(1) Roentgenographic metaphyseal cupping residual to trauma to the legs of 5 children is described for the first time. (2) The roentgenographic complex called metaphyseal cupping is made up of the following concurrent elements: shaftward depression of the metaphyses; spreading and shortening of the shaft; hypertrophy of the EOC, thinning of the cartilage plate and in some cases premature fusion with the metaphyses; and deepening of the contiguous joint space. Also, when the femoral EOC is affected, its intercondylar notch is deepened. (3) Our experience and the reports in the literature indicate that the bones at the knees are most frequently affected. Metaphyseal cupping at the knee has been associated with remote lesions at the ipsilateral hip such as tuberculosis, pyarthrosis, slipped capital femoral epiphysis and congenital dislocation, as well as purulent osteomyelitis of the femoral shaft. Residual metaphyseal cuppings at the knees and in the metatarsals have followed poliomyelitic paralysis of the muscles in the legs and feet. Some of the most severe examples of metaphyseal cupping, all at the knees, have developed during and following poisoning by vitamin A. Prolonged regional immobilization of the affected parts, due to pseudoparalysis of pain, to postpoliomyelitic paralysis and to therapeutic restraints, is a feature common to all affected patients. In sickle cell anemia, cupping of the cartilage plates of the vertebral bodies and the metaphyses of the metacarpals was not associated with prolonged immobilization. (4) Local oligemia from thrombosis secondary to stagnation of blood and slowed blood flow in the terminal epiphyseal arteries to the epiphyseal plate, induced by prolonged regional immobilization, appears to be the most likely and most frequent cause of metaphyseal cupping. In sickle cell anemia, similar oligemia is probably due to direct primary thrombosis of the sickled cells in the terminal epiphyseal arterioles. (5) The metaphyseal cupping in achondroplasia is so similar roentgenographically to the metaphyseal cupping secondary to trauma and the several other disorders mentioned above that it seems reasonable to conclude that achondroplasia is primarily due to chronic congenital oligemia induced by congenital hypoplasia of the epiphyseal arteries. All of the other dysplasias characterized by retarded cartilaginous growth chondroectodermal dysplasia, peripheral dysostosis and metaphyseal dystosis, etc., may have a similar primary causal mechanism. Osteopetrosis, on the other hand, can reasonably be explained on the basis of congenital oligemia of the metaphysis due to congenital hypoplasia of the terminal branches of the metaphyseal and perforating arteries. The primary causal mechanism of the longitudinal cartilaginous overgrowth in Marfan's syndrome could well be intrinsic hyperplasia of the epiphyseal arterioles and consequent chronic hyperemia in the epiphyseal side of the cartilage plate.