A Histological Study of Avascular Necrosis of the Femoral Head After Transcervical Fracture

Loss of osteocytes in the bone trabeculae of the femoral heads of "normal" elderly patients was patchy and distinguishable from that resulting from avascular necrosis after fracture. 2. Changes in the haemopoietic marrow were the earliest and most sensitive indicators of ischaemia, loss of osteocytes rarely being complete until three or four weeks after fracture. 3. In 109 femoral heads removed more than sixteen days after fracture the viability could be determined by histological means. All of these had suffered some damage to the vascular supply but in a number the head remained alive apart from the region of the fracture line. These heads were nourished by the blood vessels of the ligamentum teres and sometimes by retinacular arteries, usually of the inferior group. 4. Some femoral heads became completely necrotic following fracture, others were only partly affected. A variable amount of the subfoveal region commonly remained alive and it was from this site that revascularisation spread into the head. The upper segment of the femoral head least often remained alive and its subchondral region was usually the last to revascularise. 5. In a group of unselected femoral heads a third remained alive following fracture and two-thirds were partly or completely necrotic. 6. Femoral heads which were partly necrotic appeared capable of uniting and completely revascularising, there being invasion of the necrotic bone by vessels from across the fracture line and from the ligamentum teres. This contrasted with the completely necrotic femoral heads described elsewhere in this issue which united but in the absence of proliferation of ligamenturn teres vessels failed to revascularise completely and developed late segmental collapse. 7. Avascular necrosis did not appear to be the sole cause of non-union. 8. Necrotic bone showed no alteration in radiological density. Reossifying bone in areas of revascularisation sometimes caused an absolute increase of radiodensity especially when associated with halted revascularisation. This increase of radiological opacity was the result of deposition of new on dead bone with broadening of the trabeculae. Marrow calcification was minimal. 9. Obliterative sclerosis of venules in the ligamentum teres was found in "normal" patients even in infancy. No thrombosis was seen in the ligaments following fracture but where the femoral heads were completely necrotic and not revascularised the ligaments were often also necrotic. 10. There appeared to be no increase in degenerative changes in the articular cartilage of the femoral heads following fracture compared with fifty elderly controls. Some loss of chondrocytes in the deep zone of the weight-bearing area was found in about a quarter of the femoral heads. In only one head was the cartilage almost completely acellular. An almost normal depth and a smooth contour of the articular cartilage were retained.