Punctate epithelial erosions

About: Punctate epithelial erosions is a research topic. Over the lifetime, 27 publications have been published within this topic receiving 788 citations.

Classification of herpes simplex virus keratitis.

Abstract: PURPOSE We propose a nomenclature for classification of herpes simplex virus (HSV) keratitis. We hope that a more consistent classification system will lead to a better understanding of the disease processes, thus resulting in improved diagnosis, treatment, and patient outcomes. METHODS A review of the literature was performed to evaluate current HSV classification systems. These systems were evaluated in the context of both current clinical and basic science studies and our own clinical observations. RESULTS The proposed classification system is based on the anatomy and pathophysiology of the specific presentations of HSV keratitis. Anatomically, the primary level of corneal involvement, whether epithelium, stroma, or endothelium, must be elucidated. Pathophysiologically, the cause of the inflammation. whether immunologic, infectious, or neurotrophic, must be determined. There are four major categories of HSV keratitis. (1) Infectious epithelial keratitis, which is made up of cornea vesicles, dendritic ulcer, geographic ulcer, and marginal ulcer. (2) Neurotrophic keratopathy, which includes punctate epithelial erosions and neurotrophic ulcer. (3) Stromal keratitis, which is subdivided into necrotizing stromal keratitis and immune stromal keratitis. (4) Endotheliitis, which has three clinical presentations: disciform, diffuse, and linear. CONCLUSION We believe that by categorizing cases of HSV keratitis by their primary anatomic and pathophysiologic etiologic characteristics, clinicians can better understand and therefore treat all types of HSV keratitis. The four main categories of HSV keratitis are infectious epithelial keratitis, neurotrophic keratopathy, stromal keratitis, and endotheliitis. Each of these is subdivided to more specific clinical presentations.

Fluorescein punctate staining traced to superficial corneal epithelial cells by impression cytology and confocal microscopy.

Abstract: Definitions of dry eye and estimation of the severity often include the quantity and distribution of fluorescent punctate stains of the cornea.1–3 The phenomenon, superficial punctate fluorescence, is found in apparently normal subjects,4–8 contact lens wearers,9,10 and dry eyes.11–14 Synonymous terms, such as punctate epithelial erosions and punctate epithelial defects, imply loss of epithelial cells, but the anatomic basis is controversial and unproven.6,15,16 Punctate staining can be transient, appearing and disappearing over a matter of hours.17,18 Superficial punctate staining can be reduced by a high-humidity atmosphere, punctal plugging, artificial tears, and anti-inflammatory treatments.9,19–25 There is a strong correlation between the distribution of punctate stains in both eyes of a single individual, suggesting a systemic or environmental etiology, rather than a strictly local cause.18,19 Smoking, hormone changes, and medications have all been linked to changes in punctate corneal staining.26–29 The main hypothesis for punctate staining has several components. First, intercellular gaps, created by loss of tight junction integrity allow deep penetration and trapping of fluorescein between cells6,18,30–33; second, fluorescein stains desquamating, damaged, or dead cells19,30,34,35; third, surface irregularities or defects left by an absence of cells cause fluorescein to pool in punctate areas.13,18,36–39 However, irrigation does not easily remove the fluorescent punctate stains, and so pooling over surface irregularities is unlikely.40,41 Studies in rabbits and humans suggest that both living and dead cells take in fluorescein, although not all cells with fluorescein uptake are visible under the slit lamp microscope.35,42,43 The evidence that uptake is intracellular was based solely on the size and shape of the fluorescein staining spots, because organelle stains were not used.35,40 The goal of this study was to investigate the cellular basis of punctate staining by using confocal microscopy in conjunction with optimized impression cytology techniques.

Xerophthalmia in vitamin A-deficient rabbits. Clinical and ultrastructural alterations in the cornea.

Abstract: Xerophthalmia developed in the eyes of rabbits maintained on a vitamin A-deficient diet for 4 to 6 months. The earliest clinical change, a lusterless graying of the central corneal epithelium, was noted after 16 to 18 weeks on the diet. Multiple small punctate epithelial erosions appeared in the interpalpebral fissure zone within 7 to 10 days after the lusterless graying became evident. The erosions gradually became confluent, and a striking dry, glazed, peau d'orange appearance was noted. Polycystic microbullae appeared in the epithelium in some eyes. Thick keratinized epithelial plaques developed in all eyes 1 to 2 weeks after the appearance of severe peau d'orange. Electron microscopy of corneas with lusterless graying of the epithelium revealed swelling of the most superficial epithelial cells with flattened and shorter microvillous projections. In corneas with punctate epithelial erosions and keratinized plaques, microvilli were absent or decreased in number on superficial cells, and multilayered, keratinized epithelial cells were present on the surface of the cornea. The stroma appeared essentially normal with minimal edema at all stages when examined by electron microscopy. Intercellular edema was present in the endothelium in early- and late-stage xerotic corneas but could not be detected clinically. No significant clinical or microscopic alterations were seen in the corneas of control rabbits on normal diet or in rabbits on the vitamin A-deficient diet supplemented with vitamin A. The alterations seen in the corneas of vitamin A-deficient rabbits are similar to those which have been described in vitamin A-deficient humans. Rabbit therefore appears to be a good model for further studies of xerophthalmia.