Congenital aniridia is a rare genetic eye disorder characterized by the complete or partial absence of the iris from birth. Various theories and animal models have been proposed to understand and explain the pathogenesis of aniridia. In the majority of cases, aniridia is caused by a mutation in the PAX6 gene, which affects multiple structures within the eye. Treating these ocular complications is challenging and carries a high risk of side effects. However, emerging approaches for the treatment of aniridia-associated keratopathy, iris abnormalities, cataract abnormalities, and foveal hypoplasia show promise for improved outcomes. Genetic counseling plays a very important role to make informed choices. We also provide an overview of the newer diagnostic and therapeutic approaches such as next generation sequencing, gene therapy, in vivo silencing, and miRNA modulation.

Purpose: Chemical eye injury is an acute emergency that can result in vision loss. Neurotrophic keratitis (NK) is the most common long-term manifestation of chemical injury. NK due to alkali burn affects ocular surface health and is one of its most common causes. Here, we established a rabbit model of corneal alkali burns to evaluate the severity of NK-associated changes. Material methods: Alkali burns were induced in NZ rabbits by treating the cornea with (i) a 5 mm circular filter paper soaked in 0.75 N NaOH for 10 s (Mild NK) and (ii) trephination using a guarded trephine (5 mm diameter and 150-micron depth), followed by alkali burn, with a 5 mm circular filter paper soaked in 0.75 N NaOH for 10 s (a severe form of NK). Immediately after, the cornea was rinsed with 10 mL of normal saline to remove traces of NaOH. Clinical features were evaluated on Day 0, Day 1, Day 7, Day 15, and Day 21 post-alkali burn using a slit lamp, Pentacam, and anterior segment optical coherence tomography (AS-OCT). NK-like changes in epithelium, sub-basal nerve plexus, and stroma were observed using in vivo confocal microscopy (IVCM), and corneal sensation were measured using an aesthesiometer post alkali injury. After 21 days, pro-inflammatory cytokines were evaluated for inflammation through ELISA. Results: Trephination followed by alkali burn resulted in the loss of epithelial layers (manifested using fluorescein stain), extensive edema, and increased corneal thickness (550 µm compared to 380 µm thickness of control) evaluated through AS-OCT and increased opacity score in alkali-treated rabbit (80 compared to 16 controls). IVCM images showed complete loss of nerve fibers, which failed to regenerate over 30 days, and loss of corneal sensation—conditions associated with NK. Cytokines evaluation of IL6, VEGF, and MMP9 indicated an increased angiogenic and pro-inflammatory milieu compared to the milder form of NK and the control. Discussion: Using clinical parameters, we demonstrated that the alkali-treated rabbit model depicts features of NK. Using IVCM in the NaOH burn animal model, we demonstrated a complete loss of nerve fibers with poor self-healing capability associated with sub-basal nerve degeneration and compromised corneal sensation. This pre-clinical rabbit model has implications for future pre-clinical research in neurotrophic keratitis.

Purpose: To determine the visual outcome and postoperative complications of cataract surgery in patients with ocular surface disorders (OSDs). Setting: Tertiary eyecare center in North India. Design: Retrospective observational study. Methods: Patients with various OSDs with stabilized ocular surfaces who underwent cataract surgery during this period and had a minimum postoperative follow-up of 6 weeks were included. The primary outcome measures were postoperative corrected distance visual acuity (CDVA) at 6 weeks, best CDVA achieved, and postoperative complications. Results: The study included 20 men and 24 women. A total of 55 eyes were evaluated: Stevens-Johnson syndrome (SJS) 35 eyes, ocular cicatricial pemphigoid (OCP) 4 eyes, 8 eyes with dry eye disease (DED), 6 eyes with chemical injury and 2 eyes with vernal keratoconjunctivitis (VKC). The mean duration of OSD was 33.9 ± 52.17 months. The median preoperative CDVA was 2.0 (interquartile range [IQR], 1.45 to 2.0). The median CDVA ever achieved was 0.50 (IQR, 0.18 to 1.45) at 2 months and the median CDVA at 6 weeks was 0.6 (IQR, 0.3 to 1.5). Maximum improvement in CDVA was noted in patients with DED and SJS and the least in OCP. Phacoemulsification was performed in 47.27% eyes with intraoperative complications noted in 9% eyes. Postoperative surface complications occurred in 12 (21.82%) eyes. Other postoperative complications occurred in 9 (16%) eyes. Conclusions: Cataract surgery outcome can be visually rewarding in patients with OSDs provided ocular surface integrity is adequately maintained preoperatively and postoperatively.

In recent years, significant advances in tissue engineering and regenerative medicine have led to innovative approaches in addressing the various challenges associated with corneal transplants using bioengineered corneas. This mini-review aims to introduce the general ophthalmologist to the concept and technique of bioengineered cornea and provide an overview of the developments so far and an insight into the future direction. By summarizing the latest research and current limitations, we aim to highlight their potential for the future in ultimately contributing to vision restoration.

Simple limbal epithelial transplantation (SLET) has emerged as an effective treatment option for limbal stem cell deficiency (LSCD). However, the precise molecular mechanisms underlying its success remain incompletely understood. This review delves into the proposed mechanisms involving the donor limbus, host microenvironment, and the amniotic membrane as a scaffold in SLET. The donor limbus contributes to SLET efficacy through various factors secreted by limbal epithelial stem cells, including hepatocyte growth factor (HGF), soluble Fms-like tyrosine kinase-1 (sFLT-1), and pigment epithelium-derived factor (PEDF), which support corneal healing and transparency. Additionally, the presence of melanocytes, immune cells, limbal fibroblasts, and adhesion molecules within the donor tissue helps preserve the integrity of the limbal niche. The host environment plays a critical role in supporting the transplanted stem cells, with mesenchymal stem cell-secreted factors promoting proliferation and differentiation. Although the amniotic membrane has traditionally been used as a scaffold, emerging evidence suggests that it may not always be necessary. Further studies are needed to validate this scaffold-free approach and to evaluate the vitality and functional contributions of individual components used in SLET. Understanding these complex interactions and molecular mechanisms sheds light on the importance of the donor tissue, host microenvironment, and scaffold in SLET, paving the way for the optimization of this technique for the effective treatment of LSCD.