Date of Last Revision

2023-05-02 14:32:19

Major

Biology

Degree Name

Bachelor of Science

Date of Expected Graduation

Summer 2015

Abstract

Craniosynostosis is a condition in which one or more of the sutures of the skull grow together (fuse) earlier than normal in infants. Sutures are large gaps located at the bony plates or joints of the head. Craniosynostosis causes the skull to expand and grow in the direction of any normal open suture, creating craniofacial complications, such as drooping eyelids and abnormal intracranial pressure, head shape, or brain morphology. This premature fusion or ossification of sutures affects approximately 300-500 live births in 1,000,000 (Kolpakova-Hart et al., 2008) with considerable variation in phenotype, depending on which suture(s) is involved. Corrective surgery can be performed to reshape the skull and eliminate the symptom(s) present in the infant. There is no known cause of craniosynostosis or direct pattern of heritability from parent to affected infant and the condition can appear syndromically (associated with syndrome or condition) or non-syndromically. However, the majority of cases reported are sporadic, non-syndromic cases, in which pediatric patients suffer from premature fusion of only one suture (Levi et al., 2012). In the current prospective study, histological and/or immunohistochemical analyses have been conducted on sagittal synostoses as well as patent (normal open suture) tissue from the skulls of three pediatric patients. Patient surgeries were performed at Akron Children’s Hospital. The studies were begun to understand more completely the underlying etiology and possible risk factors of non-syndromic craniosynostosis. Histological staining, including toluidine blue, hematoxylin and eosin, and picrosirius red counterstained with alcian blue, has been performed for qualitatively describing tissue and cell architectural shapes and gross morphology. Immunohistochemical analysis has also been performed to study the presence of osterix, a transcription factor essential for osteoblast differentiation and bone formation. Analytical results of this work are ongoing.

Research Sponsor

Dr. William J. Landis and Dr. Jim Holda

First Reader

Sara Carlson

Second Reader

Donald Ott

Comments

Acknowledgments

The authors are thankful for the assistance in technical help given by Mr. Joshua Bundy (Department of Polymer Science, University of Akron) and by Dr. Hitomi Nakao (Department of Plastic and Reconstructive Surgery, Kinki University School of Medicine, Osaka, Japan). The authors also thank the Akron Children’s Hospital for the collection of surgical samples and the donors and their parents for providing the tissues for investigation.

Share

COinS
 
 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.