Pathogenesis of hip dysplasia Hip dysplasia is multifactorial in origin influenced by genetic and intrauterine factors, such as mechanical (rump presentation and oligohydramnios) and hormonal factors1. To ease the passage through the birth canal, the hip joint is quite mobile perinatally. Postnatally, the laxity of the ligaments will subside and the femoral head will normally position itself deeply in the acetabulum2. The theory is that if the femoral head does not migrate sufficiently into the acetabulum, dysplasia may develop because the matrice to stimulate acetabular growth is not correctly positioned. Normally, at birth the femoral head sits deep in the acetabulum held by surface tension of the synovial liquid. The growth and the hemispherical morphology of acetabulum are dependent on the presence of a normally growing and correctly placed spherical femoral head that works as a convex matrice. If for some reason the normal development is disturbed pre- or postnatally, pathologic relations may develop between the femoral head and the acetabulum3, leading to hip dysplasia.