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Comparative Anatomy and Physiology of the Mammalian Eye
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
The collagen of the vitreous measures 80 to 160 Å and has lacks obvious banding periodicity.121 This is unlike any other collagen and supports its neuroectodermal origin. The vitreous collagen is firmly anchored at the optic nerve, the posterior lens capsule, and the pars plana of the ciliary body. Hyaluronic acid, a glycosaminoglycan with a negative charge and a high affinity for water, is in highest concentration, like collagen and hyalocytes, in the peripheral vitreous.120 The concentrations of collagen and mucopolysaccharide vary between species, evident by the fluid vitreous of the owl monkey and the gel vitreous of humans (Table 4).121
Vitreoretinal
Published in Mostafa Khalil, Omar Kouli, The Duke Elder Exam of Ophthalmology, 2019
This is an avascular fibrocellular sheet or membrane that develops on the surface of the retina. It is more common in female patients. These arise from proliferation of RPE, glial cells or hyalocytes on the surface of the retina. Contracture on the retina leads to problems such as elevation of the retina and CMO.
Body Fluids
Published in Sarah Armstrong, Barry Clifton, Lionel Davis, Primary FRCA in a Box, 2019
Sarah Armstrong, Barry Clifton, Lionel Davis
VitreousContains gelatin-like protein – gives eye its spherical shapeContains phagocytes to remove unwanted debris in the visual field and hyalocytesHelps to keep the retina in placeReduced by mannitol
Hyalocyte functions and immunology
Published in Expert Review of Ophthalmology, 2022
Stefaniya K Boneva, Julian Wolf, Peter Wieghofer, J Sebag, Clemens AK Lange
Hyalocytes represent the resident myeloid cell population of the vitreous body exhibiting various properties during development, in health, and in disease [106]. They appear to be important during embryogenesis by inducing regression of the fetal vitreous vasculature, as well as in the adult for macromolecule metabolism, immune privilege and surveillance, and phagocytic activity that protects the eye from infection and other exogenous threats. Hyalocyte participation in inflammation may play an important role in autoimmune, neurodegenerative, and proliferative diseases (see article 3 in this series [3]). While the exact mechanisms by which hyalocytes mediate beneficial effects then switch to deleterious effects are currently unknown, recent research strongly indicates that this cell population is capable of being both promoters of healthy homeostasis and participants in disease.
Hyalocyte origin, structure, and imaging
Published in Expert Review of Ophthalmology, 2022
Peter Wieghofer, Michael Engelbert, Toco YP Chui, Richard B Rosen, Taiji Sakamoto, J Sebag
As the eye has long been considered a window to the body, the interplay of the eye and central nervous system is particularly intriguing. Thus, inspecting and evaluating hyalocytes in the posterior vitreous and their interaction(s) with the neural retina could afford insights to the brain in neurodegenerative disorders. The advent of new imaging modalities offers scientists and clinicians the opportunity to study human hyalocytes in vivo, enabling better understanding of cell activity (e.g. movement) during normal physiology, as well as changes in various diseased states. With further information concerning hyalocyte physiology and their departure(s) from normality as part of the pathophysiology of various pathologic conditions, the role of hyalocytes in pathogenesis can be further elucidated. This could usher in new therapeutic strategies designed to mitigate the role of these critical cells in the early stages of disease, thus stopping progression to more advanced stages. In fact, advanced knowledge could one day help to develop strategies to prevent many vitreo-retinal diseases entirely.
Hyalocytes in proliferative vitreo-retinal diseases
Published in Expert Review of Ophthalmology, 2022
Charlotte H. Jones, Wei Gui, Ricarda G. Schumann, Stefaniya K. Boneva, Clemens A. K. Lange, Koen A. van Overdam, Toco Y. P. Chui, Richard B. Rosen, Michael Engelbert, J. Sebag
Early theories on the pathogenesis of MPK focused on the retina and largely ignored the role of vitreous [23]. The two contemporary theories on etiology are breaks in the inner limiting membrane (ILM) with consequent glial cell migration, and anomalous posterior vitreous detachment (PVD) (Figure 1) [8] with vitreoschisis [13]. (Figure 2). The latter theory highlights the role of hyalocytes. Common to both theories is the role of PVD, which is found in 80–95% of cases [24–29]. Admittedly, the methods used to diagnose PVD in many of these studies may be suspect, making it possible that many cases diagnosed with total PVD are incomplete [13]. However, this prevalence is significantly higher than the 53% prevalence of PVD in the general population over age 50 [30,31]. Furthermore, it is probable that PVD in cases of MPK is anomalous with vitreoschisis.