Talk:Musculoskeletal System - Skull Development: Difference between revisions
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==2022== | |||
{{#pmid:35220463}} | |||
Calvarial bone is one of the most complex sequences of developmental events in embryology, featuring a uniquely transient, pluripotent stem cell-like population known as the cranial neural crest (CNC). The skull is formed through intramembranous ossification with distinct tissue lineages (e.g. neural crest derived frontal bone and mesoderm derived parietal bone). Due to CNC's vast cell fate potential, in response to a series of inductive secreted cues including BMP/TGF-β, Wnt, FGF, Notch, Hedgehog, Hippo and PDGF signaling, CNC enables generations of a diverse spectrum of differentiated cell types in vivo such as osteoblasts and chondrocytes at the craniofacial level. In recent years, since the studies from a genetic mouse model and single-cell sequencing, new discoveries are uncovered upon CNC patterning, differentiation, and the contribution to the development of cranial bones. In this review, we summarized the differences upon the potential gene regulatory network to regulate CNC derived osteogenic potential in mouse and human, and highlighted specific functions of genetic molecules from multiple signaling pathways and the crosstalk, transcription factors and epigenetic factors in orchestrating CNC commitment and differentiation into osteogenic mesenchyme and bone formation. Disorders in gene regulatory network in CNC patterning indicate highly close relevance to clinical birth defects and diseases, providing valuable transgenic mouse models for subsequent discoveries in delineating the underlying molecular mechanisms. We also emphasized the potential regenerative alternative through scientific discoveries from CNC patterning and genetic molecules in interfering with or alleviating clinical disorders or diseases, which will be beneficial for the molecular targets to be integrated for novel therapeutic strategies in the clinic. | |||
==2021== | |||
Candidate positive targets of LHX6 and LHX8 transcription factors in the developing upper jaw | |||
Jeffry Cesario 1 , Sara Ha 1 , Julie Kim 1 , Niam Kataria 1 , Juhee Jeong 2 | |||
Affiliations expand | |||
PMID: 34861428 DOI: 10.1016/j.gep.2021.119227 | |||
Abstract | |||
Craniofacial development is controlled by a large number of genes, which interact with one another to form a complex gene regulatory network (GRN). Key components of GRN are signaling molecules and transcription factors. Therefore, identifying targets of core transcription factors is an important part of the overall efforts toward building a comprehensive and accurate model of GRN. LHX6 and LHX8 are transcription factors expressed in the oral mesenchyme of the first pharyngeal arch (PA1), and they are crucial regulators of palate and tooth development. Previously, we performed genome-wide transcriptional profiling and chromatin immunoprecipitation to identify target genes of LHX6 and LHX8 in PA1, and described a set of genes repressed by LHX. However, there has not been any discussion of the genes positively regulated by LHX6 and LHX8. In this paper, we revisited the above datasets to identify candidate positive targets of LHX in PA1. Focusing on those with known connections to craniofacial development, we performed RNA in situ hybridization to confirm the changes in expression in Lhx6;Lhx8 mutant. We also confirmed the binding of LHX6 to several putative enhancers near the candidate target genes. Together, we have uncovered novel connections between Lhx and other important regulators of craniofacial development, including Eya1, Barx1, Rspo2, Rspo3, and Wnt11. | |||
Association between the developing sphenoid and adult morphology: A study using sagittal sections of the skull base from human embryos and fetuses | |||
Masahito Yamamoto 1 , Zhe-Wu Jin 2 , Shogo Hayashi 3 , José Francisco Rodríguez-Vázquez 4 , Gen Murakami 5 , Shinichi Abe 1 | |||
Affiliations expand | |||
PMID: 34268732 PMCID: PMC8602018 (available on 2023-12-01) DOI: 10.1111/joa.13515 | |||
Abstract | |||
The developing sphenoid is regarded as a median cartilage mass (basisphenoid [BS]) with three cartilaginous processes (orbitosphenoid [OS], ala temporalis [AT], and alar process [AP]). The relationships of this initial configuration with the adult morphology are difficult to determine because of extensive membranous ossification along the cartilaginous elements. The purpose of this study was therefore to evaluate the anatomical connections between each element of the fetal sphenoid and adult morphology. Sagittal sections from 25 embryos and fetuses of gestational age 6-34 weeks and crown-rump length 12-295 mm were therefore examined and compared with horizontal and frontal sections from the other 25 late-term fetuses (217-340 mm). The OS was identified as a set of three mutually attached cartilage bars in early fetuses. At all stages, the OS-post was continuous with the anterolateral part of the BS. The BS included the notochord and Rathke's pouch remnant in embryos and early fetuses. The dorsum sellae was absent from embryos, but it protruded from the BS in early fetuses before a fossa for the hypophysis became evident. Although not higher than the hypophysis at midterm, the dorsum sellae elongated superiorly after gestational age 25 weeks. In early fetuses, the AP was located on the side immediately anterior to the otic capsule. The AT developed on the side immediately posterior to the extraocular rectus muscles. At late term, the greater wing was formed by membranous bones from the AT and AP. The AT and AP formed a complex bridge between the BS and the greater wing. A small cartilage, future medial pterygoid process (PTmed) was located inferior to the AT in early fetuses. At midterm, one endochondral bone and multiple membranous bones formed the PTmed. The lateral pterygoid process (PTlat) was formed by a single membranous bone plate. Therefore, we connected fetal elements and the adult morphology as follows. (1) Derivative of the OS makes not only the lesser wing but also the anterior margin of the body of the sphenoid. (2) Derivatives of the BS are the body of the sphenoid including the sella turcica and the dorsum sellae. (3) Most of the greater wing including the foramen rotundum and the foramen oval originate from the AT and AP and multiple membranous bones. (4) The PTmed originate from endochondral bones and multiple membranous bones, while the PTlat derive from a single membranous bone. | |||
==2018== | |||
===Johns Hopkins Fetal Skull Collection (1918–1951)=== | |||
{{Johns Hopkins Fetal Skull Collection table}} | |||
==2017== | |||
Childs Nerv Syst. 2017 Jun;33(6):909-914. doi: 10.1007/s00381-017-3406-1. Epub 2017 Apr 10. | |||
A comprehensive review of the anterior fontanelle: embryology, anatomy, and clinical considerations. | |||
D'Antoni AV1, Donaldson OI1, Schmidt C2, Macchi V3, De Caro R3, Oskouian RJ4, Loukas M5, Shane Tubbs R6. | |||
Author information | |||
Abstract | |||
PURPOSE: | |||
Fontanelles are a regular feature of infant development in which two segments of bone remain separated, leaving an area of fibrous membrane or a "soft spot" that acts to accommodate growth of the brain without compression by the skull. Of the six fontanelles in the human skull, the anterior fontanelle, located between the frontal and parietal bones, serves as an important anatomical diagnostic tool in the assessment of impairments of the skull and brain and allows access to the brain and ventricles in the infant. | |||
METHODS: | |||
Using a standard database search, we conducted a review of the anterior fontanelle, including its embryology, anatomy, pathology, and related surgical implications. | |||
CONCLUSIONS: | |||
The diagnostic value of the anterior fontanelle, through observation of its shape, size, and palpability, makes the area of significant clinical value. It is important that clinicians are aware of the features and associated pathologies of this area in their everyday practice. | |||
KEYWORDS: | |||
Cranial calvaria; Skull; Soft spot; Suture | |||
PMID: 28396968 DOI: 10.1007/s00381-017-3406-1 | |||
==2016== | |||
===The remodeling pattern of human mandibular alveolar bone during prenatal formation from 19 to 270mm CRL=== | |||
Ann Anat. 2016 Feb 24;205:65-74. doi: 10.1016/j.aanat.2016.01.005. [Epub ahead of print] | |||
Radlanski RJ1, Renz H2, Tsengelsaikhan N2, Schuster F2, Zimmermann CA2. | |||
Abstract | |||
The underlying mechanisms of human bone morphogenesis leading to a topologically specific shape remain unknown, despite increasing knowledge of the basic molecular aspects of bone formation and its regulation. The formation of the alveolar bone, which houses the dental primordia, and later the dental roots, may serve as a model to approach general questions of bone formation. Twenty-five heads of human embryos and fetuses (Radlanski-Collection, Berlin) ranging from 19mm to 270mm (crown-rump-length) CRL were prepared as histological serial sections. For each stage, virtual 3D-reconstructions were made in order to study the morphogenesis of the mandibular molar primordia with their surrounding bone. Special focus was given to recording the bone-remodeling pattern, as diagnosed from the histological sections. In early stages (19-31mm CRL) developing bone was characterized by appositional only. At 41, in the canine region, mm CRL bony extensions were found forming on the bottom of the trough. Besides general apposition, regions with resting surfaces were also found. At a fetal size of 53mm CRL, septa have developed and led to a compartment for canine development. Furthermore, one shared compartment for the incisor primordia and another shared compartment for the molars also developed. Moreover, the inner surfaces of the dental crypts showed resorption of bone. From this stage on, a general pattern became established such that the compartmentalizing ridges and septa between all of the dental primordia and the brims of the crypts were noted, and were due to appositional growth of bone, while the crypts enlarged on their inner surfaces by resorption. By 160mm CRL, the dental primordia were larger, and all of the bony septa had become reduced in size. The primordia for the permanent teeth became visible at 225mm CRL and shared the crypts of their corresponding deciduous primordia. | |||
Copyright © 2016 Elsevier GmbH. All rights reserved. | |||
KEYWORDS: | |||
3D-reconstructions; Alveolar bone; Dental primordia; Human; Mandible | |||
PMID 26921449 | |||
==2015== | |||
===Transcriptional analysis of human cranial compartments with different embryonic origins=== | |||
Arch Oral Biol. 2015 Sep;60(9):1450-60. doi: 10.1016/j.archoralbio.2015.06.008. Epub 2015 Jul 2. | |||
Homayounfar N1, Park SS2, Afsharinejad Z3, Bammler TK3, MacDonald JW3, Farin FM3, Mecham BH4, Cunningham ML5. | |||
Abstract | |||
OBJECTIVE: | |||
Previous investigations suggest that the embryonic origins of the calvarial tissues (neural crest or mesoderm) may account for the molecular mechanisms underlying sutural development. The aim of this study was to evaluate the differences in the gene expression of human cranial tissues and assess the presence of an expression signature reflecting their embryonic origins. | |||
METHODS: | |||
Using microarray technology, we investigated global gene expression of cells from the frontal and parietal bones and the metopic and sagittal intrasutural mesenchyme (ISM) of four human foetal calvaria. qRT-PCR of a selected group of genes was done to validate the microarray analysis. Paired comparison and correlation analyses were performed on microarray results. | |||
RESULTS: | |||
Of six paired comparisons, frontal and parietal compartments (distinct tissue types of calvaria, either bone or intrasutural mesenchyme) had the most different gene expression profiles despite being composed of the same tissue type (bone). Correlation analysis revealed two distinct gene expression profiles that separate frontal and metopic compartments from parietal and sagittal compartments. TFAP2A, TFAP2B, ICAM1, SULF1, TNC and FOXF2 were among differentially expressed genes. | |||
CONCLUSION: | |||
Transcriptional profiles of two groups of tissues, frontal and metopic compartments vs. parietal and sagittal compartments, suggest differences in proliferation, differentiation and extracellular matrix production. Our data suggest that in the second trimester of human foetal development, a gene expression signature of neural crest origin still exists in frontal and metopic compartments while gene expression of parietal and sagittal compartments is more similar to mesoderm. | |||
Copyright © 2015 Elsevier Ltd. All rights reserved. | |||
KEYWORDS: | |||
Cranial suture; Differentiation; Extracellular matrix; Mesoderm; Neural crest; Proliferation | |||
PMID 26188427 | |||
==2014== | |||
===Direct Brain Recordings Reveal Impaired Neural Function in Infants With Single-Suture Craniosynostosis: A Future Modality for Guiding Management?=== | |||
J Craniofac Surg. 2014 Dec 19. [Epub ahead of print] | |||
Hashim PW1, Brooks ED, Persing JA, Reuman H, Naples A, Travieso R, Terner J, Steinbacher D, Landi N, Mayes L, McPartland JC. | |||
Abstract | |||
BACKGROUND: | |||
Patients with single-suture craniosynostosis (SSC) are at an elevated risk for long-term learning disabilities. Such adverse outcomes indicate that the early development of neural processing in SSC may be abnormal. At present, however, the precise functional derangements of the developing brain remain largely unknown. Event-related potentials (ERPs) are a form of noninvasive neuroimaging that provide direct measurements of cortical activity and have shown value in predicting long-term cognitive functioning. The current study used ERPs to examine auditory processing in infants with SSC to help clarify the developmental onset of delays in this population. | |||
