For millions of patients world-wide, primary total hip replacement (THR) is an effective way to improve quality of life. Failed THRs are often associated with extensive bone loss which makes the revision difficult. An established technique uses impacted morsellized allograft bone to reconstruct the proximal femur and ensure a rigid accommodation of the cemented revision component. There remains a fundamental lack of understanding of the impaction allografting procedure and its complications, particularly with its morphology and biomechanical characteristics.

The objectives of this thesis were to (i) describe the morphology after impaction allografting in the femur, (ii) incorporate a computer simulation that should help the orthopaedic surgeon to control the morphology during surgery, (iii) determine how the morphology affects the immediate strength of the host bone interface, and (iv) develop an animal model to investigate the changes in composite morphology and strength with postoperative healing.

Around the middle third of the stem, virtually the entire femoral canal was filled with cement, thereby forming a cement-allograft composite, whereas in other locations a pure allograft-host bone interface was found. The computer simulation suggested that cement penetration could be controlled by varying graft impaction and limiting cement volume injection. Cement penetration up to the endosteal surface significantly enhanced the host bone interface strength. In the animal study, the strength of the composite-host bone interface increased significantly at 3 weeks and was higher than the pure allograft construct. In contrast to the composite, the pure allograft construct failed at the cement-allograft interface. At 6 weeks the interface strength of the composite decreased, presumably due to cortical cancellisation caused by damaged endosteal circulation.

Cement penetration to the endosteal surface appears to be important for immediate postoperative clinical stability. However, the presence of the cement does not allow reconstitution of the host bone stock. Cortical cancellisation and medullary canal widening caused by a damaged endosteal circulation may be responsible for clinically unstable implants postoperatively. These findings suggest that the optimal reconstruction provide clinical stability without the cement reaching the endosteal surface, thereby enabling revascularisation and subsequent bone remodelling.