can result in thermal damage, leading to cell death and initiating bone resorption. By contrast, mild heat-shock has been proposed to induce bone regeneration. In this study, bone cells are exposed to heat-shock for short durations occurring during surgical cutting. Cellular viability, necrosis and apoptosis are investigated immediately after heat-shock and following recovery of 12, 24 h and 4 days, in osteocyte-like MLO-Y4 and osteoblast-like MC3T3-E1 cells, using flow cytometry. The regeneration capacity of heat-shocked Balb/c mesenchymal stem cells (MSCs) and MC3T3-E1s has been investigated following 7 and 14 day's recovery, by quantifying proliferation, differentiation and mineralization. An immediate necrotic response to heat-shock was shown in cells exposed to elevated temperatures (45 degrees C, 47 degrees C and most severe at 60 degrees C). A longer-term apoptotic response is induced in MLO-Y4s and, to a lesser extent, in MC3T3-E1s. Heat-shock-induced differentiation and mineralization by MSCs. These findings indicate that heat-shock is more likely to induce apoptosis in osteocytes than osteoblasts, which might reflect their role as sensors detecting and communicating damage within bone. Furthermore, it is shown for the first time that mild heat-shock (less than equal to 47 degrees C) for durations occurring during surgical cutting can positively enhance osseointegration by osteoprogenitors.

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