METHODS: | |||
Fifteen infants with untreated SSC and 23 typically developing controls were evaluated. ERPs were recorded during the presentation of speech sounds. Analyses focused on the P150 and N450 components of auditory processing. | |||
RESULTS: | |||
Infants with SSC demonstrated attenuated P150 amplitudes relative to typically developing controls. No differences in the N450 component were identified between untreated SSC and controls. | |||
CONCLUSIONS: | |||
Infants with untreated SSC demonstrate abnormal speech sound processing. Atypicalities are detectable as early as 6 months of age and may represent precursors to long-term language delay. Electrophysiological assessments provide a precise examination of neural processing in SSC and hold potential as a future modality to examine the effects of surgical treatment on brain development. | |||
PMID 25534054 | |||
==2012== | ==2012== | ||
===Paleontological and developmental evidence resolve the homology and dual embryonic origin of a mammalian skull bone, the interparietal=== | |||
Proc Natl Acad Sci U S A. 2012 Aug 28;109(35):14075-80. doi: 10.1073/pnas.1208693109. Epub 2012 Aug 13. | |||
Koyabu D, Maier W, Sánchez-Villagra MR. | |||
Source | |||
Palaeontological Institute and Museum, University of Zürich, 8006 Zürich, Switzerland. daisuke.koyabu@pim.uzh.ch | |||
Abstract | |||
The homologies of mammalian skull elements are now fairly well established, except for the controversial interparietal bone. A previous experimental study reported an intriguing mixed origin of the interparietal: the medial portion being derived from the neural crest cells, whereas the lateral portion from the mesoderm. The evolutionary history of such mixed origin remains unresolved, and contradictory reports on the presence or absence and developmental patterns of the interparietal among mammals have complicated the question of its homology. Here we provide an alternative perspective on the evolutionary identity of the interparietal, based on a comprehensive study across more than 300 extinct and extant taxa, integrating embryological and paleontological data. Although the interparietal has been regarded as being lost in various lineages, our investigation on embryos demonstrates its presence in all extant mammalian "orders." The generally accepted paradigm has regarded the interparietal as consisting of two elements that are homologized to the postparietals of basal amniotes. The tabular bones have been postulated as being lost during the rise of modern mammals. However, our results demonstrate that the interparietal consists not of two but of four elements. We propose that the tabulars of basal amniotes are conserved as the lateral interparietal elements, which quickly fuse to the medial elements at the embryonic stage, and that the postparietals are homologous to the medial elements. Hence, the dual developmental origin of the mammalian interparietal can be explained as the evolutionary consequence of the fusion between the crest-derived "postparietals" and the mesoderm-derived "tabulars." | |||
PMID 22891324 | |||
===The BMP Ligand Gdf6 Prevents Differentiation of Coronal Suture Mesenchyme in Early Cranial Development=== | ===The BMP Ligand Gdf6 Prevents Differentiation of Coronal Suture Mesenchyme in Early Cranial Development=== | ||
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http://onlinelibrary.wiley.com/doi/10.1111/j.1741-4520.2011.00322.x/abstract;jsessionid=D215C1671CDF1C62716033D0D5E688F1.d04t04 | http://onlinelibrary.wiley.com/doi/10.1111/j.1741-4520.2011.00322.x/abstract;jsessionid=D215C1671CDF1C62716033D0D5E688F1.d04t04 | ||
===Modeling of the human fetal skull base growth: interest in new volumetrics morphometric tools=== | |||
Early Hum Dev. 2011 Apr;87(4):239-45. doi: 10.1016/j.earlhumdev.2011.01.022. | |||
Herlin C, Largey A, deMatteï C, Daurès JP, Bigorre M, Captier G. | |||
Source | |||
Craniofacial and Plastic Pediatric Surgery Unit, Lapeyronie Hospital, Montpellier, 371 Av Doyen Gaston Giraud, 34 295 Montpellier, France. christian.herl@free.fr | |||
Abstract | |||
BACKGROUND: | |||
Research on the skull base is important to improve our understanding of the growth and development of the modern human skull. To study the growth of the human fetal skull base, we assessed a new geometric morphometric tool, which does not require the use of bone landmarks. | |||
MATERIAL AND METHODS: | |||
Seven dry fetal skulls of an estimated gestational age ranging from 15 to 27 weeks were studied. Each skull was scanned using a standard CT scan and the image sets were post-processed to extract volumetric data by segmenting the skull base into predefined regions of interest. Our method of analysis was based on the inertial properties of reconstructed volumes. | |||
RESULTS: | |||
The volumetric study of the skulls highlighted an asynchronous speed of growth between the pre and post-chordal parts of the skull base whose preferential growth are in the vertical and horizontal planes. We also found different speeds of growth in the pre-chordal part depending on the type of ossification (endochondral or membranous). The overall shape of the skull base bones were preserved during the period studied except for the petrous pyramids. The expansion of bone parts was isometric with reference to a central point that was located at the intrasphenoidal synchondrosis. Finally, the analysis of the basicranial angles corroborated data from the literature in the sagittal plane and allowed their study also in the frontal and horizontal planes. | |||
CONCLUSIONS: | |||
This three-dimensional volumetric approach is a necessary complement to studies that are performed in the sagittal plane and are based on the identification of landmarks. The geometric morphometric method used by authors permitted to obtain original informations on the growth kinetics and bone tridimensional movements of the human fetal skull base. | |||
Copyright © 2011 Elsevier Ltd. All rights reserved. | |||
PMID 21300487 | |||
==2010== | ==2010== | ||
Line 100: | Line 245: | ||
PMID 21045207 | PMID 21045207 | ||
The BMP antagonist noggin regulates cranial suture fusion STEPHEN M. WARREN, LISA J. BRUNET, RICHARD M. HARLAND, ARIS N.,ECONOMIDES & MICHAEL T. LONGAKER | |||
"During skull development, the cranial connective tissue framework undergoes intramembranous ossification to form skull bones (calvaria). As the calvarial bones advance to envelop the brain, fibrous sutures form between the calvarial plates. Expansion of the brain is coupled with calvarial growth through a series of tissue interactions within the cranial suture complex. Craniosynostosis, or premature cranial suture fusion, results in an abnormal skull shape, blindness and mental retardation. Recent studies have demonstrated that gain-of-function mutations in fibroblast growth factor receptors ( fgfr ) are associated with syndromic forms of craniosynostosis. Noggin, an antagonist of bone morphogenetic proteins (BMPs), is required for embryonic neural tube, somites and skeleton patterning. Here we show that noggin is expressed postnatally in the suture mesenchyme of patent, but not fusing, cranial sutures, and that noggin expression is suppressed by FGF2 and syndromic fgfr signalling. Since noggin misexpression prevents cranial suture fusion in vitro and in vivo , we suggest that syndromic fgfr -mediated craniosynostoses may be the result of inappropriate downregulation of noggin expression." | |||
==2009== | ==2009== | ||
Line 131: | Line 276: | ||
PMID 21887190 | PMID 21887190 | ||
==2008== | |||
===Development and tissue origins of the mammalian cranial base=== | |||
Dev Biol. 2008 Oct 1;322(1):121-32. doi: 10.1016/j.ydbio.2008.07.016. Epub 2008 Jul 22. | |||
McBratney-Owen B, Iseki S, Bamforth SD, Olsen BR, Morriss-Kay GM. | |||
Source | |||
Harvard School of Dental Medicine, Department of Developmental Biology, 190 Longwood Avenue, Boston, MA, 02115, USA. bmcbratneyowen@post.harvard.edu | |||
Abstract | |||
The vertebrate cranial base is a complex structure composed of bone, cartilage and other connective tissues underlying the brain; it is intimately connected with development of the face and cranial vault. Despite its central importance in craniofacial development, morphogenesis and tissue origins of the cranial base have not been studied in detail in the mouse, an important model organism. We describe here the location and time of appearance of the cartilages of the chondrocranium. We also examine the tissue origins of the mouse cranial base using a neural crest cell lineage cell marker, Wnt1-Cre/R26R, and a mesoderm lineage cell marker, Mesp1-Cre/R26R. The chondrocranium develops between E11 and E16 in the mouse, beginning with development of the caudal (occipital) chondrocranium, followed by chondrogenesis rostrally to form the nasal capsule, and finally fusion of these two parts via the midline central stem and the lateral struts of the vault cartilages. X-Gal staining of transgenic mice from E8.0 to 10 days post-natal showed that neural crest cells contribute to all of the cartilages that form the ethmoid, presphenoid, and basisphenoid bones with the exception of the hypochiasmatic cartilages. The basioccipital bone and non-squamous parts of the temporal bones are mesoderm derived. Therefore the prechordal head is mostly composed of neural crest-derived tissues, as predicted by the New Head Hypothesis. However, the anterior location of the mesoderm-derived hypochiasmatic cartilages, which are closely linked with the extra-ocular muscles, suggests that some tissues associated with the visual apparatus may have evolved independently of the rest of the "New Head". | |||
PMID 18680740 | |||
===Three-dimensional ontogenetic shape changes in the human cranium during the fetal period=== | |||
J Anat. 2008 May;212(5):627-35. doi: 10.1111/j.1469-7580.2008.00884.x. | |||
Morimoto N, Ogihara N, Katayama K, Shiota K. | |||
Source | |||
Laboratory of Physical Anthropology, Graduate School of Science, Kyoto University, Japan. morimoto@aim.uzh.ch <morimoto@aim.uzh.ch> | |||
Abstract | |||
Knowledge of the pattern of human craniofacial development in the fetal period is important for understanding the mechanisms underlying the emergence of variations in human craniofacial morphology. However, the precise character of the prenatal ontogenetic development of the human cranium has yet to be fully established. This study investigates ontogenetic changes in cranial shape in the fetal period, as exhibited in Japanese fetal specimens housed at Kyoto University. A total of 31 human fetal specimens aged from approximately 8 to 42 weeks of gestation underwent helical computed tomographic scanning, and 68 landmarks were digitized on the internal and external surfaces of the extracted crania. Ontogenetic shape change was then analyzed cross-sectionally and three-dimensionally using a geometric morphometric technique. The results of the present study are generally consistent with previously reported findings. It was found that during the prenatal ontogenetic process, the growth rate of the length of the cranium is greater than that of the width and height, and the growth rate of the length of the posterior cranial base is smaller than that of the anterior cranial base. Furthermore, it was observed that the change in shape of the human viscerocranium is smaller than that of the neurocranium during the fetal period, and that concurrently the basicranium extends by approximately 8 degrees due to the relative elevation of the basilar and lateral parts of occipital bone. These specific growth-related changes are the opposite of those reported for the postnatal period. Our findings therefore indicate that the allometric pattern of the human cranium is not a simple continuous transformation, but changes drastically from before to after birth. | |||
PMID 18430090 | |||
==2000== | ==2000== | ||
Line 151: | Line 321: | ||
MR imaging can show early progressive ossification of the cartilaginous skull base and its relation to intracranial structures. The study of fetal developmental anatomy may lead to a better understanding of abnormalities of the skull base. | MR imaging can show early progressive ossification of the cartilaginous skull base and its relation to intracranial structures. The study of fetal developmental anatomy may lead to a better understanding of abnormalities of the skull base. | ||
PMID 11039353 | PMID 11039353 | ||
==Historic== | |||
===1937=== | |||
The Development of the Vertebrate Skull. G. R. de Beer, M.A., D.Sc., F.L.S. 552 pp., illust., $9.50. McAinsh, Toronto, 1937. | |||
Anyone who has ever attempted even in a general way to compare the skull of man with that of lower mammals or reptiles and to determine the morphology of the different parts will realize the thorny and difficult field into which this book ventures. And it enters this field in no casual way but to a depth of 515 closely printed pages with abundant simple and clear illustrations. , | |||
The book is divided into three parts. The first deals with some general questions of the nature of cartilage and bone and goes on to review Goethe’s theory that the skull is made up of several fused vertebre. This theory of course has not stood the test of time but out of it arose the recognition of the segmental structure of the posterior end of. the skull. |
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Cite this page: Hill, M.A. (2024, June 19) Embryology Musculoskeletal System - Skull Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Musculoskeletal_System_-_Skull_Development |
2022
Liao J, Huang Y, Wang Q, Chen S, Zhang C, Wang D, Lv Z, Zhang X, Wu M & Chen G. (2022). Gene regulatory network from cranial neural crest cells to osteoblast differentiation and calvarial bone development. Cell Mol Life Sci , 79, 158. PMID: 35220463 DOI.
