Craniosynostosis, the premature fusion of one or more cranial sutures, is a common developmental disorder resulting in morphologic and functional consequences. The rat model is useful for studying pathologic and normal suture fusion because the posterior frontal suture undergoes fusion but the remaining sutures remain patent. The authors investigated the influence of regional posterior frontal dura mater on the overlying suture morphology and fate.
In 8-day-old Sprague-Dawley rats, an 8-mm calvarial disk was excised without disrupting the underlying dura mater (n = 22) and flipped so that the previously ectocranial aspect was adjacent to the dura mater. The animals were humanely killed after 5, 7, 9, 11, and 28 days, and the posterior frontal sutures were analyzed histologically. A comparison was made to control animals in which the disk was excised and then placed back into its anatomical position (n = 5). Immunohistochemistry of the transforming growth factor (TGF)-β isoforms was performed to investigate their differential, temporal, and spatial expression.
Posterior frontal suture fusion occurred on the side adjacent to the dura mater (previously patent ectocranial aspect) in an anterior-to-posterior direction, similar to that in the control group. There was specific expression of the TGF-β isoforms in the dura mater and suture mesenchyme adjacent to the dura mater.
Regional dura mater plays an important role in suture morphology, and the posterior frontal–associated dura mater possesses potent, pro-osteogenic signals that influence the overlying suture fate. The differential expression pattern of TGF-β signaling from the dura mater further supports the regional paracrine effect of the dura mater.
From the Hagey Laboratory for Pediatric Regenerative Medicine, Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University School of Medicine.
Received for publication June 12, 2008; accepted August 25, 2008.
Presented at the 53rd Annual Meeting of the Plastic Surgery Research Council, in Springfield, Illinois, May 28 through 31, 2008.
Disclosure: None of the authors has any financial or commercial association disclosures.
Michael T. Longaker, M.D., M.B.A., Stanford University School of Medicine, 257 Campus Drive, Stanford, Calif. 94305-5148, firstname.lastname@example.org