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A841. APPLICATION OF NON-DESTRUCTIVE EVALUATION TECHNIQUES FOR THE ASSESSMENT OF BONE CEMENT MICROCRACKING DURING FATIGUE



Abstract

Orthopaedic implants are often fixed into place using bone cement. The degradation of the cement mantle has been implicated as playing a major role in the loosening of these implants, and this often necessitates revision surgery. The present work has used the non-destructive acoustic emission (AE) technique to monitor the initiation and evolution of fatigue damage in bone cement constructs. Using this technique, it should be possible to gain an understanding of failure progression in cemented orthopaedic devices. Previous work in this area has focused on AE activity originating from the eventual failure location in order to identify those signatures associated with critical fatigue cracks. This usually involves analysing AE signatures associated with the final stages of failure; however, there have been limited investigations that have looked at the damage that takes up most of the crack propagation life of the sample, (i.e. microcracking formation and development), that occurs away from the failure site, but could still play a role in final failure.

In this study, dog-bone-shaped specimens of bone cement were subjected to uniaxial tensile fatigue loading, with damage monitored along the length of specimens using AE. Where specimens exhibited AE activity at locations away from the fracture site, they were sectioned and subjected to synchrotron tomography, which enabled high resolution images of these regions to be obtained. Microcracks of the order of 20 microns were observed in areas where AE had identified early, non-critical damage; in contrast, no microcracking was observed in areas that either remained unloaded or exhibited no AE. To further corroborate these observations, and characterise the damage mechanisms involved, scanning electron microscopy (SEM) was applied to the sectioned samples. In those locations where significant yet non-critical AE occurred, there was evidence of crack-bridging, suggesting that crack closure mechanisms may have slowed down or even arrested crack propagation within the bone cement.

These findings further validate the use of AE as a passive non-destructive method for the identification and understanding of damage evolution in cemented orthopaedic devices.

Correspondence should be addressed to Diane Przepiorski at ISTA, PO Box 6564, Auburn, CA 95604, USA. Phone: +1 916-454-9884; Fax: +1 916-454-9882; E-mail: ista@pacbell.net