Ischaemia resulting from increased joint pressure may play a role in the pathogenesis of necrosis of the femoral head epiphysis. We studied the effect of temporary vascular occlusion on this epiphysis in young rabbits. Occlusion for six hours resulted in necrosis of trabecular bone and of intertrabecular marrow and vascular tissue, later followed by revascularisation and repair, as has been demonstrated previously. In contrast, raised intra-articular pressure lasting for only two hours resulted in a more complex picture: trabecular osteocytes were dead, whereas the bone-forming marrow was shown by fluorochrome labelling to remain viable, and to form appositional repair bone throughout the epiphysis. We concluded that transient vascular occlusion may cause the death of trabeculae despite intact perfusion of the bone. This type of change may be important in the pathogenesis of Perthes' disease.