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Archives of Disease in Childhood Sep 2017An estimated 1.4 million of the world's children are blind. A blind child is more likely to live in socioeconomic deprivation, to be more frequently hospitalised during... (Review)
Review
An estimated 1.4 million of the world's children are blind. A blind child is more likely to live in socioeconomic deprivation, to be more frequently hospitalised during childhood and to die in childhood than a child not living with blindness. This update of a previous review on childhood visual impairment focuses on emerging therapies for children with severe visual disability (severe visual impairment and blindness or SVI/BL).For children in higher income countries, cerebral visual impairment and optic nerve anomalies remain the most common causes of SVI/BL, while retinopathy of prematurity (ROP) and cataract are now the most common avoidable causes. The constellation of causes of childhood blindness in lower income settings is shifting from infective and nutritional corneal opacities and congenital anomalies to more resemble the patterns seen in higher income settings. Improvements in maternal and neonatal health and investment in and maintenance of national ophthalmic care infrastructure are the key to reducing the burden of avoidable blindness. New therapeutic targets are emerging for childhood visual disorders, although the safety and efficacy of novel therapies for diseases such as ROP or retinal dystrophies are not yet clear. Population-based epidemiological research, particularly on cerebral visual impairment and optic nerve hypoplasia, is needed in order to improve understanding of risk factors and to inform and support the development of novel therapies for disorders currently considered 'untreatable'.
Topics: Blindness; Cataract; Child; Corneal Opacity; Eye Diseases, Hereditary; Global Health; Humans; Income; Infant, Newborn; Optic Nerve; Prevalence; Retinal Diseases; Retinopathy of Prematurity
PubMed: 28465303
DOI: 10.1136/archdischild-2016-310532 -
Ocular Immunology and Inflammation Jul 2021: While cannabis has the potential to reduce corneal pain, cannabinoids might induce side effects. This review article examines the effects of cannabinoids on the... (Review)
Review
: While cannabis has the potential to reduce corneal pain, cannabinoids might induce side effects. This review article examines the effects of cannabinoids on the cornea. As more states and countries consider the legalization of adult cannabis use, health-care providers will need to identify ocular effects of cannabis consumption.: Studies included in this review examined the connection between cannabis and the cornea, more specifically anti-nociceptive and anti-inflammatory actions of cannabinoids. NCBI Databases from 1781 up to December 2019 were consulted.: Five studies examined corneal dysfunctions caused by cannabis consumption (opacification, decreased endothelial cell density). Twelve studies observed a reduction in corneal pain and inflammation (less lymphocytes, decreased corneal neovascularization, increased cell proliferation and migration).: More than half of the studies examined the therapeutic effects of cannabinoids on the cornea. As the field is still young, more studies should be conducted to develop safe cannabinoid treatments for corneal diseases.
Topics: Cannabis; Cornea; Corneal Endothelial Cell Loss; Corneal Neovascularization; Corneal Opacity; Eye Pain; Humans; Keratitis; Medical Marijuana
PubMed: 32159404
DOI: 10.1080/09273948.2020.1726969 -
Eye (London, England) Jun 2020Corneal keratopigmentation (KTP) has a long history of use in management of patients suffering from disfiguring corneal opacities. Due to progresses and modifications in... (Review)
Review
Corneal keratopigmentation (KTP) has a long history of use in management of patients suffering from disfiguring corneal opacities. Due to progresses and modifications in KTP surgical techniques and its low rate of complications, it is taken into consideration to be used in selected groups of patients for therapeutic or functional indications. In this paper we present an overview on clinical applications of KTP in both cosmetic and functional aspects and also, we discuss the outcomes of KTP and its characteristics in experimental and histopathological studies.
