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

Osteonecrosis of the femoral head frequently leads to collapse of the articular cartilage and to disabling osteoarthritis, which ultimately may necessitate joint arthroplasty. One treatment method that has had moderate success is the so-called trapdoor approach, which involves excavation of diseased (necrotic) bone followed by bone-grafting. Augmentation of this procedure with various growth and differentiation factors may improve the outcome. We developed a canine model that mimics the clinical situation with trapdoor bone-grafting. The objective of this study was to evaluate the effect of the addition of osteogenic protein-1 on healing following the trapdoor procedure with strut-autografting.

Thirty-four skeletally mature dogs were used in the experiment. After 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, the procedure was modified by collapsing the trapdoor into the created defect intraoperatively in eighteen dogs, which were divided into three equal groups: six untreated defects were left collapsed (Group III), six were treated with bone graft (Group IV), and six were treated with bone graft augmented with osteogenic protein-1 (Group V).

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 trapdoor) had evidence of cartilage collapse. Inspection of sagittal slices and radiographs revealed an unfilled residual defect in all Group-I heads, whereas all Group-II heads were well healed. The mean normalized stiffness value was significantly larger in Group II than it was in Group I. On visual inspection, depression was noted in all of the femoral heads in Group III (untreated defect; trapdoor left collapsed). In both Group IV and Group V (grafting without and with osteogenic protein-1), the trapdoor cartilage appeared to be essentially normal. Groups IV and V had more radiographic healing than did Group III. The defects in Group V (grafting with osteogenic protein-1) healed faster radiographically than did those in Group IV (grafting without osteogenic protein-1).

Moderate-to-excellent healing was seen both radiographically and biomechanically by four months in the groups treated with grafting, with and without osteogenic protein-1, whereas untreated defects did not heal.

Symptomatic osteonecrosis of the femoral head is a clinical challenge. The animal model in the current study is a useful tool for the evaluation of methods to treat osteonecrosis of the femoral head. Studies investigating additional time-periods between implantation of osteogenic protein-1 and assessment of results as well as different doses of osteogenic protein-1 are warranted.