Calvarial bone is one of the most complex sequences of developmental events in embryology, featuring a uniquely transient, pluripotent stem cell-like population known as the cranial neural crest (CNC). The skull is formed through intramembranous ossification with distinct tissue lineages (e.g. neural crest derived frontal bone and mesoderm derived parietal bone). Due to CNC's vast cell fate potential, in response to a series of inductive secreted cues including BMP/TGF-β, Wnt, FGF, Notch, Hedgehog, Hippo and PDGF signaling, CNC enables generations of a diverse spectrum of differentiated cell types in vivo such as osteoblasts and chondrocytes at the craniofacial level. In recent years, since the studies from a genetic mouse model and single-cell sequencing, new discoveries are uncovered upon CNC patterning, differentiation, and the contribution to the development of cranial bones. In this review, we summarized the differences upon the potential gene regulatory network to regulate CNC derived osteogenic potential in mouse and human, and highlighted specific functions of genetic molecules from multiple signaling pathways and the crosstalk, transcription factors and epigenetic factors in orchestrating CNC commitment and differentiation into osteogenic mesenchyme and bone formation. Disorders in gene regulatory network in CNC patterning indicate highly close relevance to clinical birth defects and diseases, providing valuable transgenic mouse models for subsequent discoveries in delineating the underlying molecular mechanisms. We also emphasized the potential regenerative alternative through scientific discoveries from CNC patterning and genetic molecules in interfering with or alleviating clinical disorders or diseases, which will be beneficial for the molecular targets to be integrated for novel therapeutic strategies in the clinic.
2021
Candidate positive targets of LHX6 and LHX8 transcription factors in the developing upper jaw
Jeffry Cesario 1 , Sara Ha 1 , Julie Kim 1 , Niam Kataria 1 , Juhee Jeong 2 Affiliations expand PMID: 34861428 DOI: 10.1016/j.gep.2021.119227 Abstract
Craniofacial development is controlled by a large number of genes, which interact with one another to form a complex gene regulatory network (GRN). Key components of GRN are signaling molecules and transcription factors. Therefore, identifying targets of core transcription factors is an important part of the overall efforts toward building a comprehensive and accurate model of GRN. LHX6 and LHX8 are transcription factors expressed in the oral mesenchyme of the first pharyngeal arch (PA1), and they are crucial regulators of palate and tooth development. Previously, we performed genome-wide transcriptional profiling and chromatin immunoprecipitation to identify target genes of LHX6 and LHX8 in PA1, and described a set of genes repressed by LHX. However, there has not been any discussion of the genes positively regulated by LHX6 and LHX8. In this paper, we revisited the above datasets to identify candidate positive targets of LHX in PA1. Focusing on those with known connections to craniofacial development, we performed RNA in situ hybridization to confirm the changes in expression in Lhx6;Lhx8 mutant. We also confirmed the binding of LHX6 to several putative enhancers near the candidate target genes. Together, we have uncovered novel connections between Lhx and other important regulators of craniofacial development, including Eya1, Barx1, Rspo2, Rspo3, and Wnt11.
Association between the developing sphenoid and adult morphology: A study using sagittal sections of the skull base from human embryos and fetuses
Masahito Yamamoto 1 , Zhe-Wu Jin 2 , Shogo Hayashi 3 , José Francisco Rodríguez-Vázquez 4 , Gen Murakami 5 , Shinichi Abe 1 Affiliations expand PMID: 34268732 PMCID: PMC8602018 (available on 2023-12-01) DOI: 10.1111/joa.13515 Abstract
The developing sphenoid is regarded as a median cartilage mass (basisphenoid [BS]) with three cartilaginous processes (orbitosphenoid [OS], ala temporalis [AT], and alar process [AP]). The relationships of this initial configuration with the adult morphology are difficult to determine because of extensive membranous ossification along the cartilaginous elements. The purpose of this study was therefore to evaluate the anatomical connections between each element of the fetal sphenoid and adult morphology. Sagittal sections from 25 embryos and fetuses of gestational age 6-34 weeks and crown-rump length 12-295 mm were therefore examined and compared with horizontal and frontal sections from the other 25 late-term fetuses (217-340 mm). The OS was identified as a set of three mutually attached cartilage bars in early fetuses. At all stages, the OS-post was continuous with the anterolateral part of the BS. The BS included the notochord and Rathke's pouch remnant in embryos and early fetuses. The dorsum sellae was absent from embryos, but it protruded from the BS in early fetuses before a fossa for the hypophysis became evident. Although not higher than the hypophysis at midterm, the dorsum sellae elongated superiorly after gestational age 25 weeks. In early fetuses, the AP was located on the side immediately anterior to the otic capsule. The AT developed on the side immediately posterior to the extraocular rectus muscles. At late term, the greater wing was formed by membranous bones from the AT and AP. The AT and AP formed a complex bridge between the BS and the greater wing. A small cartilage, future medial pterygoid process (PTmed) was located inferior to the AT in early fetuses. At midterm, one endochondral bone and multiple membranous bones formed the PTmed. The lateral pterygoid process (PTlat) was formed by a single membranous bone plate. Therefore, we connected fetal elements and the adult morphology as follows. (1) Derivative of the OS makes not only the lesser wing but also the anterior margin of the body of the sphenoid. (2) Derivatives of the BS are the body of the sphenoid including the sella turcica and the dorsum sellae. (3) Most of the greater wing including the foramen rotundum and the foramen oval originate from the AT and AP and multiple membranous bones. (4) The PTmed originate from endochondral bones and multiple membranous bones, while the PTlat derive from a single membranous bone.
