Strut-autografting with and without osteogenic protein-1 - A preliminary study of a canine femoral head defect model

Background: Osteonecrosis of the femoral head frequently leads to collapse of the articular cartilage and to disabling osteoarthritis, which ultimatel y may necessitate joint arthroplasty. One treatment method that has had mod erate success is the so-called trapdoor approach, which involves excavation of diseased (necrotic) bone followed by bone-grafting. Augmentation of thi s procedure with various growth and differentiation factors may improve the outcome. We developed a canine model that mimics the clinical situation wi th trapdoor bone-grafting. The objective of this study was to evaluate the effect of the addition of osteogenic protein-1 on healing following the tra pdoor procedure with strut-autografting. Methods: Thirty-four skeletally mature dogs were used in the experiment. Af ter capsulotomy, a trapdoor was created in the anterolateral surface of the femoral head and a 2-cm-diameter subchondral area of bone was removed. In the phase-I experiments, seven dogs had no treatment of the defect (Group I ) and nine dogs were treated with strut-grafting (Group II). In phase II, t he procedure was modified by collapsing the trapdoor into the created defec t intraoperatively in eighteen dogs, which were divided into three equal gr oups: six untreated defects were left collapsed (Group III), six were treat ed with bone graft (Group IV), and six were treated with bone graft augment ed with osteogenic protein-1 (Group V). Results: Three of the seven femoral heads in Group I (untreated defect) and one of the nine heads in Group II (grafting without collapsing of the trap door) had evidence of cartilage collapse. Inspection of sagittal slices and radiographs revealed an unfilled residual defect in all Group-I heads, whe reas all Group-ii heads were well healed. The mean normalized stiffness val ue was significantly larger in Group II than it was in Group I. On visual i nspection, depression was noted in all of the femoral heads in Group ill (u ntreated defect; trapdoor left collapsed). In both Group IV and Group V (gr afting without and with osteogenic protein-1), the trapdoor cartilage appea red to be essentially normal. Groups IV and V had more radiographic healing than did Group Ill. The defects in Group V (grafting with osteogenic prote in-1) healed faster radiographically than did those in Group IV (grafting w ithout osteogenic protein-1). Conclusions: Moderate-to-excellent healing was seen both radiographically a nd biomechanically by four months in the groups treated with grafting, with and without osteogenic protein-1, whereas untreated defects did not heal. Clinical Relevance: Symptomatic osteonecrosis of the femoral head is a clin ical challenge. The animal model in the current study is a useful tool for the evaluation of methods to treat osteonecrosis of the femoral head. Studi es investigating additional time-periods between implantation of osteogenic protein-1 and assessment of results as well as different doses of osteogen ic protein-1 are warranted.