THE EFFECTS OF POSTNATAL HYPERTHYROIDISM ON CORONAL SUTURE COMPLEXITY IN RABBITS WITH FAMILIAL, DELAYED-ONSET CRANIOSYNOSTOSIS

Craniosynostosis results in abnormal biomechanical forces transmitted across the developing sutures and can be seen as increased interdigitation (sutural complexity). The present study was designed to examine a gene - environmental interaction by testing the hypothesis that postnatal thyroid hormone administered to rabbits with delayed-onset coronal suture synostosis (DOS) would result in an accelerated suture fusion and an increased sutural complexity compared to wild-type and in-colony normal rabbits. 138 coronal sutures were obtained from 69 rabbits, 13 wild type controls; 25 in-colony “phenotypically” normal rabbits, and; 31 rabbits with DOS. The three phenotypes were each divided into 3 treatment groups: untreated controls; vehicle controls, and; rabbits who received a 14 day course of treatment with 0.2 mg/kg of Triiodo thyronine (T3) (Sigma) in saline from 25 to 39 days of age. Longitudinal body weight and blood serum levels of T3 were taken and sutures were extirpated at 42 days of age. Suture images were captured digitally, sutural interdigitation was traced and measured using Image J, and a suture complexity index ((length/interdigitation length) x100) was calculated. Mean values were analyzed using a 3x3 (phenotype x treatment) ANOVA. Rabbits treated with T3 showed significantly (p<0.01) decreased body weight and increased (p<0.01) T3 blood serum levels by 42 days of age. DOS rabbits showed significantly more suture complexity in all three treatment groups compared to controls (F Group= 3.15; p<0.05). Only wild-type rabbits with T3 treatment showed more complexity compared to their own phenotypic controls, however, no treatment or treatment by group effects were noted (F Treatment = 0.415;NS; F Group x Treatment = 1.93;NS). Postnatal T3 exposure resulted in increased suture complexity only in wild-type control rabbits compared to rabbits with familial craniosynstosis. Results suggest that there was no statistically significant gene - environmental interaction between elevated postnatal T3 levels and craniosynostosis in this model