2018
Johns Hopkins Fetal Skull Collection (1918–1951)
Johns Hopkins Fetal Skull Collection (1918–1951) - Simplified | Full | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Specimen | Adolf H Schultz Number | Adolf H Schultz Number (Old) | Sex | Race | Basioccipital | Basisphenoid | Canines | Incisors | Incus | Left Ethmoid | Left Frontal | Left greater wing of Sphenoid | Left inferior nasal conchae | Left Lacrimal | Left lesser wing of Sphenoid | Left Mandible | Left Maxilla | Left Nasal | Left Occipital Condyle | Left Palatine | Left Parital | Left Petrous Portion of Temporal | Left Squamous portion of Temporal | Left Tympanic Ring | Left Zygomatic | Mahmood Y El Najjar Age | Malleus | Molars | Occipital | Premolar | Presphenoid | Right Ethmoid | Vomer | Right Frontal | Right greater wing of Sphenoid | Right inferior nasal conchae | Right Lacrimal | Right lesser wing of Sphenoid | Right Mandible | Right Maxilla | Right Nasal | Right Occipital Condyle | Right Palatine | Right Parietal | Right Petrous Portion of Temporal | Right Squamous portion of Temporal | Right tympanic Ring | Right Zygomatic | Stapes | Stylohyal Ossification | Ted Combs Age 1 | Ted Combs Age 2 | Ted Combs Notes | Temporal | Tympanic Ring | Tympanohyal Ossification | |
JH 001 | 6 | Blank | M | B | P | PNF | 0 | 1 | 2 | P | P | PNF | A | A | PNF | PNF | PNF | A | P | A | P | PNF | PNF | PNF | A | 5 IU | 2 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NS | 5-6 | IU | Left Occipital Condyle Missing 7/01 JR | PF PETROUS | PF SQUAMOUS | NS | |
JH 002 | 15 | 253 | M | B | P | PNF | 1 | 4 | 0 | A | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | A | 5 IU | 0 | 0 | P | 0 | PNF | A | P | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | NS | P | 0 | NS | 7 | IU | OSSIFIED | COMPLETE ROUND | NS | ||
JH 003 | 18 | Blank | M | B | P | PF | 0 | 3 | 0 | P | P | PNF | A | A | PF | PF | PNF | A | P | P | P | PF | PF | PF | P | 1y PN | 0 | 8 | P | 0 | PF | P | A | P | PF | A | A | PF | PF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NS | 11 | PN | LEFT GREATER WING MAY HAVE BEEN BROKEN | No Data | No Data | FORMING | |
JH 004 | 34 | 394 | M | B | P | PF | 2 | 7 | 0 | P | P | PF | A | A | PF | PF | PNF | P | P | P | P | PF | PF | PF | P | 9PN | 0 | 8 | P | 0 | PF | P | P | P | PF | A | A | PF | PF | PNF | P | P | P | P | PF | PF | PF | P | 0 | FORMING | 12 | PN | ENTIRE BASICRANIUM FUSED | No Data | No Data | Completely Ossified | |
JH 005 | 35 | 361 | M | B | P | PF | 0 | 7 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NS | 10 | IU | NO DATA | NO DATA | OSSIFIED | |||
JH 006 | 36 | 258 | M | B | P | PF | 0 | 0 | 1 | P | P | NS | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NS | 7 | IU | ADOLF H SCHULTZ DRAWING INCLUDED | NO DATA | NO DATA | NS | ||
JH 007 | 38 | 269 | M | B | P | PF | 0 | 0 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PNF | P | 0 | NS | 10-11 | IU | IMPROPER OSSIFICATION OF DORSUM STELLA | NO DATA | NO DATA | NS | ||
JH 008 | 51 | Blank | M | B | A | PF | 0 | 0 | 0 | A | P | ? | A | A | ? | PNF | A | A | P | P | A | A | A | A | P | 0 | 0 | A | 0 | PF | A | A | A | ? | A | A | ? | PNF | A | A | A | A | P | A | PNF | A | A | 0 | NS | 5 | IU | NOT ALL BONES BELONG HERE | NO DATA | NO DATA | NS | ||
JH 009 | 56 | 271 | M | B | P | PF | 0 | 4 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NS | 10 | IU | NO DATA | NO DATA | NS | |||
JH 010 | 58 | 340 | M | B | P | PF | 0 | 0 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NS | 9-10 | IU | NO DATA | NO DATA | NS | |||
JH 011 | 62 | Blank | M | B | P | A | 1 | 0 | 2 | P | P | A | A | A | A | PNF | PNF | A | P | P | P | PF | PF | PF | A | 1 | 3 | P | 0 | A | P | P | A | PNF | A | A | A | PNF | PNF | A | A | P | A | PF | PF | PF | A | 0 | NS | 0 | Newborn | NO DATA | NO DATA | FORMING | |||
JH 012 | 67 | 322 | M | B | P | PF | 0 | 3 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NS | 0 | Newborn | MOLAR BUDS INCLUDED | NO DATA | NO DATA | NS | ||
JH 013 | 69 | 299 | M? | B | P | PF | 0 | 1 | 2 | A | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 0 | 1 | A | 0 | PF | A | P | P | PNF | A | A | PF | PNF | PNF | A | P | A | P | PNF | PNF | PNF | P | 0 | NS | 9 | IU | CHECK SEX <- BUG!!! | NO DATA | NO DATA | NS | ||
JH 014 | 71 | 323 | M | B | P | PF | 2 | 7 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | NS | 0 | Newborn | NO DATA | NO DATA | NS | |||
JH 015 | 78 | 298 | M | B | P | PF | 0 | 0 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PNF | P | 2 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NS | 8 | IU | IMPROPER OSSIFICATION OF THE STELLA TURCICA | NO DATA | NO DATA | NS | ||
JH 016 | 83 | Blank | M | B | P | PF | 1 | 4 | 2 | P | P | PNF | A | A | PF | PNF | A | A | P | P | P | PNF | PNF | PNF | P | 2 | 3 | P | 0 | PF | P | P | A | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 7 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 017 | 91 | 334 | M | B | P | PF | 0 | 3 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 2 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | A | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 10 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 018 | 96 | 310 | M | B | P | PF | 0 | 3 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 10 | IU | SQUAMOUS PORTION OF OCCIPITAL IN 2 PIECES | NO DATA | NO DATA | NOT OBSERVED | ||
JH 019 | 109 | 315 | M | B | P | PF | 0 | 0 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 3 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 10 | IU | EXTRA BROKEN MALLEUS INCLUDED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 020 | 110 | 257 | M | B | P | PF | 0 | 4 | 2 | P | P | A | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 2 | 1 | P | 0 | PF | P | P | P | A | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 6 | IU | TEMPORALS POORLY OSSIFIED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 021 | 111 | 342 | M | B | P | PF | 0 | 1 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | A | P | 1 | NOT OBSERVED | 3 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 022 | 126 | 367 | M | B | P | PF | 1 | 4 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 1 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 10 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 023 | 135 | 250 | M | B | P | PF | 0 | 0 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | 0 | P | 0 | PF | P | A | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 8 | IU | VERY YOUNG | NO DATA | NO DATA | NOT OBSERVED | ||
JH 024 | 137 | 285 | M | B | A | PF | 0 | 6 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | A | P | P | PNF | PNF | PNF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | A | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 025 | 139 | 400 | M | B | P | PF | 2 | 5 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PNF | PF | P | 0 | NOT OBSERVED | 0 | Newborn | NO DATA | NO DATA | NOT OBSERVED | |||
JH 026 | 144 | Blank | M | B | P | PF | 1 | 0 | 0 | P | P | PNF | A | A | PF | A | PNF | A | P | P | P | PNF | PNF | A | P | 0 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | A | P | 0 | NOT OBSERVED | 10 | IU | "Two right lateral occipital bones and no left
JR 7/12/2001" |
NO DATA | NO DATA | NOT OBSERVED | ||
JH 027 | 147 | 391 | M | B | A | A | 0 | 0 | 0 | A | P | A | A | A | A | A | A | A | A | A | A | A | A | A | A | 0 | 0 | A | 0 | A | A | A | A | A | A | A | A | A | A | A | A | A | A | A | A | A | A | 0 | NO BONE | 2 | PN | LEFT FRONTAL IS THE ONLY BONE PRESENT. | NO DATA | NO DATA | NO BONE | ||
JH 028 | 155 | 355 | M | B | P | PNF | 2 | 8 | 0 | P | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 4 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 0 | Newborn | NO DATA | NO DATA | NOT OBSERVED | |||
JH 029 | 159 | 273 | M | B | A | PF | 1 | 1 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 2 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 030 | 161 | 367 | M | B | P | PF | 2 | 2 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 0 | Newborn | NO DATA | NO DATA | NOT OBSERVED | |||
JH 031 | 164 | 359 | M | B | P | PF | 3 | 6 | 2 | P | P | PNF | A | A | PF | See Note | PNF | A | P | P | P | PF | PF | PF | P | 1 | 8 | P | 0 | PF | P | P | P | PNF | A | A | PF | See Note | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 2 | PN | "MANDIBLE ONCE FUSED, NOW BROKEN" | NO DATA | NO DATA | NOT OBSERVED | ||
JH 032 | 178 | 483 | M | B | P | PF | 4 | 8 | 2 | P | P | PF | A | A | PF | PNF | PNF | A | P | A | P | PF | PF | PF | P | 2 | 6 | P | 0 | PF | P | P | P | PF | A | A | PF | PNF | PNF | A | P | A | P | PF | PF | PF | P | 2 | NOT OBSERVED | 15 | PN | MOST OF BASICRANIUM FUSED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 033 | 184 | 365 | M | B | P | PF | 4 | 5 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 2 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 034 | 189 | 377 | M | B | P | A | 4 | 7 | 1 | P | P | A | A | A | A | PNF | PNF | A | A | P | P | PF | PF | PF | P | 1 | 8 | P | 0 | A | P | P | P | A | A | A | A | PNF | PNF | A | A | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 3 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 035 | 2 | 306 | F | B | P | PF | 1 | 7 | 2 | P | P | A | A | A | A | See Note | PNF | A | P | P | P | PF | PF | PF | P | 2 | 3 | P | 0 | PF | P | P | P | A | A | A | A | See Note | PNF | A | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 0 | Newborn | MANDIBLE WAS FUSED: NOW BROKEN | NO DATA | NO DATA | NOT OBSERVED | ||
JH 036 | 8 | Blank | F | B | A | PF | 2 | 2 | 0 | A | P | PNF | A | A | PF | PNF | A | A | A | P | P | PF | PF | PF | A | 2 | 2 | P | 0 | PF | A | P | P | PNF | A | A | PF | PNF | PNF | A | A | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 037 | 14 | 236 | F | B | P | PF | 0 | 0 | 2 | A | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | 0 | P | 0 | PF | A | A | P | PNF | A | A | Broken | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVABLE | 5 | IU | NO DATA | NO DATA | NOT OBSERVABLE | |||
JH 038 | 17 | Blank | F | B | P | PF | 4 | 4 | 2 | P | P | PNF | A | A | PNF | PF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 5 | P | 0 | PF | P | P | P | PF | A | A | PF | PF | PNF | A | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 14 | PN | ADOLF H SCHULTZ DRAWING INCLUDED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 039 | 44 | 298 | F | B | P | PF | 0 | 1 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 3 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 8 | IU | EXTRA MALLEUS | NO DATA | NO DATA | NOT OBSERVED | ||
JH 040 | 45 | Blank | F | B | P | PF | 0 | 5 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 7 | P | 0 | PF | P | P | P | PF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 0 | Newborn | POOR OSSIFICATION OF THE CALVARIA | NO DATA | NO DATA | NOT OBSERVED | ||
JH 041 | 53 | 440 | F | B | A | A | 2 | 4 | 0 | P | P | A | A | A | A | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 1 | P | 0 | A | P | P | A | A | A | A | A | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 12 | PN | WHOLE SKULL BADLY OSSIFIED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 042 | 57 | 366 | F | B | P | PF | 2 | 5 | 0 | P | P | PNF | A | A | PF | A | A | A | P | P | P | PF | PF | PF | P | 0 | 4 | P | 0 | PF | P | P | A | PNF | A | A | PF | PNF | A | A | P | P | P | PF | PNF | PF | P | 2 | NOT OBSERVED | 2 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 043 | 59 | Blank | F | B | P | PF | 0 | 0 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVABLE | 8 | IU | NO DATA | NO DATA | NOT OBSERVABLE | |||
JH 044 | 61 | 340 | F | B | A | A | 0 | 2 | 0 | P | P | PNF | A | A | A | PNF | PNF | A | A | P | P | PF | PF | PF | P | 0 | 0 | P | 0 | A | P | A | A | PNF | A | A | A | A | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 9 | IU | INCOMPLETE | NO DATA | NO DATA | NOT OBSERVED | ||
JH 045 | 63 | 340BUG!!! | F | B | P | PF | 0 | 1 | 0 | P | A | PF | A | A | PF | A | A | A | A | A | A | A | A | A | A | 0 | 1 | A | 0 | PF | A | A | A | PF | A | A | PF | A | A | A | A | A | A | A | A | A | A | 0 | NO BONE | 12 | PN | - | JH 05. BAD BONE. | NO DATA | NO DATA | NO BONE | |
JH 046 | 70 | 345 | F | B | P | PF | 0 | 8 | 1 | P | P | PF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 7 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 3 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 047 | 75 | 364 | F | B | P | PF | 1 | 7 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 5 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 0 | Newborn | NO DATA | NO DATA | NOT OBSERVED | |||
JH 048 | 84 | Blank | F | B | P | PF | 0 | 2 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVABLE | 8 | IU | NO DATA | NO DATA | NOT OBSERVABLE | |||
