Related Experiment Videos
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
Summary
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.
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.