Class III malocclusion in orthodontic patients typically results from midfacial retrognathia. However, the etiology of the midfacial retrognathia remains unclear. The cranial base is considered to play an important role in the emergence of midfacial morphology due to its location within the craniofacial region as well as its dramatic growth activity during the later prenatal and early postnatal periods. Previously, the nasal septum was considered a key cranial base component which functioned to pull the maxilla anteriorly during growth. Although this nasal septal theory of midfacial advancement is generally accepted, certain midfacial abnormalities occur in the presence of normal nasal septal morphology and growth indicating that additional craniofacial regions must contribute to the control of midfacial prognathism. The purpose of this study was to describe a mouse mutant which displays midfacial retrognathia and to delineate regions of cranial base malgrowth. Further, cellular growth mechanisms responsible for causing the abnormal cranial base growth trajectories were identified. Adult 3H1 Brachyrrhine (Br) male mice, displaying midfacial retrognathia with a characteristic Class III malocclusion, were bred to normal C3H females. Litters were examined to determine whether Br offspring could be distinguished from one another between Theiler stages 23 (E15) and 27 (E19) using qualitative and quantitative methods. Results showed that two distinct groups of offspring were derived: one with midfacial retrognathia and the other without. The cranial base of Br mutants displayed a malformed sphenoidal region while the nasal septum appeared much less affected as revealed by finite element morphometric analysis. In vivo autoradiographic analysis demonstrated the existence of temporal growth sites (TGS). TGS in the sphenoidal regions were deficient in the prenatal Br mouse. Using immunohistochemistry, insulin growth factor (IGF-I) and epidermal growth factor (EGF) as well as their receptors (IGF-IR and EGF-R) were found to be expressed in cranial base chondrocytes. In order to determine whether chondrocytic responses to these growth factors were deficient in the mutant, cell cultures were established, treated with IGF-I or EGF, and cellular proliferation and differentiation were measured using (<sup>3</sup>H) -thymidine and (<sup>35</sup>S) -sulfate incorporation. Results from this analysis showed that chondrocytes from the Br posterior cranial base were less responsive to EGF compared to cells from normal posterior cranial bases. Data from this study suggest that the Br mouse displays midfacial retrognathia in a heritable fashion. Deficient growth of the Br sphenoid, particularly in the presphenoidal and sphenoethmoid region, is crucial for the establishment of midfacial retrognathia. In the Br mouse, the sphenoidal deficiency is associated with depressed proliferation in TGS. IGF-I and EGF, as well as their receptors, are expressed within the murine cranial base and the depressed level of cellular proliferation in the Br sphenoidal region results, at least in part, from a diminished response to EGF. Based on this study, I propose a "sphenoidal mechanism of midfacial advancement" whereby the sphenoid actively propels the midface forward in order to achieve proper maxillary prognathism during later prenatal and early postnatal period.
| Identifer | oai:union.ndltd.org:USASK/oai:usask.ca:etd-10212004-000813 |
| Date | 01 January 1996 |
| Creators | Ma, Wenbin |
| Contributors | Lozanoff, Scott |
| Publisher | University of Saskatchewan |
| Source Sets | University of Saskatchewan Library |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://library.usask.ca/theses/available/etd-10212004-000813 |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Saskatchewan or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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