There are differences of opinion about the pathogenesis of Perthes' disease. All are agreed that it is due to ischaemia, but the cause of this and the size and number of infarctions are in dispute. Through the generosity of the contributors six whole femoral heads and core biopsies of five other cases have been studied radiographically and histologically. The findings ranged from an ischaemic arrest of ossification in the capital articular cartilage without infarction to multiple complete infarctions of the epiphysial bone. The ensuing reparative process contributes to the pathology, which is of a range to warrant grading or grouping.
Periosteal grafting was performed in 4 patients with osteochondritis dissecans of the medial femoral condyle and 1 patient with osteonecrosis of the lateral femoral condyle following prednisone therapy. The lesions were drilled out deep into the cancellous bone. The periosteal graft was taken from the medial facet of the tibia and fixed to the excavated bony defect by the tissue glue Fibrinkleber Human Immuno (Tisseel). The patients were followed clinically, by arthroscopic examination and by radiography at 3, 6, and 12 months. After 1 year the borderline between the new and surrounding cartilage was hardly visible.
Specimens of femoral heads were studied at necropsy in two cases of Legg-Calve-Perthes' disease. One was that of a boy aged four years ten months who died from appendicitis; the other was from a boy aged six years who died from a malignant glioma. Both had been treated for one and a half years for Legg-Calve-Perthes' disease which was in a stage of repair at the time of death. The diseased femoral heads were moderately flattened but the surface cartilage was intact. Epiphysial bone and bone marrow were partly replaced by cartilage, fibrous tissue and granulation tissue, and new bone was being formed. Inflammatory reaction was inconspicuous. Enchondral bone formation was only slightly decreased, and the structure of the growth plate was undisturbed. There was no sign of systemic bone disease. In the first case the changes indicated that more than one episode of ischaemia had occurred, and an occlusion--probably from an old thrombus--was demonstrated in the posterior inferior retinacular artery of the femoral head. The last episode of ischaemia, furthermore, had caused infarction of part of the metaphysial bone. In both cases, the central area of the metaphysial bone of the affected femur contained fat, but there were few haemopoietic cells and it therefore looked pale. The findings are discussed in relation to previous work on the pathology in Legg-Calve-Perthes' disease, recent information on the vascularisation of the femoral head in children, and experimental and comparative animal studies.
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