Development of Lumbosacral Spina bifida: Three-Dimensional Computer Graphic Study of Human Embryos at Carnegie Stage Twelve

Haque, Moududul; Ohata, Kenji; Takami, Toshihiro; Soares, Sérgio; Aree, Sarun Nunta; uba, Akira Hak; Hara, Mitsuhiro

doi:10.1159/000050430

Cited by 10 publications

(5 citation statements)

References 8 publications

(18 reference statements)

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“…7a). Thus, 21-29 somites are present at stage 12 and those numbers never were and still are not 'controversial', as recently claimed [Haque et al, 2001]. Embryos with 30 or more somites belong to stage 13 or later stages.…”

Section: Discussionmentioning

confidence: 90%

“…the future third to fifth sacral vertebrae)' is incorrect and was admitted to have been based on 'bad cellular condition of the human embryos available.' In a more recent study [Haque et al, 2001] confusion was further compounded by attributing 33 somites to stage 12, whereas that number necessarily belongs to stage 13 by definition. Fig.…”

Section: The Somitic Level Of the Caudal Neuroporementioning

confidence: 99%

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Somites, Spinal Ganglia, and Centra

OʼRahilly

Müller²

2003

Cells Tissues Organs

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Serial sections of 99 human embryos from Carnegie stages 8–23 were investigated and 38 graphic reconstructions were evaluated. At stage 9 somite 1 is of appreciable size and is separated from the otic disc, as also in the next several stages by rhombomeres and pharyngeal arches 3 and 4, thereby differing from the chick. At stage 10 somite 1 begins to differentiate into sclerotome and dermatomyotome. At stage 11 spinal neural crest begins to develop. At stage 12 parts of somites 1–4 are being transformed into the hypoglossal cell cord. It is stressed that the numbers of somites present at stages 9–12 are part of the definition of those stages. At stage 13 dense and loose zones begin to be detectable rostrally in the sclerotomes and also, although out of phase, in the perinotochord. Spinal ganglia begin to develop in phase with the somites. At stages 14–16 the maximum number of somites observed was 38–39 rather than 42–44, as usually given. Moreover, they did not extend to the tapered end of the trunk, which is not a (vertebrated) ‘tail’. At stages 17–23 the maximum number of centra was 38–39, including coccygeal vertebrae 4–5. Although most of the somites appear during primary development, all of the spinal ganglia develop during secondary development (stages 13–18). The number of ganglia was at a maximum of 35 at stage 18, but was reduced to 32 already by stage 23. Important points confirmed in this study are that the number of occipital somites in the human is four, and that the level of final closure of the caudal neuropore is future somite 31, which represents approximately future sacral vertebra 2. The interpretation of relevant neural tube defects is discussed in the light of the findings. The ascensus of the conus medullaris during the fetal period is well established, but a concomitant ascent of the situs neuroporicus is proposed here, and has implications for defects that involve tethering of the spinal cord. The main results are integrated in comprehensive graphic representations of the levels and the interrelationships of (a) somites and centra, and (b) somites, neural crest, and spinal ganglia. These may aid in the elucidation of some frequently occurring anomalous conditions.

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Section: Discussionmentioning

confidence: 90%

Section: The Somitic Level Of the Caudal Neuroporementioning

confidence: 99%

Somites, Spinal Ganglia, and Centra

OʼRahilly

Müller²

2003

Cells Tissues Organs

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“…During embryogenesis, cells in the unsegmented pre‐somitic mesoderm (PSM) epithelialize and bud off rostrocaudally to form the somites, which are bilateral units of mesoderm that flank the neural tube and notochord . In humans, the 33 vertebrae along the vertebral column form from 33 pairs of somites established during embryogenesis . In mice, 65 somite pairs form to produce the 65 vertebrae seen in the adult animal .…”

Section: Vertebral Column Formationmentioning

confidence: 99%

Developmental mechanisms of intervertebral disc and vertebral column formation

Lawson

Harfe

2017

WIREs Developmental Biology

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The vertebral column consists of repeating units of ossified vertebrae that are adjoined by fibrocartilagenous intervertebral discs. These structures form from the embryonic notochord and somitic mesoderm. In humans, congenital malformations of the vertebral column include scoliosis, kyphosis, spina bifida, and Klippel Feil syndrome. In adulthood, a common malady affecting the vertebral column includes disc degeneration and associated back pain. Indeed, recent reports estimate that low back pain is the number one cause of disability worldwide. Our review provides an overview of the molecular mechanisms underlying vertebral column morphogenesis and intervertebral disc development and maintenance, with an emphasis on what has been gleaned from recent genetic studies in mice. The aim of this review is to provide a developmental framework through which vertebral column formation can be understood so that ultimately, research scientists and clinicians alike can restore disc health with appropriately designed gene and cell-based therapies. WIREs Dev Biol 2017, 6:e283. doi: 10.1002/wdev.283 For further resources related to this article, please visit the WIREs website.

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“…The primary neural tube is thought to close during Carnegie stage 12, whereas the secondary neural tube develops by a process of differentiation and canalization with the primary neural tube. This whole process occurs between Carnegie stages 13 and 20 (12,13). It has very recently been proposed that human embryos have two successive sites of fusion of the neural folds, one in the rhombencephalic region and one in the prosencephalic portion of the embryo.…”

Section: Embryologymentioning

confidence: 99%

Pathobiology and Genetics of Neural Tube Defects

2003

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Summary:Purpose: Neural tube defects (NTDs), including spina bifida and anencephaly, are common congenital malformations that occur when the neural tube fails to achieve proper closure during early embryogenesis. Based on epidemiological and clinical data obtained over the last few decades, it is apparent that these multifactorial defects have a significant genetic component to their etiology that interacts with specific environmental risk factors. The purpose of this review article is to synthesize the existing literature on the genetic factors contributing to NTD risk.Results: To date, there is evidence that closure of the mammalian neural tube initiates and fuses intermittently at four discrete locations. Disruption of this process at any of these four sites may lead to an NTD, possibly arising through closure sitespecific genetic mechanisms. Candidate genes involved in neural tube closure include genes of the folate metabolic pathway, as well as those involved in folate transport.Conclusions: Although extensive efforts have focused on elucidating the genetic risk factors contributing to the etiology of NTDs, the population burden for these malformations remains unknown. One group at high risk for having children with NTDs is epileptic women receiving antiepileptic medications during pregnancy. Efforts to better understand the genetic factors that may contribute to their heightened risk, as well as the pathogenesis of neural tube closure defects, are reviewed herein.

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Development of Lumbosacral Spina bifida: Three-Dimensional Computer Graphic Study of Human Embryos at Carnegie Stage Twelve

Cited by 10 publications

References 8 publications

Somites, Spinal Ganglia, and Centra

Somites, Spinal Ganglia, and Centra

Developmental mechanisms of intervertebral disc and vertebral column formation

Pathobiology and Genetics of Neural Tube Defects

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