Search Results (499)

Cytomegalovirus (CMV) infection of the anterior segment is increasingly recognized as an important cause of corneal endotheliitis and secondary glaucoma, even in immunocompetent individuals. CMV corneal endotheliitis typically presents with coin-shaped or linear keratic precipitates (KPs), corneal edema, mild anterior chamber inflammation, and recurrent intraocular pressure (IOP) elevation; persistent or episodic ocular hypertension may progress to glaucomatous optic neuropathy if inadequately treated. Definitive diagnosis relies on aqueous humor polymerase chain reaction (PCR) testing for CMV DNA, supported by adjunctive imaging including specular microscopy, anterior segment optical coherence tomography (AS-OCT), and in vivo confocal microscopy (IVCM). Management requires a comprehensive strategy integrating antiviral therapy, anti-inflammatory treatment, and appropriate IOP control. Topical or systemic ganciclovir remains the cornerstone, while refractory disease may necessitate surgical intervention. Older age and male sex, host immune status, prolonged or recurrent CMV infection, and pre-existing ocular conditions are major risk factors for progression and poor outcomes. The pathogenesis of secondary glaucoma is thought to involve both direct viral cytopathic effects and inflammation-mediated damage to the trabecular meshwork (TM), resulting in impaired aqueous outflow. Therefore, early recognition, accurate diagnosis, and effective treatment are essential to prevent corneal decompensation and permanent vision loss. Full article

Diabetic retinopathy (DR) is a leading cause of vision loss worldwide and represents a complex neurovascular complication of diabetes mellitus driven by chronic hyperglycemia. Increasing evidence identifies oxidative stress—defined as an imbalance between reactive oxygen species (ROS) production and antioxidant defenses—as a central pathogenic mechanism linking metabolic dysregulation to retinal injury. The retina is particularly vulnerable to oxidative damage due to its high metabolic demand, elevated oxygen consumption, and abundance of polyunsaturated fatty acids. Hyperglycemia activates multiple interconnected biochemical pathways, including the polyol and hexosamine pathways, protein kinase C signaling, advanced glycation end-product formation, and lipid peroxidation, all of which converge on excessive ROS production and mitochondrial dysfunction. Growing attention has focused on oxidative stress biomarkers as tools to characterize DR severity and progression. Elevated systemic markers of lipid, protein, and DNA oxidation, together with impaired antioxidant capacity, correlate with disease stage, while oxidative biomarkers detected in aqueous and vitreous humor reflect localized retinal injury. Importantly, oxidative stress biomarkers are also associated with functional outcomes, including best-corrected visual acuity and diabetic macular edema. Integration of systemic and ocular oxidative biomarkers with clinical staging may improve risk stratification and support personalized therapeutic strategies in DR. Full article

Daily exposure to blue light emitted by digital devices has raised concerns about oxidative stress-mediated damage to the ocular surface. Despite growing interest, validated in vitro models to study blue light-induced oxidative stress in corneal epithelial cells remain limited. A reproducible in vitro method was developed using rabbit corneal epithelial (RCE) cells exposed to blue LED light (405 nm). Irradiation parameters were optimized to induce oxidative stress without causing overt cytotoxicity. Cellular viability, intracellular ROS production, and mitochondrial oxidative stress were assessed. The model was validated using reference antioxidants (ascorbic acid and oleuropein), oleuropein formulated in a drug-in-cyclodextrin-in-liposome system (OLE-DCL), and two commercial ophthalmic formulations applied before or after irradiation. Blue light irradiation at 4.57 W/m² for 30 min significantly increased intracellular and mitochondrial ROS levels while preserving cell viability, indicating sublethal photo-oxidative stress. Ascorbic acid effectively suppressed ROS generation, whereas free oleuropein showed reduced efficacy, likely due to photosensitivity. OLE-DCL significantly enhanced antioxidant activity under irradiation. The model also discriminated between protective and restorative treatment strategies. This study establishes a validated in vitro blue light-induced oxidative stress model for corneal epithelial cells, suitable for screening antioxidant compounds, formulations, and application strategies relevant to ocular surface protection. Full article

