header advert
Orthopaedic Proceedings Logo

Receive monthly Table of Contents alerts from Orthopaedic Proceedings

Comprehensive article alerts can be set up and managed through your account settings

View my account settings

Visit Orthopaedic Proceedings at:

Loading...

Loading...

Full Access

MICRODAMAGE: IMPLICATIONS FOR IMPLANT LOOSENING



Abstract

The presence of microdamage in bone and its targeted repair by activating bone remodelling has been controversial partly because it is difficult to locate and difficult to quantify. A number of studies have now validated techniques to locate and quantify microdamage and microdamage repair in human cortical and trabecular bone samples. The purpose of this study is to determine if microcracks accumulate in the cancellous bone of the intertrochanteric region of the proximal femoral shaft and influence the strength of bone. We have used en bloc basic fuchsin staining to identify in vivo microcracks in 70 micron sections. Trabecular bone was sampled in 33 patients undergoing total hip replacement for primary osteoarthritis. The study sample had a median age of 73 years and included 18 women (aged 49 to 84 years) and 15 men (aged 45 to 85 years). Histomorphometry was used to quantify the number of cracks in each case. In a selection of 12 cases the bone sample was also biomechanically tested to determine the cancellous bone strength. We found that microcracks accumulate with age, particularly after the age of about 60 years. This indicates that the bone from the elderly is more susceptible to fatigue damage than bone from the young. In addition, an increased number of microcracks in the cancellous bone significantly reduced the ultimate failure stress of the bone. Bone screws or pins placed in cortical or trabecular bone create microdamage adjacent to an implant, and the area in which this microdamage occurs is the same as that which subsequently remodels. Microdamage may be the result primarily of procedures during prosthetic implantation, but bone screws or pins can create stress concentrations that can be sites for initiation of new cracks. Therefore, if bone remodelling targets bone microdamage for repair then accumulation of microdamage around prosthetic implants may be responsible for the biologic responses which lead to implant loosening. This phenomenon is understudied in orthopaedic research and is an area requiring further investigation.

The abstracts were prepared by Professor Jegan Krishnan. Correspondence should be addressed to him at the Flinders Medical Centre, Bedford Park 5047, Australia.