We have shown that stress fractures can be induced in the tibial diaphysis of an animal model by the repeated application of non-traumatic impulsive loads. The right hind limbs of 31 rabbits were loaded for three to nine weeks and changes in the bone were monitored by radiography and bone scintigraphy. The presence of stress fractures was confirmed histologically in some cases. Most animals sustained a stress fracture within six weeks and there was a positive correspondence between scintigraphic change and radiological evidence. Microscopic damage was evident at the sites of positive bone scans. The progression, location, and time of onset of stress fractures in this animal model were similar to those in clinical reports, making the model a useful one for the study of the aetiology of stress fractures.

The articular cartilage of the patella was studied in 100 knees at necropsy. In twenty-one of these knees the cartilage changes were related to the trabecular architecture of the underlying bone. It would appear that the initiation and location of cartilage damage and its rate and degree of progression are related to the relative stiffness of the underlying cancellous bone. On the basis of our observations we suggest that the diagnosis "chondromalacia of the patella" should be reserved for patients with asymptomatic or transiently symptomatic fibrillation of the articular cartilage of the central medial patellar facet. Those patients with persistent patellofemoral pain should be considered to have some other syndrome.