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Updated: Mar 11, 2026

An Improved Mechanical Testing Method to Assess Bone-implant Anchorage
Published on: February 10, 2014
Strain shielding in trabecular bone at the tibial cement-bone interface
Priyanka Srinivasan1, Mark A Miller2, Nico Verdonschot3
1Orthopaedic Research Laboratory, Radboud Institute for Health Sciences, Radboud university medical center, Nijmegen, The Netherlands.
Abstract:
Aseptic loosening of the tibial component remains the leading cause for revision surgery in total knee arthroplasty (TKA). Understanding the mechanisms leading to loss of fixation can offer insight into preventative measures to ensure a longer survival rate. In cemented TKA, loosening occurs at the cement-trabecular interface probably due to a stress-shielding effect of the stiffer implant material in comparison with bone. Using finite element models of lab-prepared tibial cement-trabeculae interface specimens (n=4) based on micro-CT images, this study aims to investigate the micromechanics of the interlock between cement and trabecular bone. Finite element micromotion between cement and trabeculae and bone strain were compared in the interdigitated trabeculae as well as strain in the bone distal to the interface. Lab-prepared specimens and their FE models were assumed to represent the immediate post-operative situation. The cement layer was removed in the FE models while retaining the loading conditions, which resulted in FE models that represented the pre-operative situation. Results showed that micromotion and bone strain decrease when interdigitation depth increases. Bone-cement micromotion and bone strain at the distal interdigitated region showed a dependence on bone volume fraction. Comparing the immediate post-operative and pre-operative situations, trabeculae embedded deep within the cement generally showed the highest level of strain-shielding. Strain shielding of interdigitated bone, in terms of reduction in compressive strains, was found to be between 35 and 61 % for the four specimens. Strain adaptive remodeling could thus be a plausible mechanism responsible for loss of interdigitated bone.
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