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Cover: Beijlen Grafische Communicatie Layout and Printed by Gildeprint - Enschede VoorVoorVoor het het het bijwonen bijwonen bijwonen van van van dedede openbare openbare openbare verdediging verdediging verdediging van van van hethethet proefschrift proefschrift proefschrift CraniofacialCraniofacialCraniofacial and and and Dental Dental Dental AspectsAspectsAspects of of of Crouzon Crouzon Crouzon and and and Apert Apert Apert Voor het bijwonen van SyndromeSyndromeSyndrome de openbare verdediging van het proefschrift doordoordoor JacobusJacobusJacobus Harmen Harmen Harmen Reitsma Reitsma Reitsma JacobusJacobusJacobus Harmen Harmen Harmen Reitsma Reitsma Reitsma Craniofacial and Dental Aspects of Crouzon and Apert Syndrome door Jacobus Harmen Reitsma Jacobus Harmen Reitsma Paranimfen:Paranimfen:Paranimfen: Dr.Dr.Dr. Z. Z. Z.Fourie Fourie Fourie [email protected]@[email protected] Drs.Drs.Drs. A. A. A. Fongers Fongers Fongers [email protected]@[email protected] Paranimfen: Dr. Z. Fourie OpOpOp woensdag woensdag woensdag 19 19 19 maart maart maart om om om 15.30 15.30 15.30 in in in [email protected] dedede Prof. Prof. Prof. Andries Andries Andries Queridozaal Queridozaal Queridozaal Drs. A. Fongers (Onderwijscentrum),(Onderwijscentrum),(Onderwijscentrum), Eg-370, Eg-370, Eg-370, [email protected] ErasmusMC,ErasmusMC,ErasmusMC, Dr Dr Dr Molewaterplein Molewaterplein Molewaterplein 50, 50, 50, 301530153015 CE, CE, CE, te te te Rotterdam. Rotterdam. Rotterdam. Op woensdag 19 maart om 15.30 in Jacobus Harmen Reitsma Jacobus Harmen Reitsma Jacobus Harmen Reitsma NaNaNa afloop afloop afloop van van van de de de p p romotiepromotieromotie is is is er er er de Prof. Andries Queridozaal eeneeneen receptie receptie receptie ter ter ter plaatse plaatse plaatse waarvoor waarvoor waarvoor (Onderwijscentrum), Eg-370, uu uvan van van harte harte harte bent bent bent uitgenodigd. uitgenodigd. uitgenodigd. ErasmusMC, Dr Molewaterplein 50, 3015 CE, te Rotterdam. Jacobus Harmen Reitsma Na afloop van de promotie is er JacobusJacobusJacobus Harmen Harmen Harmen Reitsma Reitsma Reitsma een receptie ter plaatse waarvoor [email protected]@[email protected] u van harte bent uitgenodigd. Jacobus Harmen Reitsma [email protected] Craniofacial and Dental Aspects of Crouzon and Apert Syndrome Jacobus Harmen Reitsma Publication of this thesis was supported by: Stichting ter Bevordering van de Orthodontie Utrecht Dental ABN AMRO Ortho = Solutions 3M Unitek Nederland ISBN: 978-94-6108-622-8 Cover: Beijlen Grafische Communicatie Layout and printed by Gildeprint - Enschede © 2014 by JH Reitsma No parts of this thesis may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, without prior permission of the author, or, when appropriate, of the publishers of the publications. Craniofacial and Dental Aspects of Crouzon and Apert Syndrome Craniofaciale en dentale aspecten van het syndroom van Crouzon en Apert Proefschrift ter verkrijging van de graad van doctor aan de Erasmus Universiteit Rotterdam op gezag van de rector magnificus Prof.dr. H.A.P. Pols en volgens besluit van het College voor Promoties. De openbare verdediging zal plaatsvinden op woensdag 19 maart 2014 om 15.30 uur door Jacobus Harmen Reitsma geboren te Dokkum Promotiecommissie: Promotoren: Prof.dr. E.B. Wolvius Prof.dr. P.F. van der Stelt Overige leden: Prof.dr. G.J. Kleinrensink Prof.dr. E.M.E.H. Lesaffre Prof.dr. I.M.J. Mathijssen Copromotor: Dr. E.M. Ongkosuwito Table of Contents Chapter 1. General Introduction 9 Chapter 2. Facial Growth in Patients With Apert and Crouzon Syndromes 31 Compared to Normal Children Cleft Palate Craniofacial Journal 2012; 49: 185-193. Chapter 3. Mandibular Asymmetry in Patients With the Syndrome of Crouzon 53 and Apert Cleft Palate Craniofacial Journal (submitted). Chapter 4. Dental Maturation in Children With the Syndrome of Crouzon and Apert 73 Cleft Palate Craniofacial Journal 2013; doi:10.1597/13-071. Chapter 5. Patterns of Tooth Agenesis in Patients With the Syndrome of Crouzon 87 or Apert Cleft Palate Craniofacial Journal 2014; 51: 178-183. Chapter 6. A Longitudinal Study of Dental Arch Morphology in Children With the 99 Syndrome of Crouzon or Apert European Journal of Oral Sciences 2013; 121: 319-327. Chapter 7. Craniofacial Stability in Patients With Crouzon or Apert Syndrome After 119 Le Fort III Distraction Osteogenesis Cleft Palate Craniofacial Journal 2013; 50: 561-569. Chapter 8. General Discussion 139 Chapter 9. Summary 155 Chapter 10. Samenvatting 161 Publications 169 Curriculum Vitae 171 PhD Portfolio 173 Acknowledgements 177 This thesis is dedicated to my teachers of life Ynskje Postma-Bijlsma Douwe Postma Chapter 1 General Introduction R1 R2 R3 R4 R5 R6 R7 R8 R9 R10 R11 R12 R13 R14 R15 R16 R17 R18 R19 R20 R21 R22 R23 R24 R25 R26 R27 R28 R29 R30 R31 R32 R33 R34 R35 R36 R37 R38 R39 10 | Chapter 1 1.1 Introduction R1 1 R2 The cranium of an infant or young child consists of different bony plates intersected by sutures. A R3 R4 calvarial suture is a type of fibrous