JH 049 | 86 | 341 | F | B | P | PF | 0 | 1 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 2 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 050 | 88 | 294 | F | B | A | PF | 0 | 2 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 051 | 101 | 290 | F | B | P | PF | 0 | 0 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PNF | P | 1 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 052 | 107 | Blank | F | B | P | PF | 0 | 0 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 053 | 118 | 311 | F | B | P | PF | 0 | 5 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PF | PF | P | 2 | NOT OBSERVED | 9 | IU | NASAL BONES FUSED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 054 | 120 | 252 | F | B | P | PF | 0 | 0 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PNF | P | 1 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PNF | P | 2 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 055 | 121 | 276 | F | B | P | PNF | 0 | 2 | 2 | P | P | PNF | A | A | PNF | A | PNF | P | P | P | P | PNF | PF | PF | P | 2 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | A | P | 1 | NOT OBSERVED | 6 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 056 | 122 | 313 | F | B | A | A | 0 | 0 | 1 | A | ? | A | A | A | A | A | A | A | A | A | A | A | A | A | A | 0 | 0 | P | 0 | A | A | A | ? | A | A | A | A | A | A | A | A | A | A | A | A | A | A | 0 | NO BONES | ? | ? | TWO FRONTALS FROM TWO SPECIMENS (SIDES IN DISPUTE) EAR OSSICLES WITH SMALL....(?) | NO DATA | NO DATA | NO BONES | ||
JH 057 | 127 | 307 | F | B | P | PF | 0 | 2 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 2 | NOT OBSERVED | 10 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 058 | 132 | 354 | F | B | P | PF | 1 | 8 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 4 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 059 | 149 | 290 | F | B | P | A | 0 | 0 | 1 | A | P | PNF | A | A | A | PNF | PNF | A | P | P | P | PF | PF | PNF | P | 1 | 0 | P | 0 | A | A | P | P | A | A | A | A | PNF | A | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 060 | 150 | 2825 | F | B | P | PF | 0 | 4 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 0 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVABLE | See Note | See Note | Age estimated as 8 months to Newborn | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 061 | 169 | 340 | F | B | P | PF | 2 | 3 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 8 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 0 | Newborn | NO DATA | NO DATA | NOT OBSERVED | |||
JH 062 | 172 | 283 | F | B | P | PF | 0 | 2 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 7 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 063 | 185 | 345 | F | B | P | PF | 1 | 4 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | A | A | A | P | 2 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | A | A | A | P | 0 | NOT OBSERVED | 10 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 064 | 190 | 331 | F | B | P | PF | 0 | 3 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 2 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 065 | 191 | 256 | F | B | P | PNF | 0 | 0 | 0 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | A | 0 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | A | 0 | NOT OBSERVED | 5-6 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 066 | 10 | 240 | M | W | P | PNF | 0 | 0 | 2 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PNF | A | P | P | PNF | A | A | A | PNF | PNF | P | P | P | P | PNF | A | PNF | P | 1 | NOT OBSERVED | 5 | IU | NO DATA | NODATA | NOT OBSERVED | |||
JH 067 | 20 | Blank | M | W | P | PF | 1 | 0 | 1 | P | P | A | A | A | PF | PNF | PNF | P | P | A | P | PF | PF | PF | P | 0 | 3 | P | 0 | PF | P | A | A | PNF | A | A | PF | A | PNF | A | P | A | P | PF | PF | PF | P | 0 | NOT OBSERVED | 0 | Newborn | Reported missing by JR 7/001 | NO DATA | NO DATA | NOT OBSERVED | ||
JH 068 | 40 | Blank | M | W | P | PF | 2 | 2 | 1 | A | P | PF | A | A | PF | PNF | PNF | A | A | A | P | PF | PF | PF | A | 2 | 2 | P | 0 | PF | A | A | P | PF | A | A | PF | PNF | "PF, Zygomatic" | A | A | A | P | PF | PF | PF | P | 1 | NOT OBSERVED | 2 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 069 | 48 | 340 | M | W | P | PNF | 1 | 4 | 1 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | 1 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 7 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 070 | 49 | 274 | M | W | P | PNF | 0 | 0 | 2 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 6-7 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 071 | 74 | 332 | M | W | P | PF | 1 | 2 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 10 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 072 | 77 | 336 | M | W | P | PF | 1 | 0 | 1 | P | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PF | PF | P | 2 | 1 | P | 0 | PF | P | P | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PF | PF | P | 2 | NOT OBSERVED | 10 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 073 | 89 | 344 | M | W | P | PF | 0 | 1 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PNF | P | 1 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 074 | 92 | 279 | M | W | P | PNF | 0 | 0 | 1 | P | P | PNF | A | A | PNF | PNF | PNF | P | A | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | A | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 6 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 075 | 105 | Blank | M | W | P | PNF | 0 | 0 | 2 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 6 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 076 | 108 | 280 | M | W | P | PF | 0 | 1 | 2 | P | P | A | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 1 | P | 0 | PF | A | A | P | PNF | A | A | PF | PNF | PNF | P | P | A | P | PF | PF | PF | A | 0 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 077 | 129 | 340 | M | W | P | PF | 2 | 5 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 5 | P | 0 | PF | P | A | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 1 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 078 | 131 | 364 | M | W | P | PNF | 2 | 2 | 2 | P | P | PNF | A | A | PNF | PNF | PNF | A | A | P | P | PF | PF | PF | P | 2 | 6 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 079 | 136 | 363 | M | W | P | PF | 0 | 6 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 080 | 138 | 355 | M | W | P | PF | 0 | 0 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 3 | PN | KERKRING'S CENTER OBSERVED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 081 | 141 | 347 | M | W | P | PF | 1 | 3 | 2 | P | P | PNF | A | A | PF | See Note | PNF | P | P | P | P | PF | PF | PF | P | 2 | 5 | P | 0 | PF | P | P | P | PNF | A | A | PF | See Note | PNF | A | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 2 | PN | MANDIBLE ONCE FUSED NOW BROKEN | NO DATA | NO DATA | NOT OBSERVED | ||
JH 082 | 143 | 326 | M | W | P | PF | 3 | 6 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 3 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 0 | Newborn | EXTRA MALLEUS INCLUDED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 083 | 146 | 320 | M | W | P | PF | 0 | 2 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 2 | P | 0 | PF | A | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 9 | IU | THREE PARIETAL FRAGMENTS | NO DATA | NO DATA | NOT OBSERVED | ||
JH 084 | 151 | 353 | M | W | A | PF | 3 | 4 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 4 | P | 0 | PF | A | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 3 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 085 | 156 | 364 | M | W | P | PF | 1 | 2 | 1 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 6 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 2 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 086 | 157 | 288 | M | W | P | PF | 1 | 2 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | 1 | P | 0 | PF | A | P | P | A | A | A | PF | PNF | PNF | A | P | P | P | PNF | PNF | A | P | 0 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 087 | 162 | 374 | M | W | P | PF | 2 | 4 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | A | P | P | PNF | PNF | PNF | P | 2 | 3 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | A | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 088 | 166 | 382 | M | W | P | PF | 0 | 0 | 1 | P | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | 1 | P | 0 | PF | P | P | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 4 | PN | MANY TOOTH FRAGMENTS | NO DATA | NO DATA | NOT OBSERVED | ||
JH 089 | 171 | 380 | M | W | P | PNF | 1 | 3 | 1 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | 4 | P | 0 | PNF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 10 | IU | NASAL BONES FUSED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 090 | 179 | Blank | M | W | P | PNF | 3 | 4 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | 7 | P | 0 | PNF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 3 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 091 | 186 | 373 | M | W | P | PF | 1 | 2 | 2 | P | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | 7 | P | 0 | PF | P | P | P | PF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 9 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 092 | 188 | Blank | M | W | P | PNF | 0 | 2 | 1 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PF | PF | PNF | P | 1 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NOT OBSERVED | 8 | IU | NO DATA | NO DATA | NOT OBSERVED | |||
JH 093 | 192 | 328 | M | W | P | PNF | 0 | 0 | 1 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 0 | NOT OBSERVED | 7 | IU | KERKRING'S CENTER OBSERVED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 094 | 13 | Blank | F | W | P | A | 0 | 0 | 2 | P | P | A | A | A | A | PNF | PNF | P | A | P | P | PF | PF | PF | P | 2 | 5 | P | 0 | A | P | P | P | A | A | A | A | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 0 | Newborn | TEETH FRAGMENTS | NO DATA | NO DATA | NOT OBSERVED | ||
JH 095 | 23 | 352 | F | W | P | PF | 4 | 8 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | NOT OBSERVED | 4 | PN | TYMPANIC MEMBRANE INTACT | NO DATA | NO DATA | NOT OBSERVED | ||
JH 096 | 43 | 268 | F | W | P | PNF | 0 | 0 | 1 | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PNF | P | P | P | PNF | A | A | PNF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | NOT OBSERVED | 5 | IU | ADOLF H SCHULTZ DRAWING INCLUDED | NO DATA | NO DATA | NOT OBSERVED | ||
JH 097 | 47 | 313 | F | W | P | PF | 0 | 0 | 0 | P | P | PNF | A | A | PF | PNF | PNF | P | P | A | P | PF | PF | PNF | P | 1 | 1 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | A | P | PF | PF | PNF | P | 0 | NOT OBSERVED | 8 | IU | ONE BONE FRAGMENT - SQUAMOUS TYPE | NO DATA | NO DATA | NOT OBSERVED | ||
JH 098 | 64 | 364 | F | W | P | PF | 0 | 3 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | A | PNF | P | P | P | P | PF | PF | PF | P | 1 | NOT OBSERVED | 3 | PN | NO DATA | NO DATA | NOT OBSERVED | |||
JH 099 | 95 | 350 | F | W | A | A | 0 | 0 | 0 | A | P | A | A | A | A | A | A | A | A | A | P | A | A | A | A | 0 | 0 | P | 0 | A | A | A | P | A | A | A | A | A | A | A | ?(BROKEN) | A | P | A | A | A | A | 0 | NO BONES | 4 | PN | HYDROCEPHALIC | NO DATA | NO DATA | NO BONES | ||
JH 100 | 100 | 365 | F | W | P | PF | 0 | 5 | 2 | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 2 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 1 | NO | 0 | Newborn | NO DATA | NO DATA | NOT OBSERVABLE | |||
