The Development of the Human Intervertebral Disc
Peter Ghosh in The Biology of the Intervertebral Disc, 2019
In embryos of 2 mm or more C.R.L. (crown to rump length) (3 weeks gestation) a continuous mesenchymal column is formed around the cylindrical notochord. This is said to be due to the active proliferation and medial migration of somitic mesoderm from the ventromedial portions of the somites — termed sclerotomes.19 The notochord becomes separated from the gut tube and aorta ventrally and from the neural tube dorsally, as mesenchyme appears around it. The column appears first cranially and, at a later stage, caudally.16Neural processes appear as condensations of the somitic mesenchyme at each side of the neural tube. These extend dorsally from the continuous column around the notochord. According to Verbout,18 the loose axial mesenchyme, which develops first around the notochord, differs morphogenetically from the somitic mesenchyme and may not be initially derived from it. However, “commissural” communications are later established with the somitic mesoderm on each side. The continuous mesenchymal column thus formed around the notochord constitutes the anlagen of the vertebral bodies and intervertebral discs.
Cell Recruitment for Intervertebral Disc
Raquel M. Gonçalves, Mário Adolfo Barbosa in Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
An important aspect that, together with other factors, might contribute to IVD degeneration is the progressive loss of notochordal cells. The NP tissue derives from the endoderm, being a remnant of the notochord (Roberts et al. 2006). Depending on the species, the notochord cells may persist to adulthood. Many animal species retain the presence of these cells (Hunter, Matyas, and Duncan 2004); however, in humans, the number of notochordal cells decreases drastically following birth, being nonidentifiable after 4 years (Roberts et al. 2006). Still, the presence or loss of notochordal cells in humans remains debatable, as the presence of these cells was demonstrated in human adult discs (Weiler et al. 2010). The loss or decrease of notochordal cells in IVD tissue might have implications on proteoglycan synthesis rate and distribution, therefore representing a key factor in the IVD degeneration process (Cappello et al. 2006).
Prenatal Development of the Facial Skeleton
D. Dixon Andrew, A.N. Hoyte David, Ronning Olli in Fundamentals of Craniofacial Growth, 2017
One of the two zones that does not become infiltrated by mesenchymal cells is the small, circular prochordal plate that lies toward one end of the elongating embryonic disc, in front of the developing neural tube. The plate denotes the site of the future oropharyngeal membrane where ectoderm and endoderm remain in intimate contact, forming a delicate partition between the primitive mouth cavity and the foregut. The neural tube has elaborated as a sinking-in of a more elementary neural plate, a longitudinal strip of ectoderm, induced by the axially placed notochordal process beneath it to differentiate into the neuroectoderm, as the first essential step in an initially simple but later complex sequence of events that will lead in due time to the completion of the definitive central nervous system. Induction has been defined as operable when one cell population effects a change in the behavior of another group of cells in a developmentally significant way (Holtfreter, 1968). The notochord plays another, coincidental role, for it designates for the first time the right and left sides of the embryo. Thus the prochordal region may be said to occupy a cephalic or cranial position in the rapidly growing embryonic disc.
Focal Pachymeningitis Induced Papilloedema as an Early Manifestation of Relapsing Polychondritis
Published in Neuro-Ophthalmology, 2023
Majda Rachdi, Abraham J. Beun, Stelianos Kampouridis, François Willermain, Tom Buelens
The exact aetiology of RPC remains currently unknown, but it is considered to involve genetic predisposition and both the humoral and cell-mediated immune systems.1,17 One study that examined the immunogenetics of RPC identified human leukocyte antigen (HLA)-DR4 as the major risk allele for RPC.18 In addition to genetic susceptibility, circulating antibodies against several types of collagen (mainly collagens II, IX, and XI) have been detected, as well as against other cartilage proteins, such as cartilage matrix protein (or matrilin-1) and cartilage oligomeric matrix proteins.1,17,19 Up to one-third of patients with RPC present with other autoimmune disease, whether this association with other diseases is purely coincidental or representative of a shared genetic predisposition is currently unknown.16,19 Nervous system involvement is uncommon, especially at disease onset, and may be related to vasculitis20 or meningoencephalitis.21,22 It has also been speculated that remnants of the notochord could serve as antigens, or that the central nervous system may contain an antigen distinct from collagen.23
Transgenic zebrafish larvae as a non-rodent alternative model to assess pro-inflammatory (neutrophil) responses to nanomaterials
Published in Nanotoxicology, 2022
Suzanne Gillies, Rachel Verdon, Vicki Stone, David M. Brown, Theodore Henry, Lang Tran, Carl Tucker, Adriano G. Rossi, Charles R. Tyler, Helinor J. Johnston
Zebrafish larvae (3 dpf) were anesthetized in 4.2% tricaine (MS-222, Sigma-Aldrich), in E3 medium (adjusted to pH 7) for 15 min. Anesthetized larvae were then placed onto a clean glass microscope slide (Fisher-Scientific, UK) on the stage of a Leica M205 FCA fluorescence stereomicroscope. The larvae were manipulated into a right lateral recumbent position, using a superfine eyelash tool (Agar Scientific, UK). Using a sterile #23 scalpel blade (Swann-Morton, UK), the tail fins of the larvae were transected distally from the tip of the notochord to induce a moderate injury (Figure S1). The larvae were then imaged in a bright field and with an EGFP filter (488 nm), using a Leica DFC7000 T digital color camera connected to the Leica M205 FCA microscope. Larvae were imaged again at 4, 6, 8, 24, and 48 h post-injury.
Intrasellar hemorrhagic chordoma masquerading as pituitary apoplexy: case report and review of the literature
Published in British Journal of Neurosurgery, 2021
Boyi Li, Michael G. Kim, Jose F. Dominguez, Eric Feldstein, George Kleinman, Fawaz Al-Mufti, Matthew Kim, Simon Hanft
Chordomas are neoplasms arising from the remnants of the embryological notochord.1 They account for approximately 1% of intracranial tumors, with 35% arising from the skull base, 50% from the sacrococcygeal region, and 15% from the vertebrae.2,3 They are generally centrally located, expansile soft tissue lesions often causing lytic bone destruction.1 Clinical presentation varies based on location. For clival chordomas, symptoms typically include headache and progressive neurological deficits, such as cranial neuropathies (most commonly manifesting as diplopia), over weeks to months due to slow invasion into local structures of the skull base.2,4 Hemorrhagic presentation is exceedingly rare. Here we report a case of apoplectic intrasellar chordoma in an adult male, which presented similarly to pituitary apoplexy.
Related Knowledge Centers
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