Bone adaptation to load: microdamage as a stimulus for bone remodelling

Authors

  • T. C. Lee,

    Corresponding author
    1. Department of Anatomy, Royal College of Surgeons in Ireland, St Stephen's Green, Dublin 2, Ireland
    2. Trinity Centre for Bio-Engineering, Department of Mechanical and Manufacturing Engineering, Trinity College, Dublin 2, Ireland
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  • A. Staines,

    1. Department of Public Health Medicine and Epidemiology, University College Dublin, Dublin 2, Ireland
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  • D. Taylor

    1. Trinity Centre for Bio-Engineering, Department of Mechanical and Manufacturing Engineering, Trinity College, Dublin 2, Ireland
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T. C. Lee, Department of Anatomy, Royal College of Surgeons in Ireland, St Stephen's Green, Dublin 2, Ireland. Tel. + 353 1402 2264; fax: + 353 1402 2355; e-mail: tclee@rcsi.ie

Abstract

Mechanical loading in the proximal radius was increased by ulnar osteotomy (Group O), altered by Steinmann pinning (Group P) or unaltered in sham operated controls (Group C) in skeletally mature female sheep, aged 2–4 years. A series of intravenous fluorochromes were given to label bone formation and fuchsin-stained microdamage assessed at intervals of up to 24 weeks. Microcracks were present in all groups and were found in the original cortex near the periosteal surface. No microcracks were found in the new, fibrolamellar bone laid down at periosteal or endosteal surfaces. Mean microcrack length (49 µm, SD 10 µm) did not differ between groups or over time. Microcrack numerical and surface densities and resorption cavity density peaked in all groups at 6 weeks, consistent with a regional acceleratory phenomenon (RAP), but the peaks were significantly greater in Group O. The density of refilling or secondary osteons peaked at 10 weeks and the mean time required for the formation of an osteon was 7.51 ± 0.59 weeks. Fatigue-induced microdamage is normally present in bone and is increased due to repetitive loading of the mechanically overloaded radius. The location and timing of microcracks, resorption cavities and secondary osteons are consistent with the activation-resorption-formation remodelling cycle and suggest that microdamage is a stimulus for bone remodelling.

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