JH 101 | 114 | 396 | F | W | P | PF | 3 | 3 | 0 | P | P | PNF | A | A | PF | See Noe | PNF | A | P | P | P | PF | PF | PF | P | 0 | 8 | P | 0 | PF | P | P | P | PNF | A | A | PF | See Note | PNF | A | P | P | P | PF | PF | PF | P | 0 | NO | 5 | PN | MANDIBLE ONCE FUSED NOW BROKEN | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 102 | 116 | 400 | F | W | P | PF | 0 | 0 | 2 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | 0 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 2 | NO | 2 | PN | TEETH NOT COUNTED | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 103 | 117 | 290 | F | W | P | A | 0 | 0 | 0 | A | P | A | A | A | A | A | PNF | A | A | A | P | PF | PF | PNF | A | 0 | 0 | P | 0 | A | A | A | P | A | A | A | A | A | PNF | A | P | A | P | PF | PF | PNF | P | 0 | NO | 7 | IU | TWO TOOTH BUDS | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 104 | 128 | 368 | F | W | P | PF | 0 | 0 | 2 | P | P | PF | A | A | PF | PF | PNF | A | P | P | P | PF | PF | PF | A | 2 | 0 | P | 0 | PF | P | P | P | PF | A | A | PF | PF | PNF | A | P | P | P | PF | PF | PF | A | 0 | NO | 5 | PN | TOOTH FRAGMENTS | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 105 | 134 | Blank | F | W | P | PF | 1 | 0 | 0 | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | 4 | P | 0 | PF | P | P | P | PNF | A | A | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NO | 9 | IU | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 106 | 148 | 290 | F | W | P | PNF | 2 | 0 | 0 | P | P | A | A | A | PNF | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | 0 | P | 0 | PNF | P | P | P | A | A | A | A | PNF | PNF | A | P | P | P | PNF | PNF | PNF | P | 0 | NO | 8 | IU | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 107 | 160 | 60 | F | W | P | PNF | 2 | 3 | 2 | P | P | PNF | P | A | PNF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 2 | 5 | P | 0 | PNF | P | P | P | PNF | P | A | PNF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NO | 2 | PN | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 108 | 167 | 372 | F | W | P | PF | 1 | 3 | 0 | P | P | PNF | P | P | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 1 | 2 | P | 0 | PF | P | P | P | PNF | P | P | PF | PNF | PNF | A | P | P | P | PF | PF | PF | P | 0 | NO | 1 | PN | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 109 | 168 | 316 | F | W | P | PF | 0 | 1 | 2 | P | P | PNF | P | A | PF | PNF | PNF | P | P | P | P | PNF | PF | PF | P | 2 | 3 | P | 0 | PF | P | P | P | PNF | P | A | PF | PNF | PNF | A | P | P | P | PNF | PF | PF | P | 0 | NO | 8 | IU | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 110 | 170 | 331 | F | W | P | PF | 0 | 3 | 2 | P | P | PNF | P | P | PF | PNF | PNF | P | P | P | P | A | PF | PF | P | 1 | 5 | P | 0 | PF | P | P | P | PNF | P | A | PF | PNF | PNF | P | P | P | P | PF | PF | PF | P | 0 | NO | 0 | Newborn | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 111 | 175 | 342 | F | W | A | PF | 0 | 1 | 2 | P | P | PNF | P | P | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 4 | A | 0 | PF | P | P | P | PNF | P | P | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 0 | NO | 10 | IU | EAR OSSICLES PRESENT - NO COUNT | NO DATA | NO DATA | NOT OBSERVABLE | ||
JH 112 | 194 | 317 | F | W | P | PF | 0 | 1 | 2 | P | P | PNF | P | P | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 2 | 0 | P | 0 | PF | P | P | P | PNF | P | P | PF | PNF | PNF | P | P | P | P | PNF | PNF | PNF | P | 0 | NO | 8 | IU | NO DATA | NO DATA | NOT OBSERVABLE | |||
Johns Hopkins Fetal Skull Collection (1918–1951) - The collection was begun by Adolph Hans Schultz (1891–1976) - fetal, stillbirths, newborns, and infants up to approximately one year of age. Collection of 112 specimens was transferred to the Cleveland Museum of Natural History on a permanent loan in 1973. |
2017
Childs Nerv Syst. 2017 Jun;33(6):909-914. doi: 10.1007/s00381-017-3406-1. Epub 2017 Apr 10. A comprehensive review of the anterior fontanelle: embryology, anatomy, and clinical considerations. D'Antoni AV1, Donaldson OI1, Schmidt C2, Macchi V3, De Caro R3, Oskouian RJ4, Loukas M5, Shane Tubbs R6. Author information Abstract PURPOSE: Fontanelles are a regular feature of infant development in which two segments of bone remain separated, leaving an area of fibrous membrane or a "soft spot" that acts to accommodate growth of the brain without compression by the skull. Of the six fontanelles in the human skull, the anterior fontanelle, located between the frontal and parietal bones, serves as an important anatomical diagnostic tool in the assessment of impairments of the skull and brain and allows access to the brain and ventricles in the infant. METHODS: Using a standard database search, we conducted a review of the anterior fontanelle, including its embryology, anatomy, pathology, and related surgical implications. CONCLUSIONS: The diagnostic value of the anterior fontanelle, through observation of its shape, size, and palpability, makes the area of significant clinical value. It is important that clinicians are aware of the features and associated pathologies of this area in their everyday practice. KEYWORDS: Cranial calvaria; Skull; Soft spot; Suture PMID: 28396968 DOI: 10.1007/s00381-017-3406-1
2016
The remodeling pattern of human mandibular alveolar bone during prenatal formation from 19 to 270mm CRL
Ann Anat. 2016 Feb 24;205:65-74. doi: 10.1016/j.aanat.2016.01.005. [Epub ahead of print]
Radlanski RJ1, Renz H2, Tsengelsaikhan N2, Schuster F2, Zimmermann CA2.
Abstract
The underlying mechanisms of human bone morphogenesis leading to a topologically specific shape remain unknown, despite increasing knowledge of the basic molecular aspects of bone formation and its regulation. The formation of the alveolar bone, which houses the dental primordia, and later the dental roots, may serve as a model to approach general questions of bone formation. Twenty-five heads of human embryos and fetuses (Radlanski-Collection, Berlin) ranging from 19mm to 270mm (crown-rump-length) CRL were prepared as histological serial sections. For each stage, virtual 3D-reconstructions were made in order to study the morphogenesis of the mandibular molar primordia with their surrounding bone. Special focus was given to recording the bone-remodeling pattern, as diagnosed from the histological sections. In early stages (19-31mm CRL) developing bone was characterized by appositional only. At 41, in the canine region, mm CRL bony extensions were found forming on the bottom of the trough. Besides general apposition, regions with resting surfaces were also found. At a fetal size of 53mm CRL, septa have developed and led to a compartment for canine development. Furthermore, one shared compartment for the incisor primordia and another shared compartment for the molars also developed. Moreover, the inner surfaces of the dental crypts showed resorption of bone. From this stage on, a general pattern became established such that the compartmentalizing ridges and septa between all of the dental primordia and the brims of the crypts were noted, and were due to appositional growth of bone, while the crypts enlarged on their inner surfaces by resorption. By 160mm CRL, the dental primordia were larger, and all of the bony septa had become reduced in size. The primordia for the permanent teeth became visible at 225mm CRL and shared the crypts of their corresponding deciduous primordia. Copyright © 2016 Elsevier GmbH. All rights reserved. KEYWORDS: 3D-reconstructions; Alveolar bone; Dental primordia; Human; Mandible
PMID 26921449
2015
Transcriptional analysis of human cranial compartments with different embryonic origins
Arch Oral Biol. 2015 Sep;60(9):1450-60. doi: 10.1016/j.archoralbio.2015.06.008. Epub 2015 Jul 2.
Homayounfar N1, Park SS2, Afsharinejad Z3, Bammler TK3, MacDonald JW3, Farin FM3, Mecham BH4, Cunningham ML5.
Abstract
OBJECTIVE: Previous investigations suggest that the embryonic origins of the calvarial tissues (neural crest or mesoderm) may account for the molecular mechanisms underlying sutural development. The aim of this study was to evaluate the differences in the gene expression of human cranial tissues and assess the presence of an expression signature reflecting their embryonic origins. METHODS: Using microarray technology, we investigated global gene expression of cells from the frontal and parietal bones and the metopic and sagittal intrasutural mesenchyme (ISM) of four human foetal calvaria. qRT-PCR of a selected group of genes was done to validate the microarray analysis. Paired comparison and correlation analyses were performed on microarray results. RESULTS: Of six paired comparisons, frontal and parietal compartments (distinct tissue types of calvaria, either bone or intrasutural mesenchyme) had the most different gene expression profiles despite being composed of the same tissue type (bone). Correlation analysis revealed two distinct gene expression profiles that separate frontal and metopic compartments from parietal and sagittal compartments. TFAP2A, TFAP2B, ICAM1, SULF1, TNC and FOXF2 were among differentially expressed genes. CONCLUSION: Transcriptional profiles of two groups of tissues, frontal and metopic compartments vs. parietal and sagittal compartments, suggest differences in proliferation, differentiation and extracellular matrix production. Our data suggest that in the second trimester of human foetal development, a gene expression signature of neural crest origin still exists in frontal and metopic compartments while gene expression of parietal and sagittal compartments is more similar to mesoderm. Copyright © 2015 Elsevier Ltd. All rights reserved. KEYWORDS: Cranial suture; Differentiation; Extracellular matrix; Mesoderm; Neural crest; Proliferation PMID 26188427
2014
Direct Brain Recordings Reveal Impaired Neural Function in Infants With Single-Suture Craniosynostosis: A Future Modality for Guiding Management?
J Craniofac Surg. 2014 Dec 19. [Epub ahead of print]
Hashim PW1, Brooks ED, Persing JA, Reuman H, Naples A, Travieso R, Terner J, Steinbacher D, Landi N, Mayes L, McPartland JC.
Abstract
BACKGROUND: Patients with single-suture craniosynostosis (SSC) are at an elevated risk for long-term learning disabilities. Such adverse outcomes indicate that the early development of neural processing in SSC may be abnormal. At present, however, the precise functional derangements of the developing brain remain largely unknown. Event-related potentials (ERPs) are a form of noninvasive neuroimaging that provide direct measurements of cortical activity and have shown value in predicting long-term cognitive functioning. The current study used ERPs to examine auditory processing in infants with SSC to help clarify the developmental onset of delays in this population. METHODS: Fifteen infants with untreated SSC and 23 typically developing controls were evaluated. ERPs were recorded during the presentation of speech sounds. Analyses focused on the P150 and N450 components of auditory processing. RESULTS: Infants with SSC demonstrated attenuated P150 amplitudes relative to typically developing controls. No differences in the N450 component were identified between untreated SSC and controls. CONCLUSIONS: Infants with untreated SSC demonstrate abnormal speech sound processing. Atypicalities are detectable as early as 6 months of age and may represent precursors to long-term language delay. Electrophysiological assessments provide a precise examination of neural processing in SSC and hold potential as a future modality to examine the effects of surgical treatment on brain development.
PMID 25534054
2012
Paleontological and developmental evidence resolve the homology and dual embryonic origin of a mammalian skull bone, the interparietal
Proc Natl Acad Sci U S A. 2012 Aug 28;109(35):14075-80. doi: 10.1073/pnas.1208693109. Epub 2012 Aug 13.
Koyabu D, Maier W, Sánchez-Villagra MR. Source Palaeontological Institute and Museum, University of Zürich, 8006 Zürich, Switzerland. daisuke.koyabu@pim.uzh.ch
Abstract
The homologies of mammalian skull elements are now fairly well established, except for the controversial interparietal bone. A previous experimental study reported an intriguing mixed origin of the interparietal: the medial portion being derived from the neural crest cells, whereas the lateral portion from the mesoderm. The evolutionary history of such mixed origin remains unresolved, and contradictory reports on the presence or absence and developmental patterns of the interparietal among mammals have complicated the question of its homology. Here we provide an alternative perspective on the evolutionary identity of the interparietal, based on a comprehensive study across more than 300 extinct and extant taxa, integrating embryological and paleontological data. Although the interparietal has been regarded as being lost in various lineages, our investigation on embryos demonstrates its presence in all extant mammalian "orders." The generally accepted paradigm has regarded the interparietal as consisting of two elements that are homologized to the postparietals of basal amniotes. The tabular bones have been postulated as being lost during the rise of modern mammals. However, our results demonstrate that the interparietal consists not of two but of four elements. We propose that the tabulars of basal amniotes are conserved as the lateral interparietal elements, which quickly fuse to the medial elements at the embryonic stage, and that the postparietals are homologous to the medial elements. Hence, the dual developmental origin of the mammalian interparietal can be explained as the evolutionary consequence of the fusion between the crest-derived "postparietals" and the mesoderm-derived "tabulars."
