Aims/hypothesis Corneal confocal microscopy is a rapid non-invasive ophthalmic imaging technique that identifies peripheral and central neurodegenerative disease. Quantification of corneal sub-basal nerve plexus morphology, however, requires either time-consuming manual annotation or a less-sensitive automated image analysis approach. We aimed to develop and validate an artificial intelligence-based, deep learning algorithm for the quantification of nerve fibre properties relevant to the diagnosis of diabetic neuropathy and to compare it with a validated automated analysis program, ACCMetrics. Methods Our deep learning algorithm, which employs a convolutional neural network with data augmentation, was developed for the automated quantification of the corneal sub-basal nerve plexus for the diagnosis of diabetic neuropathy. The algorithm was trained using a high-end graphics processor unit on 1698 corneal confocal microscopy images; for external validation, it was further tested on 2137 images. The algorithm was developed to identify total nerve fibre length, branch points, tail points, number and length of nerve segments, and fractal numbers. Sensitivity analyses were undertaken to determine the AUC for ACCMetrics and our algorithm for the diagnosis of diabetic neuropathy. Uazman Alam and Yalin Zheng are joint senior authors.

Meibomian gland dysfunction is the most frequent cause of evaporative dry eye, yet its underlying pathophysiology is unknown. To gain insight into this pathophysiology, we characterized the time-dependent tear film and ocular surface changes occurring in X-linked anhidrotic-hypohidrotic ectodermal dysplasia mice (Tabby), which lack the meibomian gland. These mice sequentially developed corneal epithelial defects, central corneal stromal edema, neovascularization, and pannus 8 to 16 weeks after birth. Aqueous tear secretion was normal, whereas tear break-up time and ex vivo tear evaporation times were all shortened. Corneal epithelial microvilli were less numerous, conjunctival goblet cell density was unaffected, and MUC5AC and MUC5B gene expression was increased. Markers of squamous metaplasia (cytokeratin 10 and small proline-rich protein 1B) were noticed in the corneal epithelium of Tabby mice as early as the fourth week. Taken together, the Tabby mouse is a relevant meibomian gland dysfunction-related dry eye model that may lead to a better understanding of how meibomian glands are related to ocular surface health. This model may also help with discovering novel drug options for treating evaporative dry eye.

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of increased corneal subbasal nerve tortuosity in dry eye disease and its correlation with clinical parameters.

Objectives: To investigate ocular surface alterations and in vivo confocal microscopic characteristics of the cornea in dry eye disease (DED) with contact lens wear (CLW). Methods: Sixty participants were divided into three groups: DED with CLW (n=20), DED without CLW (n=20), and normal control (n=20). Ocular surface parameters were evaluated. Basal tears and in vivo confocal microscopy images of the cornea were collected. Multiplex bead analysis was used to assess interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, nerve growth factor (NGF), and substance P (SP) in tears. Nerve morphology and dendritic cell density in corneal subbasal nerve images were calculated. Results: The DED with CLW group showed significantly higher ocular surface staining scores (P=0.022) and higher levels of IL-1β, NGF, and SP in tears (P=0.014, P=0.004 and P=0.025) than the DED without CLW group. Corneal dendritic cell density in the DED with CLW group was significantly higher than that in the normal controls (P=0.001) and DED without CLW group (P=0.043). Tear cytokine levels of IL-1β, NGF, and SP were correlated with ocular surface parameters in the DED with CLW group. Moreover, the years of CLW were positively correlated with corneal dendritic cell density (r=0.527, P=0.017) and negatively correlated with corneal nerve density (r=−0.511, P=0.021). Conclusions: Patients with DED with CLW showed greater epithelial damage, elevated inflammatory cytokines and neuromediators in tears, and higher corneal dendritic cell density than patients with DED without CLW. The immune and nervous systems may be involved in contact lens–related DED.