From the facts presented, it would seem logical to conclude that the etiology of congenital dislocation of the hip is a developmental fault of the hip system produced by extrinsic factors—growth circumstances—with a combination of hereditary and environmental faults which alter the normal growth potential or the intrinsic mosaic pattern. Congenital dislocation and congenital dysplasia are developmental deformities produced by secondary adaptive changes. Inherited characteristics and environmental factors may alter the intrinsic mosaic pattern by a faulty timing in development. Patten states that "local overgrowth may be responsible for certain anomalies, just as local arrests may be responsible for others. . .".

Our concept of congenital dysplasia of the hip and congenital dislocation is that, through a developmental fault, the acetabulum has failed to deepen and the head and neck of the femur have become anteverted. The anteversion tends to turn the head forward, displacing the cartilaginous sphere laterally, so that the glenoidal labrum and acetabulum cover less of the head than usual. The poor adaptation of the head and acetabulum continues dynamically to require altered growth changes, altering the intrinsic mosaic pattern. These growth changes are manifested in subluxation or acetabular dysplasia by pushing upward of the glenoidal labrum, widening of the socket, and enlargement of the head (Fig. 8). If the head escapes completely past the edge of the glenoidal labrum, a true dislocation results. The glenoidal labrum, unobstructed, returns by its elasticity to its proper position, lying between the head and the acetabulum. The head of the dislocated hip no longer has the stimulus for overgrowth seen in the subluxation, so that it remains small and round, although becoming flattened on the side if in contact with the ilium.

This mechanism is in complete accord with the pathological findings in early postnatal hip dysplasias, demonstrated by arthrograms and by operative findings. It is to be remembered that anteversion occurs below the trochanter's and actually is associated with torsion of the femoral shaft.

It would seem a logical hypothesis that the rotation of the limb buds may be an important factor in the abnormal development. Presumably there must be an adaptive alteration in the change of position, from the origin of the hip joint in the first few weeks of embryonic life to the 90 degrees of rotation and adduction of the hip in the second four weeks of life. Interference with the orderly timing of this rotation—the embryo being held in a position overlong for even a short time—could produce a failure, mild or severe, in the intrinsic mosaic design. The altered environment could produce the adaptive features which are seen in all the structures of the hip joint, and not a primary change in the acetabulum alone.

These studies lead to the following hypothesis : Congenital dislocation and congenital dysplasia of the hip may be regarded as the result of faulty development, due to environmental factors extrinsic to the hip joint. An inherited fault in the timing of development may produce these extrinsic changes. The loss of the normal dynamic reciprocal relationship of the component parts of the hip joint during the stage of rotational adjustment of the limb buds may produce the secondary adaptive changes which lead to acetabular dysplasia or congenital dislocation. Heredity can play an important part in altering the growth and time factors. The known embryological development of the hip joint is certainly opposed to the theory of a primary inherited failure of development of a portion of the acetabulum.