PMID 22891324
The BMP Ligand Gdf6 Prevents Differentiation of Coronal Suture Mesenchyme in Early Cranial Development
PLoS One. 2012;7(5):e36789. Epub 2012 May 31.
Clendenning DE, Mortlock DP. Source Department of Molecular Physiology and Biophysics, Center for Human Genetics Research, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America.
Abstract
Growth Differentiation Factor-6 (Gdf6) is a member of the Bone Morphogenetic Protein (BMP) family of secreted signaling molecules. Previous studies have shown that Gdf6 plays a role in formation of a diverse subset of skeletal joints. In mice, loss of Gdf6 results in fusion of the coronal suture, the intramembranous joint that separates the frontal and parietal bones. Although the role of GDFs in the development of cartilaginous limb joints has been studied, limb joints are developmentally quite distinct from cranial sutures and how Gdf6 controls suture formation has remained unclear. In this study we show that coronal suture fusion in the Gdf6-/- mouse is due to accelerated differentiation of suture mesenchyme, prior to the onset of calvarial ossification. Gdf6 is expressed in the mouse frontal bone primordia from embryonic day (E) 10.5 through 12.5. In the Gdf6-/- embryo, the coronal suture fuses prematurely and concurrently with the initiation of osteogenesis in the cranial bones. Alkaline phosphatase (ALP) activity and Runx2 expression assays both showed that the suture width is reduced in Gdf6+/- embryos and is completely absent in Gdf6-/- embryos by E12.5. ALP activity is also increased in the suture mesenchyme of Gdf6+/- embryos compared to wild-type. This suggests Gdf6 delays differentiation of the mesenchyme occupying the suture, prior to the onset of ossification. Therefore, although BMPs are known to promote bone formation, Gdf6 plays an inhibitory role to prevent the osteogenic differentiation of the coronal suture mesenchyme.
PMID 22693558
The human calvaria: a review of embryology, anatomy, pathology, and molecular development
Childs Nerv Syst. 2012 Jan;28(1):23-31. Epub 2011 Nov 27.
Tubbs RS, Bosmia AN, Cohen-Gadol AA. Source Department of Neurosurgery, Children's Hospital, Ambulatory Care Center, 1600 7th Avenue South, Birmingham, AL 35294, USA. shane.tubbs@chsys.org
Abstract
INTRODUCTION: The human skull is a complex structure that deserves continued study. Few studies have directed their attention to the development, pathology, and molecular formation of the human calvaria. MATERIALS AND METHODS: A review of the medical literature using standard search engines was performed to locate studies regarding the human calvaria. RESULTS: The formation of the human calvaria is a complex interaction between bony and meningeal elements. Derailment of these interactions may result in deformation of this part of the skull. CONCLUSIONS: Knowledge of the anatomy, formation, and pathology of the human calvaria will be of use to the clinician that treats skull diseases. With an increased understanding of genetic and molecular biology, treatment paradigms for calvarial issues may change.
PMID 22120469
Principles of cranial base ossification in humans and rats
Acta Otolaryngol. 2012 Apr;132(4):349-54. doi: 10.3109/00016489.2011.642814. Epub 2011 Dec 27.
Santaolalla-Montoya F, Martinez-Ibargüen A, Sánchez-Fernández JM, Sánchez-del-Rey A. Source Otorhinolaryngology Department, School of Medicine, University of the Basque Country, Spain. Francisco.santaolalla@ehu.es Abstract CONCLUSIONS: 1. The principle of bilateral symmetry depends on the chordal cartilage that is the keystone in cranial base ossification in rats and humans, due to its anatomical situation and for the production of the chordin protein that regulates the bone morphogenetic protein BMP-7. 2. In humans and in rats, foramen lacerum closure follows a line of intramembranous ossification that depends on BMP-7, regulated by the first branchial pouch. 3. The cranial base ossification patterns and centres are similar in humans and in rats, except in the otic capsule, palate and the lateral pterygoid plate. 4. The neural crest may induce cranial ossification through the cranial nerves. OBJECTIVES: To study the patterns of cranial base ossification in humans and in rats, considering the chordal cartilage, and the otic, nasal and orbit capsules, as well as the participation of the branchial arches and pouches. METHODS: This was a light microscopy study of human fetal specimens obtained from spontaneous abortions with the following crown-rump-lengths (crl) 45, 74, 90, 134, 145 and 270 mm, and a 1-day-old neonate (360 mm crl), who had died of sudden death syndrome. We also examined Webster albino rat embryos of 16, 18 and 20 days of gestation and a postnatal series of rats 8 h and 1, 3, 4, 6, 7, 10 and 13 days old, as well as adult animals. RESULTS: In the 45 mm human fetus, the chordal cartilage with the nasal, otic and orbit capsules initiates cranial base ossification. Foramen lacerum closure begins in the 16-day-old rat embryo, following a line of membranous ossification between the external pterygoid process and the lateral alisphenoidal wing at ovalis foramen level. This is not a timing symmetrical process, which may persist until the 10th postnatal day in the rat. In the human fetus of 74 mm, the foramen lacerum space is closed by a membranous fusion ossification between the chordal cartilage and otic capsule, finishing at the 270 mm specimen. Endochondral ossification of the human otic capsule first appeared in the 145 mm (18 weeks) fetal specimen with four ossifying centres. The rat otic cartilaginous capsule showed rapid endochondral ossification, in the third and fourth postnatal day specimens.
PMID 22201370
http://informahealthcare.com/doi/abs/10.3109/00016489.2011.642814
2011
Morphological and morphometric study on sphenoid and basioccipital ossification in normal human fetuses
Congenit Anom (Kyoto). 2011 Sep;51(3):138-48. doi: 10.1111/j.1741-4520.2011.00322.x.
Zhang Q, Wang H, Udagawa J, Otani H. Source Department of Developmental Biology, Shimane University, Izumo, Japan.
Abstract
Congenital anomalies of the brain frequently correspond to cranial base anomalies, and a detailed description of morphology and individual variations in the developing cranial base is of clinical importance for diagnosing anomalies. Development of the human cranial base has been studied using dissection, computed tomography, and magnetic resonance imaging, each of which has advantages and disadvantages. We here examined development of the normal human fetal cranial base using bone staining, which allows for direct observation of the ossification centers and precise three-dimensional measurements. We observed alizarin red S-stained sphenoids and basiocciputs of 22 normal formalin-fixed human fetuses with crown-rump lengths (CRL) of 115-175 mm. We defined landmarks and measured sphenoids and basiocciputs using a fine caliper. Growth patterns of these ossifying bones were obtained, and we found similarities and differences among the growth patterns. We also observed individual variations in the ossification patterns, in particular, single- or double-ossification center patterns for the basisphenoid. The orbitosphenoid and basisphenoid widths and ratios of the widths to the total cranial base width were significantly different between the two pattern groups, whereas the other measurements and their ratios to the total cranial base did not differ between the groups. We measured the cerebrum and pons in different sets of 22 human fetuses with CRLs of 105-186 mm and found close relationships with the development of corresponding parts of the cranial base. The results contribute to the quantitative and qualitative information about the growth patterns and variations during human fetal cranial base development. © 2011 The Authors. Congenital Anomalies © 2011 Japanese Teratology Society.
PMID 21848997
Modeling of the human fetal skull base growth: interest in new volumetrics morphometric tools
Early Hum Dev. 2011 Apr;87(4):239-45. doi: 10.1016/j.earlhumdev.2011.01.022.
Herlin C, Largey A, deMatteï C, Daurès JP, Bigorre M, Captier G. Source Craniofacial and Plastic Pediatric Surgery Unit, Lapeyronie Hospital, Montpellier, 371 Av Doyen Gaston Giraud, 34 295 Montpellier, France. christian.herl@free.fr Abstract BACKGROUND: Research on the skull base is important to improve our understanding of the growth and development of the modern human skull. To study the growth of the human fetal skull base, we assessed a new geometric morphometric tool, which does not require the use of bone landmarks. MATERIAL AND METHODS: Seven dry fetal skulls of an estimated gestational age ranging from 15 to 27 weeks were studied. Each skull was scanned using a standard CT scan and the image sets were post-processed to extract volumetric data by segmenting the skull base into predefined regions of interest. Our method of analysis was based on the inertial properties of reconstructed volumes. RESULTS: The volumetric study of the skulls highlighted an asynchronous speed of growth between the pre and post-chordal parts of the skull base whose preferential growth are in the vertical and horizontal planes. We also found different speeds of growth in the pre-chordal part depending on the type of ossification (endochondral or membranous). The overall shape of the skull base bones were preserved during the period studied except for the petrous pyramids. The expansion of bone parts was isometric with reference to a central point that was located at the intrasphenoidal synchondrosis. Finally, the analysis of the basicranial angles corroborated data from the literature in the sagittal plane and allowed their study also in the frontal and horizontal planes. CONCLUSIONS: This three-dimensional volumetric approach is a necessary complement to studies that are performed in the sagittal plane and are based on the identification of landmarks. The geometric morphometric method used by authors permitted to obtain original informations on the growth kinetics and bone tridimensional movements of the human fetal skull base.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID 21300487
2010
Design and construction of a brain phantom to simulate neonatal MR images
Comput Med Imaging Graph. 2010 Dec 10. [Epub ahead of print]
Kazemi K, Moghaddam HA, Grebe R, Gondry-Jouet C, Wallois F.
Department of Electrical and Electronics Engineering, Shiraz University of Technology, Shiraz, Iran; GRAMFC EA 4293, Faculty of Medicine, University of Picardie Jules Verne, 80036 Amiens, France. Abstract This paper presents the design and construction of a 3D digital neonatal neurocranial phantom and its application for the simulation of brain magnetic resonance (MR) images. Commonly used digital brain phantoms (e.g. BrainWeb) are based on the adult brain. With the growing interest in computer-aided methods for neonatal MR image processing, there is a growing demand a digital phantom and brain MR image simulator especially for the neonatal brains. This is due to the pronounced differences between adult and neonatal brains not only in terms of size but also, more importantly, in terms of geometrical proportions and the need to subdivide white matter into two different tissue types in neonates. Therefore the neonatal brain phantom created in the here presented work consists of 9 different tissue types: skin, fat, muscle, skull, dura mater, gray matter, myelinated white matter, nonmyelinated white matter and cerebrospinal fluid. Each voxel has a vector consisting of 9 components, one for each of these nine tissue types. This digital phantom can be used to map simulated magnetic resonance signal intensities resulting in simulated MR images of the newborns head. These images with controlled degradation of the image data present a representative, reproducible data set ideal for development and evaluation of neonatal MRI analysis methods, e.g. segmentation and registration algorithms.
