The long bones in eleven newborn infants who had neuromuscular disease
were studied and were found to be thin, hypomineralized, and elongated. In
most of the bones, there were multiple diaphyseal or metaphyseal fractures,
or both. By light microscopy, the outstanding findings were fractures
through the growth plate and diaphysis and thinning of the cortices. The
etiology of the fractures and the insufficient substance of the bone is the
reduction in the intrauterine motion of the fetus, which leads to fragility
of the bones and contractures of the joints. The severity of the
alterations may have been related to the time of the onset of the
abnormalities and to the duration and degree of the intrauterine
akinesia.