Topics: Coloring Agents; Cornea; Corneal Opacity; Humans; Tattooing
PubMed: 31896801
DOI: 10.1038/s41433-019-0750-2 -
Experimental Eye Research Jan 2016The corneal wound healing response, including the development of stromal opacity in some eyes, is a process that often leads to scarring that occurs after injury,... (Review)
Review
The corneal wound healing response, including the development of stromal opacity in some eyes, is a process that often leads to scarring that occurs after injury, surgery or infection to the cornea. Immediately after epithelial and stromal injury, a complex sequence of processes contributes to wound repair and regeneration of normal corneal structure and function. In some corneas, however, often depending on the type and extent of injury, the response may also lead to the development of mature vimentin+ α-smooth muscle actin+ desmin+ myofibroblasts. Myofibroblasts are specialized fibroblastic cells generated in the cornea from keratocyte-derived or bone marrow-derived precursor cells. The disorganized extracellular matrix components secreted by myofibroblasts, in addition to decreased expression of corneal crystallins in these cells, are central biological processes that result in corneal stromal fibrosis associated with opacity or "haze". Several factors are associated with myofibroblast generation and haze development after PRK surgery in rabbits, a reproducible model of scarring, including the amount of tissue ablated, which may relate to the extent of keratocyte apoptosis in the early response to injury, irregularity of stromal surface after surgery, and changes in corneal stromal proteoglycans, but normal regeneration of the epithelial basement membrane (EBM) appears to be a critical factor determining whether a cornea heals with relative transparency or vision-limiting stromal opacity. Structural and functional abnormalities of the regenerated EBM facilitate prolonged entry of epithelium-derived growth factors such as transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF) into the stroma that both drive development of mature myofibroblasts from precursor cells and lead to persistence of the cells in the anterior stroma. A major discovery that has contributed to our understanding of haze development is that keratocytes and corneal fibroblasts produce critical EBM components, such as nidogen-1, nidogen-2 and perlecan, that are essential for complete regeneration of a normal EBM once laminin secreted by epithelial cells self-polymerizes into a nascent EBM. Mature myofibroblasts that become established in the anterior stroma are a barrier to keratocyte/corneal fibroblast contributions to the nascent EBM. These myofibroblasts, and the opacity they produce, often persist for months or years after the injury. Transparency is subsequently restored when the EBM is completely regenerated, myofibroblasts are deprived of TGFβ and undergo apoptosis, and the keratocytes re-occupy the anterior stroma and reabsorb disordered extracellular matrix. The aim of this review is to highlight factors involved in the generation of stromal haze and its subsequent removal.
Topics: Animals; Apoptosis; Basement Membrane; Corneal Injuries; Corneal Keratocytes; Corneal Opacity; Corneal Stroma; Epithelium, Corneal; Extracellular Matrix Proteins; Humans; Myofibroblasts; Wound Healing
PubMed: 26675407
DOI: 10.1016/j.exer.2014.09.012 -
BMJ Open Ophthalmology 2022This review assesses different clinical aspects of the various known drug-induced corneal deposits, based on the corneal layer involved (epithelium, stroma and/or... (Review)
Review
This review assesses different clinical aspects of the various known drug-induced corneal deposits, based on the corneal layer involved (epithelium, stroma and/or endothelium), and based on the drug class. The most well-known condition caused by drug deposits is vortex keratopathy, or corneal verticillata, which is a whorl-like opacity in the corneal epithelium. Vortex keratopathy is commonly caused by certain cationic amphiphilic drugs such as amiodarone, antimalarials, suramin, tamoxifen, chlorpromazine and non-steroidal anti-inflammatory drugs. These deposits usually occur once a certain dose of the drug is reached. Most cases present with mild to moderate symptoms with minimal visual impairment. Most of these deposits resolve automatically, after months to years of drug cessation. Notably, other drug classes can cause deposits in all three layers of the cornea. Chlorpromazine, gold, rifabutin, indomethacin and tyrosine kinase inhibitors can cause stromal deposits, with reduced visual acuity when the anterior stroma is involved. Chlorpromazine and rifabutin can also cause deposits in the endothelial layer of the cornea. Regardless of the type of corneal deposit, local therapies such as topical lubricants or corticosteroids may help improve symptoms. Drug cessation or modification can also be helpful but should be weighed against the systemic risks of the underlying disease.