Copyright © 2010 Elsevier Ltd. All rights reserved. PMID 21146956
Fibroblast growth factor receptor signaling crosstalk in skeletogenesis
Sci Signal. 2010 Nov 2;3(146):re9.
Miraoui H, Marie PJ.
Laboratory of Osteoblast Biology and Pathology, INSERM UMR606 and University Paris Diderot, Paris 75475, Cedex 10, France. Abstract Fibroblast growth factors (FGFs) play important roles in the control of embryonic and postnatal skeletal development by activating signaling through FGF receptors (FGFRs). Germline gain-of-function mutations in FGFR constitutively activate FGFR signaling, causing chondrocyte and osteoblast dysfunctions that result in skeletal dysplasias. Crosstalk between the FGFR pathway and other signaling cascades controls skeletal precursor cell differentiation. Genetic analyses revealed that the interplay of WNT and FGFR1 determines the fate and differentiation of mesenchymal stem cells during mouse craniofacial skeletogenesis. Additionally, interactions between FGFR signaling and other receptor tyrosine kinase networks, such as those mediated by the epidermal growth factor receptor and platelet-derived growth factor receptor α, were associated with excessive osteoblast differentiation and bone formation in the human skeletal dysplasia called craniosynostosis, which is a disorder of skull development. We review the roles of FGFR signaling and its crosstalk with other pathways in controlling skeletal cell fate and discuss how this crosstalk could be pharmacologically targeted to correct the abnormal cell phenotype in skeletal dysplasias caused by aberrant FGFR signaling.
PMID 21045207 The BMP antagonist noggin regulates cranial suture fusion STEPHEN M. WARREN, LISA J. BRUNET, RICHARD M. HARLAND, ARIS N.,ECONOMIDES & MICHAEL T. LONGAKER
"During skull development, the cranial connective tissue framework undergoes intramembranous ossification to form skull bones (calvaria). As the calvarial bones advance to envelop the brain, fibrous sutures form between the calvarial plates. Expansion of the brain is coupled with calvarial growth through a series of tissue interactions within the cranial suture complex. Craniosynostosis, or premature cranial suture fusion, results in an abnormal skull shape, blindness and mental retardation. Recent studies have demonstrated that gain-of-function mutations in fibroblast growth factor receptors ( fgfr ) are associated with syndromic forms of craniosynostosis. Noggin, an antagonist of bone morphogenetic proteins (BMPs), is required for embryonic neural tube, somites and skeleton patterning. Here we show that noggin is expressed postnatally in the suture mesenchyme of patent, but not fusing, cranial sutures, and that noggin expression is suppressed by FGF2 and syndromic fgfr signalling. Since noggin misexpression prevents cranial suture fusion in vitro and in vivo , we suggest that syndromic fgfr -mediated craniosynostoses may be the result of inappropriate downregulation of noggin expression."
2009
Pediatric craniofacial surgery for craniosynostosis: Our experience and current concepts: Part -1
J Pediatr Neurosci. 2009 Jul;4(2):86-99. doi: 10.4103/1817-1745.57327.
Anantheswar YN, Venkataramana NK. Source Department of Plastic Surgery, Manipal Hospital, Kengeri, Bangalore, India.
Abstract
Craniostenosis is a disease characterized by untimely fusion of cranial sutures resulting in a variety of craniofacial deformities and neurological sequelae due to alteration in cranial volume and restriction of brain growth. This involves vault sutures predominantly, but cranial base is not immune. Association with a variety of syndromes makes the management decision complex. These children need careful evaluation by multiple specialists to have strategic treatment options. Parental counseling is an important and integral part of the treatment. Recent advancements in the surgical techniques and concept of team approach have significantly enhanced the safety and outcome of these children. We had an opportunity of treating 57 children with craniostenosis in the last 15 years at our craniofacial service. Out of them, 40 were nonsyndromic and 17 were syndromic variety. We describe our successful results along with individualized operative technical modifications adopted based on the current understanding of the disease.
PMID 21887189
Pediatric craniofacial surgery for craniosynostosis: Our experience and current concepts: Parts -2
J Pediatr Neurosci. 2009 Jul;4(2):100-7. doi: 10.4103/1817-1745.57328.
Anantheswar YN, Venkataramana NK. Source Department of Plastic Surgery, Manipal Hospital, Kengeri, Bangalore, India.
Abstract
Craniostenosis associated with other syndromes poses several clinical and management challenges. Involvement of cranial, facial, and systemic defects with an underlying genetic abnormality needs comprehensive understanding, to plan appropriate and safe treatment modalities. Often, these children require staging involving several/multiple surgical procedures. Unsuccessful outcomes and retrusion of the deformities are common in comparison to the nonsyndromic variety. We present our experience in treating 17 children with syndromic craniostenosis with successful outcomes and minimal morbidity. We also describe the principles behind the staging. Technology adoption has improved the results as well as reduced the complications to an acceptable minimum.
PMID 21887190
2008
Development and tissue origins of the mammalian cranial base
Dev Biol. 2008 Oct 1;322(1):121-32. doi: 10.1016/j.ydbio.2008.07.016. Epub 2008 Jul 22.
McBratney-Owen B, Iseki S, Bamforth SD, Olsen BR, Morriss-Kay GM. Source Harvard School of Dental Medicine, Department of Developmental Biology, 190 Longwood Avenue, Boston, MA, 02115, USA. bmcbratneyowen@post.harvard.edu Abstract The vertebrate cranial base is a complex structure composed of bone, cartilage and other connective tissues underlying the brain; it is intimately connected with development of the face and cranial vault. Despite its central importance in craniofacial development, morphogenesis and tissue origins of the cranial base have not been studied in detail in the mouse, an important model organism. We describe here the location and time of appearance of the cartilages of the chondrocranium. We also examine the tissue origins of the mouse cranial base using a neural crest cell lineage cell marker, Wnt1-Cre/R26R, and a mesoderm lineage cell marker, Mesp1-Cre/R26R. The chondrocranium develops between E11 and E16 in the mouse, beginning with development of the caudal (occipital) chondrocranium, followed by chondrogenesis rostrally to form the nasal capsule, and finally fusion of these two parts via the midline central stem and the lateral struts of the vault cartilages. X-Gal staining of transgenic mice from E8.0 to 10 days post-natal showed that neural crest cells contribute to all of the cartilages that form the ethmoid, presphenoid, and basisphenoid bones with the exception of the hypochiasmatic cartilages. The basioccipital bone and non-squamous parts of the temporal bones are mesoderm derived. Therefore the prechordal head is mostly composed of neural crest-derived tissues, as predicted by the New Head Hypothesis. However, the anterior location of the mesoderm-derived hypochiasmatic cartilages, which are closely linked with the extra-ocular muscles, suggests that some tissues associated with the visual apparatus may have evolved independently of the rest of the "New Head".
PMID 18680740
Three-dimensional ontogenetic shape changes in the human cranium during the fetal period
J Anat. 2008 May;212(5):627-35. doi: 10.1111/j.1469-7580.2008.00884.x.
Morimoto N, Ogihara N, Katayama K, Shiota K. Source Laboratory of Physical Anthropology, Graduate School of Science, Kyoto University, Japan. morimoto@aim.uzh.ch <morimoto@aim.uzh.ch> Abstract Knowledge of the pattern of human craniofacial development in the fetal period is important for understanding the mechanisms underlying the emergence of variations in human craniofacial morphology. However, the precise character of the prenatal ontogenetic development of the human cranium has yet to be fully established. This study investigates ontogenetic changes in cranial shape in the fetal period, as exhibited in Japanese fetal specimens housed at Kyoto University. A total of 31 human fetal specimens aged from approximately 8 to 42 weeks of gestation underwent helical computed tomographic scanning, and 68 landmarks were digitized on the internal and external surfaces of the extracted crania. Ontogenetic shape change was then analyzed cross-sectionally and three-dimensionally using a geometric morphometric technique. The results of the present study are generally consistent with previously reported findings. It was found that during the prenatal ontogenetic process, the growth rate of the length of the cranium is greater than that of the width and height, and the growth rate of the length of the posterior cranial base is smaller than that of the anterior cranial base. Furthermore, it was observed that the change in shape of the human viscerocranium is smaller than that of the neurocranium during the fetal period, and that concurrently the basicranium extends by approximately 8 degrees due to the relative elevation of the basilar and lateral parts of occipital bone. These specific growth-related changes are the opposite of those reported for the postnatal period. Our findings therefore indicate that the allometric pattern of the human cranium is not a simple continuous transformation, but changes drastically from before to after birth.
PMID 18430090
2000
MR, CT, and plain film imaging of the developing skull base in fetal specimens
AJNR Am J Neuroradiol. 2000 Oct;21(9):1699-706.
Nemzek WR, Brodie HA, Hecht ST, Chong BW, Babcook CJ, Seibert JA. Source Department of Radiology, University of California, Davis Medical Center, Sacramento 95817, USA. Abstract BACKGROUND AND PURPOSE: The developing fetal skull base has previously been studied via dissection and low-resolution CT. Most of the central skull base develops from endochondral ossification through an intermediary chondrocranium. We traced the development of the normal fetal skull base by using plain radiography, MR imaging, and CT. METHODS: Twenty-nine formalin-fixed fetal specimens ranging from 9 to 24 weeks' gestational age were examined with mammographic plain radiography, CT, and MR imaging. Skull base development and ossification were assessed. RESULTS: The postsphenoid cartilages enclose the pituitary and fuse to form the basisphenoid, from which the sella turcica and the posterior body of the sphenoid bone originate. The presphenoid cartilages will form the anterior body of the sphenoid bone. Portions of the presphenoid cartilage give rise to the mesethmoid cartilage, which forms the central portion of the anterior skull base. Ossification begins in the occipital bone (12 weeks) and progresses anteriorly. The postsphenoid (14 weeks) and then the presphenoid portion (17 weeks) of the sphenoid bone ossify. Ossification is seen laterally (16 weeks) in the orbitosphenoid, which contributes to the lesser wing of the sphenoid, and the alisphenoid (15 weeks), which forms the greater wing. CONCLUSION: MR imaging can show early progressive ossification of the cartilaginous skull base and its relation to intracranial structures. The study of fetal developmental anatomy may lead to a better understanding of abnormalities of the skull base. PMID 11039353
Historic
1937
The Development of the Vertebrate Skull. G. R. de Beer, M.A., D.Sc., F.L.S. 552 pp., illust., $9.50. McAinsh, Toronto, 1937.
Anyone who has ever attempted even in a general way to compare the skull of man with that of lower mammals or reptiles and to determine the morphology of the different parts will realize the thorny and difficult field into which this book ventures. And it enters this field in no casual way but to a depth of 515 closely printed pages with abundant simple and clear illustrations. ,
The book is divided into three parts. The first deals with some general questions of the nature of cartilage and bone and goes on to review Goethe’s theory that the skull is made up of several fused vertebre. This theory of course has not stood the test of time but out of it arose the recognition of the segmental structure of the posterior end of. the skull.