Dry eye disease (DED) is an ocular surface disorder characterized by tear film instability, inflammation, epithelial damage, and neurosensory abnormalities. Due to its multifactorial etiology and pathophysiology, conventional therapies that focus on lubrication and immunosuppression often fall short in addressing the neuropathic component of ocular pain experienced by a growing subset of patients. Recent developments in sensory neuroscience have highlighted the pivotal role of ion channels in mediating ocular surface homeostasis, pain signaling, and inflammation. This review examines the role of the following major ion channel families in the pathophysiology of DED and neuropathic ocular pain: transient receptor potential (TRP) channels, voltage-gated sodium (Nav) channels, and purinergic P2X receptors. The review details their anatomical distribution, molecular function, and responses to environmental stimuli such as heat, cold, osmolarity, and injury. Current treatments, such as artificial tears, anti-inflammatory drops, and systemic neuromodulators, are also reviewed in relation to their effects on ion channel modulation. Additionally, emerging therapies that directly target sensory transduction pathways are introduced. This review highlights the therapeutic potential of ion channel modulation in personalizing treatment for patients with ocular surface pain, particularly those with neuropathic features unresponsive to standard care. Full article

Background: Dry Eye Disease (DED) is a multifactorial disorder characterized by tear film instability and ocular surface inflammation. Murine models based on environmental stress are widely used to mimic evaporative DED, although many focus on limited disease features. This study aimed to provide an integrated characterization of ocular surface alterations induced by chronic desiccating stress. Methods: Adult mice were housed in a Controlled-Environmental Chamber (CEC) with low humidity and increased airflow for up to 21 days and sacrificed after 14 or 21 days. Corneal damage was assessed by fluorescein staining. Conjunctival histology was evaluated for epithelial morphology, goblet cell (GC) size, and mucin composition. Complement fractions C3 and C5a were assessed by immunohistochemistry. Expression of inflammatory markers (Major Histocompatibility Complex, Class II, DR, HLA-DR; interleukin-1β, IL-1β; tumor necrosis factor-α, TNF-α) was quantified by Real-Time PCR (RT-PCR) in corneal and conjunctival epithelium. Results: Fluorescein staining revealed progressive corneal epithelial damage over time. Histological analysis demonstrated conjunctival epithelial alterations characterized by a significant reduction in GC size and in neutral mucin-positive GCs, consistent with mucin remodeling of the ocular surface epithelium. Increased epithelial deposition of complement fractions C3 and C5a was observed, while molecular analysis confirmed upregulation of inflammatory markers, including HLA-DR, IL-1β, and TNF-α. Collectively, these findings indicate that the model captures key pathophysiological components of DED. Conclusions: The CEC model reproduces major features of evaporative DED, including epithelial damage, GC remodeling, immune activation, and inflammation. As a non-invasive desiccating stress model, it represents a relevant experimental platform for studying ocular surface inflammation and for preclinical evaluation of therapeutic strategies. Full article

As the prevalence of myopia, or near-sightedness, continues to rise globally, it becomes imperative to determine the mechanisms driving myopia so that appropriate interventions to mitigate it can be developed. Light appears to be critical for normal ocular development, and over the past several decades research has explored the connection between light exposure and myopia development. This review explores the growing field of photobiomodulation, or the use of light to modulate biological processes, to prevent myopia development. To complete this review, relevant texts published from January 1990 to December 2025 were retrieved from the PubMed database using a combination of search terms covering myopia and ocular development, light exposure conditions related to myopia, myopia development in relation to circadian and diurnal regulation, nonvisual opsins and myopia, and light-induced ocular damage. Through this review, we see that photobiomodulation offers a potential intervention to control myopia progression, but the mechanisms behind light’s influence on ocular development remain complex and incompletely understood. This review aims to summarize what is currently known to serve as a basis for future research and to delineate important findings. Full article

