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Inelastic strain accumulation in cortical bone during rapid transient tensile loading.

M T Fondrk1, E H Bahniuk, D T Davy

  • 1Department of Mechanical & Aerospace Engineering, Case Western Reserve University, Cleveland, OH 44106, USA.

Journal of Biomechanical Engineering
|January 14, 2000
PubMed
Summary
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A damage model for nonlinear tensile behavior of cortical bone.

Journal of biomechanical engineering·1999

Cortical bone exhibits nonlinear stress-strain behavior under rapid loading, similar to creep loading. This indicates bone damage accumulation and potential for biological repair responses.

Area of Science:

  • Biomechanics
  • Biomaterials Science
  • Orthopedic Research

Background:

  • Cortical bone's mechanical properties are crucial for skeletal function.
  • Understanding bone's response to rapid loading is vital for injury prevention and treatment.

Purpose of the Study:

  • To investigate the tensile stress-strain behavior of human and bovine cortical bone under rapid, high-amplitude load cycles.
  • To determine if nonlinear stress-strain behavior observed in creep loading also occurs during transient loading at physiological rates.

Main Methods:

  • Experimental study using machined bovine and human cortical bone samples.
  • Subjected samples to rapid load cycles (+/- 420 MPa/s) with load reversal at pre-selected strain levels.
  • Measured axial and transverse strain behavior to assess nonlinearity and residual strain.

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Main Results:

  • Cortical bone demonstrated significant nonlinearity in axial strain during the first load cycle, while transverse strain remained largely linear.
  • A substantial portion of maximum nonlinear strain accumulated after load reversal in both human (29.1%) and bovine (35.1%) bone.
  • Significant residual axial and volumetric strains were observed upon unloading, indicating internal damage.

Conclusions:

  • Nonlinear stress-strain behavior in cortical bone occurs during transient loading at physiological rates, mirroring creep loading behavior.
  • Damage accumulation, evidenced by internal voids and new surfaces, is a primary driver of this nonlinear behavior.
  • Residual volume increases and structural disruptions may act as a stimulus for bone's biological repair mechanisms.