Abstract
Proximal femoral bone loss is often observed after total hip arthroplasty (THA) and continues to complicate revisions. The purpose of this study was to evaluate the clinical and radiographic outcomes of patients with the unusual finding of proximal femoral cortical hypertrophy after THA or endoprosthesis.
Three patients were identified with femoral stem tip perforation through the posterolateral femoral shaft cortex. Known risk factors for perforation were osteoporosis, distal osteolysis causing late stem migration, and endoprosthesis after previous fracture/internal fixation. Two patients had dual energy x-ray absorptiometry (DXA) of both hips. Follow-up was 16, 17 and 28 years.
All three patients had clinically stable femoral components and none had thigh loading pain. All three patients had dense cortical bone buttressing the undersuface of the implant collar and a dense medial femoral cortex. Proximal femoral DXA regions of interest were 120 and 145% of the contralateral femur in the migration and post-fracture endoprosthesis patients, respectively.
The endoprosthesis patient was revised to a THA 28 years post-operatively due to acetabular erosion. Excess dense cortical bone in the proximal femur was removed with a high speed bur and enabled revision with a primary non-cemented femoral component.
Common factors which appeared to be necessary for a stable implant with proximal femoral densification included collared femoral components, stem alignment more vertical than the femoral neck axis, stem perforating the posterolateral femoral cortex, no inhibition of translation along the stem axis by cement or biological ingrowth, and not having the implant revised despite its unorthodox appearance.
Long-term maintenance of the proximal femoral cortex after THA or endoprosthesis is possible. Paradoxically, a rare subset of the complication of femoral shaft perforation demonstrated by these anomalous cases suggested an alternative approach to the prevention of stress shielding bone loss after THA.
The abstracts were prepared by Nico Verdoschot. Correspondence should be addressed to him at Orthopaedic Research Laboratory, Universitair Medisch Centrum, Orthopaedie / CSS1, Huispost 800, Postbus 9101, 6500 HB Nijmegen, Th. Craanenlaan 7, 6525 GH Nijmegen, The Netherlands.