Background/Objectives: Childhood-onset Sjögren disease (cSjD) is a rare autoimmune disorder with heterogeneous manifestations and ongoing diagnostic challenges, as there are no validated paediatric criteria. Our study aims to characterise the clinical, laboratory, and imaging features of children diagnosed with cSjD at a single Romanian paediatric rheumatology centre between 2015 and 2025 and contextualise these findings within the most recent literature. Methods: A retrospective review of 15 consecutive cSjD patients was conducted, including clinical features, autoantibodies, imaging, biopsy findings, treatment, and outcomes. Results: Our cohort showed a significant female predominance (80%) and a broad age range at disease onset (3–15 years). Extraglandular manifestations were more common at presentation than glandular phenotypes (53.3% vs. 40%). Lupus-like extraglandular presentations frequently led to initial misdiagnosis as childhood-onset systemic lupus erythematosus (SLE) in our cohort. Sicca symptoms were present at diagnosis in only 3 of 15 patients (20%) and developed later during follow-up in an additional 4 patients (26.7%). Notably, the cohort included novel findings, such as an unprecedented presentation with acute exudative pericarditis complicated by cardiac tamponade. Anti-SSA antibodies and salivary gland ultrasound abnormalities were highly prevalent (86.7% and 100%, respectively). Anti-SSB antibodies were detected in seven patients (46.7%), with titres showing more variability than those of anti-SSA, ranging from just above the positivity threshold to mildly elevated levels. The association with macro-creatine kinase type I was another distinctive feature of this series. Chronic musculoskeletal pain and dryness were our patients’ most frequently reported symptoms at the last assessment, affecting up to 5/15 (33.3%) in each domain. One patient showed irreversible ocular damage during our study. Conclusions: Extraglandular presentations of cSjD are highly heterogeneous and diagnostically challenging, often occurring without glandular symptoms. Lupus-like systemic features—including facial vasculitic purpura, with or without arthralgia, and occasional pericarditis, as observed in our cohort—may contribute to frequent initial diagnostic misattribution to SLE. Early salivary gland ultrasonography, targeted autoantibody testing, and selective biopsy are essential for timely diagnosis, underscoring the urgent need for paediatric-specific validated classification criteria. Full article

Background/Objectives: Rosacea is a chronic inflammatory dermatosis that may involve the eye, causing surface and adnexal damage that can precede cutaneous signs. Detecting subclinical ocular changes is clinically important because early ocular surface dysfunction may be missed on routine examination yet progress to corneal complications, allowing earlier preventive management when identified. We prospectively evaluated subclinical ocular alterations in cutaneous rosacea using a combined, fully non-invasive high-tech imaging workflow—tear film interferometry, infrared meibography, and exploratory retinal optical coherence tomography angiography (OCT-A)—including patients without clinically evident ocular involvement. Methods: Sixteen patients with cutaneous rosacea (mean age 44.3 ± 11.2 years; 4 males, 12 females) were enrolled and divided into: Group 1—rosacea with clinically evident ocular involvement (n = 11); Group 2—rosacea without clinical ocular involvement (n = 5). Six age-matched healthy subjects served as controls (Group 3). All underwent LipiView II^® interferometry and meibography to quantify lipid-layer thickness (LLT, nm) and meibomian gland (MG) loss score (1 = normal–4 = severe), plus retinal OCT-A (Optovue Inc., Fremont, CA, USA). ANOVA with post hoc Tukey test assessed inter-group differences. Results: OCT-A showed no significant alterations in superficial or deep retinal plexuses across groups (p > 0.05). Conversely, LLT was significantly reduced in both rosacea groups vs. controls (OD: 45.5 ± 21.4 nm and 67.4 ± 10.1 nm vs. 92.7 ± 8.2 nm; OS: 40.4 ± 15.3 nm and 66.4 ± 10.1 nm vs. 96.0 ± 6.7 nm; p < 0.001). MG score was markedly higher (worse) in rosacea (OD: 3.63 ± 0.50 and 3.20 ± 0.83 vs. 1.83 ± 0.75; OS: 3.45 ± 0.68 and 3.40 ± 0.54 vs. 1.66 ± 0.81; p < 0.001). Ocular symptoms were reported by 85% of patients yet slit-lamp examination revealed surface alterations in 58% of asymptomatic cases. Conclusions: Tear film interferometry and meibography detect early ocular surface impairment in rosacea—even in the absence of clinical signs—while retinal microvasculature appears unaffected. Routine ophthalmologic screening of all rosacea patients could enable prompt treatment of subclinical dysfunction, potentially preventing corneal complications. Retinal OCTA metrics were not significantly different in this small pilot cohort, and these negative findings should be interpreted cautiously pending larger studies. Full article

