Abstract
The side distribution of single spinal curves in our school screening referrals for 1988–99 (n=218) suggests that the mechanism(s) determining curve laterality for the upper spine differs from those for the lower spine. We address here the laterality of right thoracic AIS. In the search to understand the aetiology of AIS some workers focus on mechanisms initiated in embryonic life including a disturbance of bilateral symmetry. The normal external bilateral symmetry of the body, highly conserved in vertebrates, results from a default process involving mesodermal somites. The normal internal asymmetry of the heart, major blood vessels, lungs and gut with its glands is also highly conserved among vertebrates. There is recent evidence that vertebrates retain an archaic asymmetric visceral organization in thoracic and abdominal organs (Cooke). In early embryonic life the visceral asymmetry develops from the breaking of the initial bilateral symmetry by a binary asymmetry switch producing asymmetric gene expression around the embryonic node and/or in the lateral plate mesoderm. In the mouse this switch occurs during gastrulation by cilia driving a leftward flow of fluid and morphogen(s) at the embryonic node (nodal flow) favouring precursors of heart, great vessels and viscera on the left. Based on the non-random laterality of thoracic AIS curves, we suggest that the binary asymmetry switch – through genetic/environmental factors extending to involve anomalously left-sided mesodermal precursors of vertebrae, ribs and/or muscles (positively or negatively), explains the distribution of right/left thoracic AIS. Some support for this hypothesis is the prevalence of scoliosis curve laterality associated with situs inversus.
Correspondence should be addressed to: Dr Caroline Goldberg, The Research Centre, Our Lady’s Children’s Hospital Crumlin, Dublin 12, Ireland.