Topics: Chlorpromazine; Corneal Dystrophies, Hereditary; Corneal Opacity; Humans; Rifabutin; Vision Disorders
PubMed: 35415268
DOI: 10.1136/bmjophth-2021-000943 -
BMC Ophthalmology Dec 2022Axenfeld-Rieger syndrome (ARS) is a rare kind of anterior segment dysgenesis (ASD). The most common ocular features of ARS are posterior embryotoxon and iris hypoplasia,... (Review)
Review
BACKGROUND
Axenfeld-Rieger syndrome (ARS) is a rare kind of anterior segment dysgenesis (ASD). The most common ocular features of ARS are posterior embryotoxon and iris hypoplasia, while some patients may manifest as corneal opacity and edema. However, the current understanding of how ARS affects the cornea is still incomplete. This study reports a novel histopathological finding of ARS, complicating corneal abnormalities, including congenital corneal opacity and irreversible endothelial decompensation.
METHODS
This retrospective study included 6 eyes of 3 ARS patients, 5 of which underwent keratoplasty for irreversible endothelial decompensation from May 2016 to January 2019. No eye had a history of surgery. We reviewed the data of epidemiology, clinical manifestations and histopathologic examinations.
RESULTS
Five eyes developed irreversible endothelial decompensation, among which 4 were born with corneal opacity. One eye exhibited transparent cornea but showed a continuous loss of endothelial cells in the absence of surgery and elevated intraocular pressure thereafter. Anterior segment optical coherence tomography photographs showed that anterior synechia existed in the area with corneal opacities, where we found the interlayer splitting of the Descemet membrane inserted by hypoplastic iris and a basement membrane-like structure under a light microscope.
CONCLUSION
Anterior synechia might be associated with corneal abnormalities in ARS patients. The novel histopathologic finding revealed the internal relation between anterior segment dysgenesis and would help explore the inner mechanism of corneal abnormalities in ARS.
Topics: Humans; Endothelial Cells; Retrospective Studies; Anterior Eye Segment; Eye Abnormalities; Corneal Diseases; Corneal Opacity; Iris Diseases
PubMed: 36577962
DOI: 10.1186/s12886-022-02754-8 -
Experimental Eye Research Dec 2014Stromal transparency is a critical factor contributing to normal function of the visual system. Corneal injury, surgery, disease and infection elicit complex wound... (Review)
Review
Stromal transparency is a critical factor contributing to normal function of the visual system. Corneal injury, surgery, disease and infection elicit complex wound healing responses that serve to protect against insults and maintain the integrity of the cornea, and subsequently to restore corneal structure and transparency. However, in some cases these processes result in prolonged loss of corneal transparency and resulting diminished vision. Corneal opacity is mediated by the complex actions of many cytokines, growth factors, and chemokines produced by the epithelial cells, stromal cells, bone marrow-derived cells, lacrimal tissues, and nerves. Myofibroblasts, and the disorganized extracellular matrix produced by these cells, are critical determinants of the level and persistence of stromal opacity after corneal injury. Decreases in corneal crystallins in myofibroblasts and corneal fibroblasts contribute to cellular opacity in the stroma. Regeneration of a fully functional epithelial basement membrane (BM) appears to have a critical role in the maintenance of corneal stromal transparency after mild injuries and recovery of transparency when opacity is generated after severe injuries. The epithelial BM likely has a regulatory function whereby it modulates epithelium-derived growth factors such as transforming growth factor (TGF) β and platelet-derived growth factor (PDGF) that drive the development and persistence of myofibroblasts from precursor cells. The purpose of this article is to review the factors involved in the maintenance of corneal transparency and to highlight the mechanisms involved in the appearance, persistency and regression of corneal opacity after stromal injury.