Background/Objectives: Dry eye disease (DED) is a multifactorial condition affecting the ocular surface. It is characterized by tear film instability, hyperosmolarity, inflammation, and oxidative stress. First-line treatment for DED relies on lubricating and hydrating eye drops, usually containing hyaluronic acid (HA), which supports tear film stability and epithelial healing. However, HA alone cannot correct oxidative stress, a key driver of cellular damage and inflammation in DED. Accordingly, this study aimed to evaluate the antioxidant capacity of Malva sylvestris tincture (MalvaT) and its physicochemical properties in experimental eye-drop formulations containing HA. Methods: The antioxidant activity of reconstituted MalvaT lyophilisate (Malva) was assessed in cell-free assays against several oxygen radicals and in cell-based assays using the human HaCat keratinocyte cell line. The refractive index was measured in eye-drop formulations containing 0.15% or 0.3% HA and 0.5% MalvaT. Surface tension was assessed in eye-drop formulations containing 0.15% HA and increasing concentrations (0.25–2.0%) of MalvaT. Results: Malva showed potent oxygen radical scavenging activity in both cell-free and cell-based assays, indicating its antioxidant capacity and the efficient cellular uptake of antioxidant components. The refractive indices of experimental eye-drop solutions containing HA and MalvaT were close to that of tear fluid (1.334). The surface tension of the experimental eye-drop formulations, while not impacted by 0.15% HA, was significantly reduced by increasing concentrations of MalvaT (p < 0.0001). At the concentration of 0.5% MalvaT, the mean surface tension was reduced from 68.17 mN/m (HA control) to 59.80 mN/m (HA + MalvaT), thereby bringing it closer to that of tear fluid. Conclusions: This pre-clinical study suggests that combining the antioxidant properties of Malva tincture with the lubricating and hydrating effects of HA in eye-drop formulations exhibiting optimal rheological characteristics may offer a promising therapeutic approach for managing DED. Full article

Vernal keratoconjunctivitis (VKC) represents far more than a typical allergic eye disease. It is a distinct and often underestimated chronic inflammatory condition that primarily affects children during critical stages of physical and emotional development. Though frequently grouped with seasonal allergic conjunctivitis, VKC differs significantly in its immunopathology, clinical presentation, and long-term implications. Its intense ocular symptoms and its potential for corneal damage and substantial psychosocial burden require, rather than symptom control, coordinated and multidisciplinary management. This narrative review explores VKC from every angle, with a particular focus on its implications for pediatric care. VKC, in fact, represents a genuine clinical challenge: as its symptoms can mimic milder forms of conjunctivitis, its course is often unpredictable, and its treatment requires balancing efficacy and safety in vulnerable age groups. We examined the immunological mechanisms that make it a model of localized Th2 inflammation, the diagnostic pitfalls that delay recognition, and the evolving treatment landscape, from conventional therapies like cyclosporine A and tacrolimus to innovative agents such as omalizumab and dupilumab. We also highlighted the role of emerging biomarkers, the influence of environmental and microbiome factors, and the urgent need for standardized care pathways. As research continues to expand our understanding, VKC is emerging as a prime example of how personalized medicine and translational science can intersect to address complex immune-mediated diseases in children. For the ones treating pediatric allergic disorders, VKC is no longer a rare curiosity: it is a clinical challenge worth understanding deeply. Full article

Background: Pediatric orbital floor fractures differ from adult injuries due to bone elasticity and a higher incidence of trapdoor-type defects with extraocular muscle entrapment, often presenting with limited external signs but carrying a high risk of functional impairment. Early recognition and prompt surgical release are essential to prevent irreversible neuromuscular damage and persistent binocular vision disturbances. Case Presentation: A 13-year-old patient sustained an orbital floor blow-out fracture with inferior rectus muscle incarceration following blunt trauma. The child presented with vertical diplopia, ocular motility restriction, and infraorbital hypoesthesia. Computed tomography demonstrated a posteriorly located linear orbital floor defect with soft-tissue entrapment, supporting the indication for urgent surgical intervention to avoid ischemic injury. Management and Outcome: Through a transconjunctival retroseptal approach, the entrapped muscle was promptly released, and orbital floor continuity was restored using an autologous bone graft harvested from the anterior maxillary wall with piezosurgery. This technique allowed controlled and precise bone harvesting while preserving adjacent anatomical and developing dental structures. Postoperative recovery was uneventful, with complete resolution of diplopia and full restoration of binocular ocular motility during follow-up. Conclusion: Early surgical intervention plays a pivotal role in achieving functional recovery in pediatric orbital floor fractures with muscle entrapment. Autologous reconstruction supported by piezosurgical bone harvesting represents a safe and effective approach in growing patients, providing reliable functional and anatomical outcomes. This case reinforces the clinical relevance of timely intervention and highlights practical considerations in pediatric orbital trauma management. Full article

