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Originally discovered in the nineteenth century, hyalocytes are the resident macrophage cell population in the vitreous body. Despite this, a comprehensive understanding of their precise function and immunological significance has only recently emerged. In this article, we summarize recent in-depth investigations deciphering the critical role of hyalocytes in various aspects of vitreous physiology, such as the molecular biology and functions of hyalocytes during development, adult homeostasis, and disease. Hyalocytes are involved in fetal vitreous development, hyaloid vasculature regression, surveillance and metabolism of the vitreoretinal interface, synthesis and breakdown of vitreous components, and maintenance of vitreous transparency. While sharing certain resemblances with other myeloid cell populations such as retinal microglia, hyalocytes possess a distinct molecular signature and exhibit a gene expression profile tailored to the specific needs of their host tissue. In addition to inflammatory eye diseases such as uveitis, hyalocytes play important roles in conditions characterized by anomalous posterior vitreous detachment (PVD) and vitreoschisis. These can be hypercellular tractional vitreo-retinopathies, such as macular pucker, proliferative vitreo-retinopathy (PVR), and proliferative diabetic vitreo-retinopathy (PDVR), as well as paucicellular disorders such as vitreo-macular traction syndrome and macular holes. Notably, hyalocytes assume a significant role in the early pathophysiology of these disorders by promoting cell migration and proliferation, as well as subsequent membrane contraction, and vitreoretinal traction. Thus, early intervention targeting hyalocytes could potentially mitigate disease progression and prevent the development of proliferative vitreoretinal disorders altogether, by eliminating the involvement of vitreous and hyalocytes.

The transparent vitreous body, which occupies about 80% of the eye’s volume, is laden with numerous enzymatic and non-enzymatic antioxidants that could protect the eye from oxidative stress and disease. Aging is associated with degeneration of vitreous structure as well as a reduction in its antioxidant capacity. A growing body of evidence suggests these age-related changes may be the precursor of numerous oxidative stress-induced vitreo-retinopathies, including vision degrading myodesopsia, the clinically significant entoptic phenomena that can result from advanced vitreous degeneration. Adequate intravitreal antioxidant levels may be protective against vitreous degeneration, possibly preventing and even improving vision degrading myodesopsia as well as mitigating various other vitreo-retinopathies. The present article is, therefore, a review of the different antioxidant molecules within vitreous and the inter-relationships between vitreous antioxidant capacity and degeneration.

In myopia, diabetes and ageing, fibrous vitreous liquefaction and degeneration is associated with the formation of opacities inside the vitreous body that cast shadows on the retina, appearing as ‘floaters’ to the patient. Vitreous opacities degrade contrast sensitivity function and can cause notable impairment in vision-related quality of life. Here we introduce ‘nanobubble ablation’ for safe destruction of vitreous opacities. Following intravitreal injection, hyaluronic acid-coated gold nanoparticles and indocyanine green, which is widely used as a dye in vitreoretinal surgery, spontaneously accumulate on collagenous vitreous opacities in the eyes of rabbits. Applying nanosecond laser pulses generates vapour nanobubbles that mechanically destroy the opacities in rabbit eyes and in patient specimens. Nanobubble ablation might offer a safe and efficient treatment to millions of patients suffering from debilitating vitreous opacities and paves the way for a highly safe use of pulsed lasers in the posterior segment of the eye.Vitreous opacities, which are collagen aggregates that form in the eye and cause vision impairment (eye floaters), are currently treated with invasive surgical intervention or high-energy laser photoablation. In this paper, the authors show that exposing gold nanoparticles or indocyanine green to low-energy laser pulses generates vapour nanobubbles that can disrupt collagen aggregates in the eyes of rabbit, suggesting a milder strategy for the treatment of eye floaters.

With increased knowledge about the origins and pathophysiology of vitreo-retinal disorders—and, in particular, the central role of anomalous posterior vitreous detachment in vitreo-maculopathies—a paradigm shift from surgery to pharmacotherapy is taking place with the development of pharmacologic vitreolysis. The first approved agent for pharmacologic vitreolysis therapy is ocriplasmin, a truncated form of the nonspecific serine protease plasmin. Twelve studies comprise the current ocriplasmin clinical trial program, demonstrating the efficacy and safety of a single intravitreal injection of ocriplasmin for the treatment of patients with symptomatic vitreo-macular adhesion or vitreo-macular traction, including patients with macular holes. Although post-approval implementation of ocriplamsin in clinical practice has shown success rates of up to 78 %, there have been recent case reports of acute, transient visual dysfunction. There are thus new initiatives to further refine clinical indications for case selection and to identify possible untoward effects. Although more studies are warranted, it appears that ocriplasmin offers a good alternative to surgery. The future lies in pharmacologic vitreolysis, and the future of pharmacologic vitreolysis lies in prevention. Thus, long-term studies are needed to define a role for pharmacologic vitreolysis, in particular with ocriplasmin, in the prevention of progressive diabetic retinopathy and age-related macular degeneration.

PurposeContrast sensitivity function (CSF) declines with age. When unassociated with cataracts, this is hypothesized to be due to macular ganglion cell complex (GCC) thinning. However, other studies found associations with increased vitreous echodensity and posterior vitreous detachment (PVD). We investigate the relationship between CSF, vitreous echodensity, PVD, and GCC thickness as related to age in the same subjects.MethodsAge, CSF (Weber index: %W), vitreous echodensity (quantitative ultrasonography [QUS]), lens status (phakia or pseudophakia), best-corrected visual acuity (BCVA), and GCC thickness (SD-OCT) were evaluated in 57 eyes of 57 subjects with (n = 32, mean age = 62 years) and without (n = 25, mean age = 44 years) PVD (P < 0.001). A multivariate linear regression analysis was performed to assess the effects of independent variables on CSF.ResultsCSF was 51.2% worse in eyes with PVD (2.98 ± 0.31 %W) compared to no PVD (1.97 ± 0.24 %W; P < 0.001). QUS was 55.8% greater in eyes with PVD than those without (P < 0.001). Among all subjects, PVD status, vitreous echodensity, and age were the only independent variables demonstrating significant effects on CSF. Lens status, BCVA, and GCC thickness did not demonstrate association with CSF.ConclusionsPVD, vitreous echodensity, and age are determinants of CSF. PVD and increased vitreous echodensity are each associated with diminished CSF, independent of age. Thus, in the absence of GCC thinning and cataracts, vitreous changes may be a cause of decreased CSF with age.