Etiologic Factors in Congenital Displacement of the Hip and Myelodysplasia

Abstract

The two prime factors in the mechanism of intrauterine displacement of the hip are mesenchymal tissue abnormalities and mechanical stress placed on the fetal hip joint by the leg-folding mechanism. The somatic changes involve general laxity of the articular ligaments, attributable to either the physiologic effects of progesterone or a genetic trait consisting of familial joint laxity. The ligamentous laxity not only interferes with the folding mechanism of the fetal legs but also influences the torsional effect on the hip joints. This facilitates the displacement of the femoral head over the posterior rim of the acetabulum. The mechanical stress caused by the delay in leg folding also appears to play a role in a genetically determined occult form of myelodysplasia. Its prevalence has already been partially revealed by sensory evoked potential tests. Possibly, a more refined motor evoked potential test might help to explain a large percentage of the idiopathic cases. Thus, many of the etiologic factors in congenital hip displacement, previously considered to be caused by pre- and postnatal environmental influences, may well have genetic origins. These origins may be associated with varying degrees of underlying myelodysplasia. The relatively high incidence of firstborn affected, the ratio of female to male patients, the seasonal incidence of birth, and familial and racial prevalence may prove to be genetically predetermined.