As steroid-induced osteonecrosis of the femoral condyle is a relatively rare disease, literature regarding its treatment and histology is sparse [1, 2], and there are no prospective randomized trials comparing treatment options. Thus, especially in young patients, surgeons often have difficulties in selecting an appropriate treatment. Several reports have described surgical procedures for the treatment of steroid-induced osteonecrosis of the femoral condyle [7–10]. However, there are no clear indications established for these surgical methods or for conservative treatment. As for the primary spontaneous osteonecrosis of the knee (SONK), P.J. Yates et al. reported that middle aged patients presenting with primary SONK not visible on plain radiographs, can expect a relatively rapid and complete recovery with a simple non-operative treatment . Lotke et al. described that conservative treatment will do well if the size of the lesion is small (less than 45% of the condylar width, or less than 3.5 square centimeters), however, thereafter degenerative changes will develop in almost all patients. However there are few literatures described of clinical course and prognosis of steroid-induced osteonecrosis of the femoral condyle. Prosthetic replacement remains the most predictable modality for treating the advanced disease, however as compared to osteoarthritis, the complication rate may be higher and the ultimate success rate slightly lower [3, 13]. In addition, for young patients such as our patients, this option may be considered an over indication and is not the ideal from the view point of articular cartilage regeneration and restoration. There are other choices of treatment in clinical use such as debridement , abrasion chondroplasty, subchondral drilling , and microfracture . These methods are based on the perforation of the underlying subchondral bone and enable the migration of pluripotent mesenchymal stem cells from the bone marrow into the defect zone. Wiedel et al. reported his experience with arthroscopic evaluation and treatment of ten knees with steroid-induced osteonecrosis of the knee . He suggested that arthroscopic debridement provides reasonable symptomatic relief, allowing the patients to return to activities of daily living. However these methods have led to the formation of fibrocartilagious scar tissue with structural and biomechanical properties that are inferior to those of hyaline cartilage [16, 18, 19]. To this end, osteochondral allo/autografting has recently received much attention as an alternative approach for repairing joint surfaces. Osteochondral allografting is one of the available techniques for transplantation of osteochondral bone, however it has the potential risks of disease transmission or immune graft rejection [20–23]. Therefore, in three cases presented here, we indicated the osteochondral autografting for the young patients with steroid-induced osteonecrosis of the femoral condyle who were resistant to conservative treatments including restricted weight-bearing with crutches, nonsteroidal anti-inflammatory drugs, and intra-articular injection of hyaluronic acid.
Recently, use of an autogenous osteochondral graft has gained in clinical popularity because of its technical feasibility and cost effectiveness. Animal and clinical studies have shown that osteochondral plugs maintain hyaline cartilage coverage over the subchondral bone . However, there are few studies regarding autogenous osteochondral graft transplantation for steroid-induced osteonecrosis of the femoral condyle. Here we reported three cases of steroid-induced osteonecrosis of the femoral condyle treated successfully with autogenous osteochondral graft transplantation. Nakagawa et al. also previously reported a case of steroid-induced osteonecrosis of the femoral condyle measuring 10 cm2 treated by osteochondral graft transplantation with a satisfactory result . In contrast, Ching-Jen Wang et al. reported a poor result in one patient with a 6 cm2 defect undergoing osteochondral autograft for steroid-induced osteonecrosis of the femoral condyle . In our cases, the average defect size was 2.83 cm2 (range 1.5 to 5.0 cm2) and all patients received satisfactory results. One of the factors for the success of autogenous osteochondral mosaicplasty is the size of osteochondral articular cartilage defect. Hangody et al. reported that the defect size between 1 and 4 cm2 is the promising factor for the success of the procedure. Lane et al. suggested that because of the difficulty of matching the topography of recipient and donor joint surfaces, the amount of tissue that can be successfully transferred in most surgeons’ hands is limited to less than 2 cm2. Since autogenous osteochondral graft transplantation is a surgical procedure with free bone graft transplantation, the engraftment of the transplanted graft is an important issue, however no detailed analysis of this issue has been reported in cases of surgically treated steroid-induced osteonecrosis of the femoral condyle. Our study has shown that the transplanted grafts remained viable up to two years after surgeries based on MRIs examination and arthroscopic evaluation. However, the lesion in case 2 was partially associated with fibrous tissue formation according to a second-look arthroscopic evaluation despite a good clinical outcome. In this patient we were unable to completely perform osteochondral autograft transplantation and only performed microfracture at the deep posterior part of the lesion because of the location of the lesion. In case 3, similarly, the posterior aspect of the lesion was difficult to reach for grafting even with the knee fully flexed. A previous study suggested that osteochondral graft stability plays an important role in preserving the histologic properties of the cartilage . As a result, in our cases, appropriate press-fit techniques to the peripheral lesion may have led to the reconstruction of smooth articular cartilage despite fibrous tissue coverage at the non-grafting site. However, our cases need to be followed for a longer period since our follow-up period is not long enough for the evaluation of the graft integrity, especially under steroid induced pathology.