Introduction to Crouzon Syndrome

What is/are Crouzon Syndrome?

Crouzon Syndrome - Demarcations of pathological regions in Cri du chat, Velo-cardio-Facial syndrome and Crouzon syndrome were mapped. ^[1] OBJECTIVE Crouzon syndrome with acanthosis nigricans (CAN) is a rare and clinically complex subtype of Crouzon syndrome. ^[2] In the current report, we present the first case in the literature of an internal distraction associated zygomatic-maxillary fracture in a patient with Crouzon syndrome. ^[3] Crouzon syndrome is an autosomal dominant type of craniosynostosis, first reported by French neurologist Octave Crouzon in 1912. ^[4] The compression ratio at the level of the odontoid process was comparable with that in controls; the compression ratio at the level of the foramen magnum was significantly higher in patients with Crouzon syndrome (+27. ^[5] Hereditary spherocytosis (HS) and craniosynostosis syndromes such as Crouzon syndrome or Pfeiffer syndrome are rare genetic disorders that do not commonly have overlapping symptoms or etiologies. ^[6] BACKGROUND The goal of this study is to analyze the safety of reconstructive surgeries for Crouzon syndrome, and to understand the deformities and complications related to the surgical procedure. ^[7] The aim of this study was to report on a single center's experience with spring-assisted cranial vault expansion (SAE) in patients with Crouzon syndrome and sagittal suture synostosis. ^[8] With the increasing possibilities of surgical treatment addressing the complex spectrum of defects in Crouzon syndrome (CS), it is of utmost importance to obtain accurate assessment of the malformation. ^[9] Background: Obstructive sleep apnea is common in patients with Crouzon syndrome, yet it may be caused by multiple factors. ^[10] Eight children were diagnosed with Apert Syndrome, two with Saethre Chotzen syndrome, one with Crouzon syndrome, and one with Greig cephalopolysyndactyly syndrome. ^[11] Method A total of 133 preoperative CT scans (nonsyndromic bicoronal synostosis, n=38; Apert syndrome bicoronal synostosis subtype, n=33; Crouzon syndrome bicoronal synostosis subtype, n=10; controls, n=52) were included. ^[12] Summary Purpose This study aims to investigate the influence of different cranial vault suture synostoses on orbital and periorbital morphological development in Crouzon syndrome. ^[13] OBJECTIVE This retrospective radiographic controlled study investigates the dental phenotype in patients with Crouzon syndrome to determine if differences are observed as suggested by the FGFR2C342Y/+ Crouzon mouse models, and whether these models could be of interest to study the role of this mutation in tooth development. ^[14] Diagnoses differed between procedures, with more Crouzon Syndrome in LF3 and more Apert Syndrome in LF2ZR. ^[15] FGFR3 is associated with multiple skeletal dysplasias including thanatophoric dysplasia, achondroplasia, and Crouzon syndrome and hypochondroplasia. ^[16] The most frequent syndromes in this group are: Crouzon syndrome, suture synostosis, microsomia, cerebral anomalies and midface clefts. ^[17] Rationale: Crouzon syndrome is a craniofacial malformation caused by premature fusion of fibrous sutures in infants. ^[18] Crouzon syndrome (CS) is an autosomal dominant disorder seen in about 1 in 60000 live births. ^[19] Multisuture synostoses are typically associated with distinct craniofacial syndromes, including Muenke syndrome, Apert syndrome, Crouzon syndrome, and Pfeiffer syndrome, and are thus categorized under syndromic craniosynostoses. ^[20] Craniofacial syndromes such as Crouzon syndrome or Apert syndrome are typically associated with a major hypoplasia in the midface responsible for exophthalmos, leading to palpebral malocclusion and frequent corneal complications. ^[21] Syndromes were identified in 38 patients (90%), with Crouzon syndrome being the most common (n = 16, 42%). ^[22] The most commonly occurring syndromic craniosynostoses are Apert syndrome, Crouzon syndrome, Pfeiffer syndrome, and Saethre-Chotzen syndrome. ^[23] According to ClinVarFGFR3 gene was associated with Crouzon syndrome with acanthosis nigricans, PDGFRA, EGFR and TP53 gene mutations were corellated with Idiopathic hypereosinophilic syndrome, Lung cancer and Glioma susceptibility respectively. ^[24] Possible diagnoses include cleft lip and palate, ocular anomalies such as hypertelorism and orbital dystopia, oligo‐ and polydactyly, conjoined twinning, clubfoot, Down syndrome, Crouzon syndrome, and Seckel syndrome. ^[25] We report an unusual case of bilateral optic nerve glioma without chiasmatic involvement in a 17-month old male patient with craniosynostosis and Crouzon Syndrome, an autosomal dominant disorder caused by activating FGFR2 mutations associated with craniosynostosis and optic atrophy. ^[26] Ultrasound depicts Pfeiffer syndrome or other acrocephalosyndactyly syndromes (Apert syndromes, Saethre-Chotzen) or other syndromic forms of craniosynostosis like Crouzon syndrome. ^[27] Purpose Children with Crouzon syndrome have a characteristic inversion of the orientation of the palpebral fissures, an increase of the interorbital distance, telecanthus, and exorbitism. ^[28] Crouzon syndrome is a rare form of syndromic craniosynostosis (SC) characterized by premature fusion of the cranial and facial sutures, elevated intracranial pressure, varying degrees of ocular exposure due to exorbitism, and airway compromise caused by midface retrusion. ^[29] Background : Constricted head or cloverleaf deformity in Crouzon syndrome is a severe form of the syndrome involving trilobed coronal and lambdoid synostosis. ^[30] 95 cm3), in Crouzon syndrome 700. ^[31] We conducted semi-structured qualitative interviews with 11 adults with Goldenhar or Crouzon syndrome. ^[32] Six syndrome-based categories were distinguished: Crouzon syndrome, Pfeiffer syndrome, Apert syndrome, cloverleaf skull syndrome, and others (Muenke syndrome, Sensenbrenner syndrome, unclassified). ^[33]