joint in the cranium. The growth of the cranium is effectuated R5 mainly in the sutures. Two important functions of the calvarial sutures are to secure flexibility R6 of the cranium during passage of a baby through the birth canal, and to facilitate growth and R7 separation of the calvarial bones during intrauterine and perinatal life (Posnick and Ruiz, 2000). It R8 is normal that the calvarial bones are separated by the sutures at the time of birth. Until the age R9 of six years the sutures allow bones of the skull to move. After the age of six years skull growth R10 mostly takes place by apposition of bone at the outer side of the skull and resorption of bone R11 tissue on the inner side of the skull (Herring, 2008). R12 Premature fusion of one or more sutures in the skull is defined as craniosynostosis (Virchow, R13 1851; Herring, 2008). The prevalence of craniosynostosis occurs one in 2,000 to 2,500 live R14 births (Cohen and MacLean, 2000). The prevalence of nonsyndromic craniosynostosis at birth is R15 estimated to be three to five per 10,000 births. The prevalence of syndromic synostosis at birth is R16 significantly lower, estimated in the range of 0.15 per 10,000 births (Cohen and MacLean, 2000). R17 When craniosynostosis is part of a syndrome, different syndromes with craniosynostosis R18 R19 show unique phenotypes, but share clinical features (Cohen, 1986; Gorlin et al., 2001). Initially R20 syndromes were classified on the basis of the clinical findings, but now most of the syndromes R21 are defined according to specific genetic mutations (Glass et al., 1994). Frequently children with R22 craniosynostosis have associated anomalies and conditions including adverse effects on sensory, R23 motoric, cardiovascular and respiratory functions (Cohen and Kreiborg, 1993; Turvey et al., 1996; R24 Anderson et al., 1997; Renier et al., 2000; Bhattacharjee et al., 2009). The Apert, Crouzon, R25 Saethre-Chotzen and Muenke syndromes represent the more commonly identified syndromes R26 with craniosynostosis. These familial craniosynostosis syndromes share many common features, R27 including midface hypoplasia, cranial base growth abnormalities, abnormal facies, and limb R28 abnormalities. A short overview is given of the common syndromes. R29 R30 R31 1.2 Common craniosynostosis syndromes R32 R33 R34 The pattern of inheritance in the Crouzon syndrome is autosomal dominant (mainly due to R35 mutations on the fibroblast growth factor receptor 2 (FGFR2), and rarely due to the FGFR1 R36 or FGFR3 gene). The specific gene mutation for the Crouzon syndrome is found in the third R37 extracellular immunoglobulin domain of FGFR2 (Reardon et al., 1994; Wilkie et al., 1995). A R38 R39 General Introduction | 11 R1 mutation of FGFR3 leads to a Crouzon syndrome with acanthosis nigricans, a skin disorder with R2 velvety hyperpigmentated skin. Even more severe manifestations can be seen, such as stenosis R3 of the choanae and malformation of the brain (Arnaud-López et al., 2007). The prevalence of R4 this manifestation is 1 in 25,000 live births (Reardon et al., 1994). The Crouzon syndrome is R5 characterized by premature fusion of calvarial sutures, midface hypoplasia, shallow orbits, and R6 ocular proptosis. The intelligence of patients with Crouzon syndrome is overall significantly better R7 than the intelligence of patients with Apert syndrome, with a mean IQ of 84 to 92 (Da Costa et R8 R9 al., 2006). The Pfeiffer syndrome is an autosomal dominant syndrome (mutations on the FGFR1 R10 or FGFR2 gene) (Muenke et al., 1994; Cornejo-Roldan et al., 1999). Genetically the Pfeiffer and R11 the Crouzon syndrome can often not be distinguished from each other (Rutland et al., 1995). R12 Both syndromes may belong to the same broad spectrum of the same disease (De Jong, 2012). R13 Mutations in FGFR1 usually give a less expressive phenotype than FGFR2 mutations in the Pfeiffer R14 patients. R15 The Apert syndrome is characterized by craniosynostosis, exorbitism, midface hypoplasia R16 and symmetric complex syndactyly of both hands and feet. The reported prevalence is one R17 in 60,000 live births (Cohen and Kreiborg, 1992). Most cases are sporadic, although several R18 cases with autosomal dominant transmission have been reported (mutations on the FGFR2 R19 gene). The specific gene mutations in Apert syndrome are found between the second and third R20 extracellular immunoglobulin domains of FGFR2 (Wilkie et al., 1995). 99% of sporadic cases of R21 Apert syndrome are caused by 1 or 2 common mutations in the FGFR2 gene, S252W or P253R R22 (Glacer et al., 2003). The heredity of Apert syndrome shows an autosomal dominance in most R23 R24 of the cases (Gorlin et al., 2001). The intelligence varies from near normal to mentally retarded R25 with a mean IQ of 62 to 74 (Da Costa et al., 2006). Apert is the most severe type of syndromic R26 craniosynostosis. R27 The Muenke syndrome is an autosomal dominant disorder (P250R mutation on the FGFR3 R28 gene) (Glass et al., 1994).
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