Topics: Animals; Corneal Opacity; Corneal Stroma; Extracellular Matrix; Humans
PubMed: 25281830
DOI: 10.1016/j.exer.2014.09.013 -
Romanian Journal of Ophthalmology 2022To compare ultrasonic energy delivered into the eye [cumulative dissipated energy, (CDE)] and frequencies of required auxiliary surgical methods during... (Observational Study)
Observational Study
To compare ultrasonic energy delivered into the eye [cumulative dissipated energy, (CDE)] and frequencies of required auxiliary surgical methods during phacoemulsification surgery in eyes with and without corneal opacity. The study was designed as a retrospective comparative observational study. The study group [Corneal Opacity Group, (COG)] was comprised of 31 eyes of 31 cataract patients with corneal opacity. Only nebular and macular corneal opacities (according to slit-lamp based classification of Agrawal) were included in the study. The control group (CG) was comprised of 40 eyes of 40 cataract patients without corneal opacity. The CDE values were obtained using the Centurion system (Alcon, Fort Worth, TX) and the patients were followed-up postoperatively for a period of one month. The mean age of the subjects was 71.46 ± 8.86 years (52-89) in COG and 66.12 ± 5.96 years (55-80) in CG (p >0.05). In COG, the most common etiologic factors were trauma, keratitis, and degenerative diseases. The mean CDE value was 15.16 ± 8.71 (2.20-42.65) in COG and 10.04 ± 6.28 (3.77-31.80) in CG and it was found as significantly higher in COG (p=0.003). Some auxiliary surgical methods including posterior synechiolysis and anterior capsule staining were more commonly performed in COG (p=0.044 and p=0.040, respectively). No intraoperative or postoperative complication was observed. More ultrasonic energy is delivered into the eye and more auxiliary surgical methods are needed in cataract patients with corneal opacity who underwent phacoemulsification. CDE = Cumulative dissipated energy, COG = Corneal Opacity Group, CG = Control group, IOL = Intraocular lens, LOCS = Lens Opacities Classification System, BCVA = best-corrected visual acuity, SRK/T = Sanders, Retzlaff, and Kraff theoretical, OVD = ophthalmic viscosurgical device, SPSS = Statistical Package for the Social Sciences.
Topics: Humans; Middle Aged; Aged; Aged, 80 and over; Retrospective Studies; Visual Acuity; Phacoemulsification; Cataract; Corneal Opacity
PubMed: 36349172
DOI: 10.22336/rjo.2022.45 -
The Ocular Surface Jan 2021Corneal stromal wound healing is a complex event that occurs to restore the transparency of an injured cornea. It involves immediate apoptosis of keratocytes followed by... (Review)
Review
Corneal stromal wound healing is a complex event that occurs to restore the transparency of an injured cornea. It involves immediate apoptosis of keratocytes followed by their activation, proliferation, migration, and trans-differentiation to myofibroblasts. Myofibroblasts contract to close the wound and secrete extracellular matrix and proteinases to remodel it. Released proteinases may degenerate the basement membrane allowing an influx of cytokines from overlying epithelium. Immune cells infiltrate the wound to clear cellular debris and prevent infections. Gradually basement membrane regenerates, myofibroblasts and immune cells disappear, abnormal matrix is resorbed, and transparency of the cornea is restored. Often this cascade deregulates and corneal opacity results. Factors that prevent corneal opacity after an injury have always intrigued the researchers. They hold clinical relevance as they can guide the outcomes of corneal surgeries. Studies in the past have shed light on the role of various factors in stromal healing. TGFβ (transforming growth factor-beta) signaling is the central player guiding stromal responses. Other major regulators include myofibroblasts, basement membrane, collagen fibrils, small leucine-rich proteoglycans, biophysical cues, proteins derived from extracellular matrix, and membrane channels. The knowledge about their roles helped to develop novel therapies to prevent corneal opacity. This article reviews the role of major regulators that determine the outcome of stromal healing. It also discusses emerging therapies that modulate the role of these regulators to prevent stromal opacity.
Topics: Cornea; Corneal Injuries; Corneal Opacity; Corneal Stroma; Humans; Wound Healing
PubMed: 33127599
DOI: 10.1016/j.jtos.2020.10.006 -
Indian Pediatrics Mar 2005
Topics: Cornea; Corneal Opacity; Humans; Infant, Newborn; Sclera
PubMed: 15817979
DOI: No ID Found