Drug delivery to the ocular system is affected by anatomical factors like the corneal epithelium, blinking reflex, aqueous blood barrier, and retinal blood barrier, which lead to quick removal from the site and inefficient drug delivery. Developing a drug delivery mechanism that targets specific eye tissue is a major hurdle for researchers. Our study examines the challenges of drug absorption in these pathways. Hydrogels have been researched as a suitable delivery method to overcome some obstacles. These are developed alone or in conjunction with other technologies, such as nanoparticles. Many polymer hydrogel nanoparticle systems utilizing both natural and synthetic polymers have been created and investigated; each has pros and cons. The complex release mechanism of encapsulated agents from hydrogel nanoparticles depends on three key factors: hydrogel matrix swelling, drug-matrix chemical interactions, and drug diffusion. This mechanism exists regardless of the type of polymer. This study provides an overview of the classification of hydrogels, release mechanisms, and the role of controlled release systems in pharmaceutical applications. Additionally, it highlights the integration of nanotechnology in ocular disease therapy, focusing on different types of nanoparticles, including nanosuspensions, nanoemulsions, and pharmaceutical nanoparticles. Finally, the review discusses current commercial formulations for ocular drug delivery and recent advancements in non-invasive techniques. The objective is to present a comprehensive overview of the possibilities for enhancing ocular medication delivery through hydrogel nanoparticle systems.

Dry eye disease (DED), also known as keratoconjunctivitis sicca, is a multifactorial ocular disease characterized by tear film insufficiency due to diverse etiologies including aging, incomplete and infrequent blinking, hormonal changes, medications, and systemic diseases. Classified into aqueous-deficient dry eye (ADDE), evaporative dry eye (EDE), and mixed subtypes, DED presents with symptoms such as irritation, stinging, redness, foreign body sensation, sensitivity to light, and blurred or fluctuating vision. While rare, severe cases may lead to vision loss. With its rising global prevalence across age groups, DED poses a significant public health challenge. Primary care physicians (PCPs), often the first point of contact for DED patients, require timely screening and management strategies. This review explores the epidemiology, pathophysiology, clinical manifestations, diagnosis, and management of DED, emphasizing practical approaches for PCPs. This narrative review was conducted by searching MEDLINE, PubMed, and Google Scholar databases for relevant articles. Diagnostic approaches, including detailed history taking, patient-reported questionnaires, differential diagnosis, and assessments are discussed alongside management strategies, including symptomatic ophthalmic treatment, risk factor mitigation (e.g., reduced digital device screen time), prevention, and nutrition. By providing a synopsis of early symptoms that PCPs are often the first to encounter, practical approaches to screening and managing DED in the primary care setting, and guidelines on when to refer to specialty care, this comprehensive review aims to equip PCPs with the knowledge to improve DED screening and optimize patient outcomes.

Persistent corneal epithelial defects (PCEDs) are a challenging ocular condition characterized by the failure of complete corneal epithelial healing after an insult or injury, even after 14 days of standard care. There is a lack of therapeutics that target this condition and encourage re-epithelialization of the corneal surface in a timely and efficient manner. This review aims to provide an overview of current standards of management for PCEDs, highlighting novel, emerging treatments in this field. While many of the current non-surgical treatments aim to provide lubrication and mechanical support, novel non-surgical approaches are undergoing development to harness the proliferative and healing properties of human mesenchymal stem cells, platelets, lufepirsen, hyaluronic acid, thymosin ß4, p-derived peptide, and insulin-like growth factor for the treatment of PCEDs. Novel surgical treatments focus on corneal neurotization and limbal cell reconstruction using novel scaffold materials and cell-sources. This review provides insights into future PCED treatments that build upon current management guidelines.

Mustard gas keratopathy (MGK), a complication of exposure to sulfur mustard, is a blinding ocular surface disease involving key cellular pathways, including apoptosis, oxidative stress, and inflammation. Recent studies indicate that cellular senescence contributes to the pathophysiology of mustard gas toxicity. This study aimed to assess senescence and stress-related pathways—particularly mitogen-activated protein kinase (MAPK) signaling—in nitrogen mustard (NM)-induced corneal injury. In vitro, primary human corneal epithelial (P-HCECs), primary human corneal mesenchymal stromal cells (hcMSCs), and human corneal–limbal epithelial cell (HCLE) lines were exposed to varying concentrations of NM. The results demonstrated a dose-dependent increase in cellular senescence, characterized by reduced Ki67 expression, elevated p16, and p21 mRNA levels, as well as activation of the MAPK pathway activation. Treatment with a selective p38-MAPK inhibitor significantly reduced senescence markers and improved cell proliferation following exposure to NM. Overall, these studies indicate that NM exposure triggers cellular senescence and stress-related MAPK signaling, while p38-MAPK inhibition mitigates these effects, suggesting a potential therapeutic strategy.