Background: Chronic work-related stress, including exposure to mobbing, is associated with a wide range of psychological and somatic consequences. However, its potential impact on visual function, particularly in the absence of structural ocular damage, remains underexplored. This narrative review critically examines the evidence linking chronic stress, autonomic nervous system (ANS) dysregulation, and functional visual disorders, focusing on accommodative function and asthenopia. Methods: A qualitative narrative review of the literature published between 2000 and 2025 was conducted using major biomedical databases. Studies addressing chronic stress, ANS activity, accommodative function, digital eye strain, and functional ocular symptoms were identified and integrated into a coherent pathophysiological framework. Results: The ocular system, being richly innervated by the ANS, may represent a peripheral target of prolonged stress-related autonomic alterations. Available evidence suggests that chronic stress is associated with asthenopia, accommodative inefficiency, and ocular discomfort even in the absence of overt ocular pathology. In particular, altered parasympathetic control of the ciliary muscle emerges as a plausible mediating mechanism. Conclusions: Functional visual disorders may represent peripheral manifestations of stress-related ANS dysregulation. Although causality cannot be established conclusively, the proposed framework supports the need for multidisciplinary research to clarify the clinical and medico-legal relevance of stress-related visual dysfunction. Full article

Background/Objectives: Keratitis is an ocular disease caused by microbial infection or by non-infectious damage due to UV light exposure, chemical exposure, or eye injuries. Methods: Moxifloxacin-loaded ufasomes (MOX-UFAs) were optimized using a full factorial design (1².2³) after being prepared by the vortex mixing method. The study evaluated the effects of the oleic acid amount, surface active agent (SAA) amount, and SAA type as independent factors on the entrapment efficiency percent (EE%), particle size (PS), polydispersity index (PDI), zeta potential (ZP), and the amount released after 6 h (Q6h%). Results: The optimized ufasomes (UFAs) formulation was spherical, with an EE% of 78.37 ± 3.91%, PS of 203.13 ± 20.31 nm, PDI of 0.334 ± 0.016, and ZP of −25.42 ± 1.27 mV. The in vitro release of moxifloxacin (MOX) from the UFAs was maintained for more than 6 h in the range of 40.0–75.0%. The optimum MOX-UFAs formulation was incorporated into an in situ gel (Pluronic F-127/HPMC K4M). The ex vivo studies (corneal permeation and confocal laser scanning microscopy) proved the successful retention of the MOX-UFAs-laden in situ gel. Furthermore, the in vitro and in vivo antimicrobial studies revealed their significant antimicrobial effect against Pseudomonas aeruginosa. In addition, the Draize test proved the tolerability of MOX-UFAs-laden in situ gel in animals. Conclusions: The incorporation of MOX-UFAs into Pluronic F-127/HPMC K4M in situ gel could successfully provide sustained ocular delivery and improve the bioavailability of MOX for the management of keratitis. Full article

Corneal nerves are essential for maintaining the functional integrity of the ocular surface. Damage to corneal nerves can lead to corneal issues and impaired vision. Current treatments for corneal nerve damage are inadequate, thus highlighting the need for innovative therapeutic approaches. In this study, we present a hydrogel microneedle system designed to facilitate the sustained release of recombinant human nerve growth factor (rhNGF). The microneedle features a tip composed of glycidyl methacrylate modified silk fibroin (SFMA) loaded with rhNGF, photopolymerized for structural integrity, while its base is formed using silk fibroin (SF). This design allows the microneedles to penetrate the corneal epithelium and deliver rhNGF to the sub-epithelial layer. The crosslinking process not only provides the mechanical strength required for microneedle penetration but also enables sustained drug release. The proposed rhNGF-loaded SF hydrogel microneedle provides a platform for drug delivery, serving as a novel therapeutic option for corneal tissue engineering. Full article

Dry eye disease (DED) is a common condition that can be associated with cataract surgery, requiring pre- and postoperative considerations. Pre-existent DED and disruption of the tear film homeostasis due to incisional corneal nerve damage, intra-operative ocular surface drying, microscope phototoxicity, or the toxic effects of preservatives and active ingredients of postoperative drops or a combination thereof, represents a potential mechanism for worsening or developing DED after cataract surgery. Recent diagnostic advancements have enabled us better to understand the pathophysiology of DED after cataract surgery. For patients with pre-existing DED before cataract surgery, early intervention can improve surgical outcomes. In contrast, failure to recognize DED risk factors or subtle signs can result in inaccurate refractive measurements, poor surgical outcomes, including serious complications, worsening of dry eye symptoms, patient dissatisfaction, and decreased quality of life. This review presents an overview of the perioperative management of DED in patients undergoing cataract surgery with an emphasis on pre-operative diagnosis and treatment, and its impact on improving surgical refractive outcomes and decreasing complications. Full article