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synostosis/phosphatase
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14 Ergebnisse
Unilateral coronal synostosis: a histomorphometric study.
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OBJECTIVE
This histomorphometric study compared the open and prematurely fused side of the coronal suture in subjects with unilateral coronal synostosis (UCS).
METHODS
Sutures and parasutural bone were obtained from seven subjects with nonsyndromic UCS during operative correction at 3 to 24 months
A study on the occurrence of alkaline phosphatase in the sutura interfrontalis of Wistar rats.
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The aim of the present study was to determine the presence of alkaline phosphatase during various stages in development and closure of the sutura interfrontalis. The histological sections reveal that this enzyme could primarily be demonstrated in the dura mater of this suture. In further
The presence of alkaline phosphatase in the coronal suture of rat.
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The purpose of the present study was to determine the presence of alkaline phosphatase within the coronal suture, the dura mater and the pericranium. The histologic sections reveal that no alkaline phosphatase activity could be observed within the coronal suture as well as the dura mater, while the
Plagiocephaly: premature unilateral closure of the coronal suture: a potentially localized disorder of cellular metabolism.
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Osteoblasts from involved and noninvolved sutures and normal membranous bone in patients with premature unilateral coronal synostosis were harvested and grown in tissue culture. The cultures were characterized to establish specific basal metabolic parameters of cellular growth and the production of
Remodeling of the sagittal suture in osteopetrotic (op/op) mice associated with cranial flat bone growth.
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It is well known that cranial flat bone experiences growth and development at the sutural interface, which is regarded as a neutral zone to control mechanical stimuli. In osteopetrotic (op/op) mice, meanwhile, cranial deformation is produced by the deficiency of osteoclasts and the subsequent defect
Cranial manifestations of hypophosphatasia in childhood nephrotic syndrome.
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A 7-year-old boy was referred to the children's hospital because of gross oedema and tiredness. Massive proteinuria was found and the condition was diagnosed as a childhood nephrotic syndrome. Concomitantly, pathologically low levels of serum alkaline phosphatase were recorded, and this, together
Scaphocephaly: premature closure of the sagittal suture: a localized disorder of cellular metabolism?
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Osteoblasts derived from sagittal sutures with premature synostosis, noninvolved coronal sutures, and normal frontal bone were harvested and cultured as cells in an attempt to determine if osteoblasts at the site of premature fusion exhibited altered in vitro cellular dynamics. Basal metabolic
Morphological change of the nasopremaxillary suture in growing "toothless" osteopetrotic (op/op) mice.
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Osteopetrotic (op/op) mice are known to commonly show a failure of tooth eruption. It is also well understood that masticatory function is highly associated with the craniofacial morphology of the growing mouse; however, the effects on sutural growth have not been studied. The present study was
Dihydrotestosterone stimulates proliferation and differentiation of fetal calvarial osteoblasts and dural cells and induces cranial suture fusion.
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BACKGROUND
The higher prevalence of metopic and sagittal suture synostosis in male infants suggests a role for androgens in early craniofacial development. These experiments characterize the influence of androgen stimulation on growth and differentiation of fetal dural and calvarial bone cells and
Craniosynostosis in transgenic mice overexpressing Nell-1.
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Previously, we reported NELL-1 as a novel molecule overexpressed during premature cranial suture closure in patients with craniosynostosis (CS), one of the most common congenital craniofacial deformities. Here we describe the creation and analysis of transgenic mice overexpressing Nell-1. Nell-1
FGFR2c-mediated ERK-MAPK activity regulates coronal suture development.
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Fibroblast growth factor receptor 2 (FGFR2) signaling is critical for proper craniofacial development. A gain-of-function mutation in the 2c splice variant of the receptor's gene is associated with Crouzon syndrome, which is characterized by craniosynostosis, the premature fusion of one or more of
Aberrantly activated Wnt/β-catenin pathway co-receptors LRP5 and LRP6 regulate osteoblast differentiation in the developing coronal sutures of an Apert syndrome (Fgfr2 S252W /+ ) mouse model
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Background: Apert syndrome is an autosomal, dominant inherited disorder characterized by craniosynostosis and syndactyly caused by gain-of-function mutations in the fibroblast growth factor receptor 2 (FGFR2) gene. Wnt/β-catenin signaling
Severe skeletal toxicity from protracted etidronate therapy for generalized arterial calcification of infancy.
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Generalized arterial calcification (AC) of infancy (GACI) is an autosomal recessive disorder that features hydroxyapatite deposition within arterial elastic fibers. Untreated, approximately 85% of GACI patients die by 6 months of age from cardiac ischemia and congestive heart failure. The
Evidence that homozygous PTPRD gene microdeletion causes trigonocephaly, hearing loss, and intellectual disability.
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BACKGROUND
The premature fusion of metopic sutures results in the clinical phenotype of trigonocephaly. An association of this characteristic with the monosomy 9p syndrome is well established and the receptor-type protein tyrosine phosphatase gene (PTPRD), located in the 9p24.1p23 region and
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