fibroblast growth factor

In this study, we investigated the levels of mRNA and protein expression related to cellular differentiation of Crouzon syndrome patient‐derived DPSCs (CS‐DPSCs) with a Gly338Arg fibroblast growth factor receptor 2 mutation. ^[1] ABSTRACT Crouzon syndrome is considered as one of the most common craniosynostosis syndromes with a prevalence of 1 in 65,000 individuals, and has a close relationship with variants in fibroblast growth factor receptor 2. ^[2] Rationale: Crouzon syndrome is an autosomal dominant genetic disorder caused by mutations in fibroblast growth factor receptor 2 (FGFR2) and one of the most common types of craniosynostosis. ^[3] OBJECTIVES Mutations in the fibroblast growth factor receptor 2 (FGFR2) gene are responsible for several severe forms of craniosynostotic disorders, such as Apert and Crouzon syndromes. ^[4] Crouzon syndrome is caused by mutation in the fibroblast growth factor receptor-2 (FGFR-2) gene resulting in premature closure of suture lines. ^[5] Crouzon syndrome is one of the most common craniosynostosis facial syndromes caused by a mutation in the fibroblast growth factor receptor 2 (FGFR2) gene. ^[6]

bicoronal synostosis n

Methods: A total of 125 computed tomographic scans were included (nonsyndromic bicoronal synostosis, n = 36; Apert syndrome associated with bicoronal synostosis, n = 24; Crouzon syndrome associated with bicoronal synostosis, n = 11; and controls, n = 54). ^[1]

crouzon syndrome patient

In this study, we investigated the levels of mRNA and protein expression related to cellular differentiation of Crouzon syndrome patient‐derived DPSCs (CS‐DPSCs) with a Gly338Arg fibroblast growth factor receptor 2 mutation. ^[1] Crouzon syndrome patients develop normal intracranial volume and potential restricted posterior cranial fossa volume with growth. ^[2]