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Contact lens wear shown to induce reduction of corneal epithelial layers
More precise measurement of corneal epithelium thickness and number of epithelial layers following contact lens wear would be useful, physician says.
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The human corneal epithelium has five to eight cell layers and is 50 µm to 52 µm thick. It is the most regular arrangement of stratified epithelium in the human body. The cell layers of the epithelium include three to four outer flattened squamous cells, one to three layers of wing cells and a single layer of columnar basal cells.
The corneal epithelium is self-renewing, and in the cornea, complete turnover occurs in approximately 5 to 7 days. The function of the corneal epithelium is twofold: to form a barrier between the environment and the stroma of the cornea, and, through its interaction with the tear film, to form a smooth refractive surface. Adjacent superficial epithelial cells are joined by zonula occludens, creating a barrier that resists bacterial adherence.
Influence of contact lenses
There are corneal dystrophies and systemic metabolic disorders that involve the cornea only at the level of the epithelium. What about the influence of contact lenses on the corneal epithelium?
We found a significant reduction of epithelial opacities in two patients with Fabry’s disease after they had worn daily polymethylmethacrylate (PMMA) and HEMA contact lenses for 4 months. Upon discontinuation of the contact lens, there was a renewed increase of typical vortex opacities.
Walter Lisch
Bourne reported on three patients with Meesmann corneal dystrophy in whom the wearing of soft contact lenses had led to significant decrease in the epithelial microcysts. The symptoms returned in 3 to 4 weeks when the contact lenses were discontinued. We reported on two unrelated female patients with Lisch epithelial corneal dystrophy and the beneficial effect of soft contact lens wearing. Discontinued wearing of contact lenses again induced a progression of opacity. The etiology of this phenomenon is interpreted as a contact lens-induced reduction of corneal epithelial layers.
Corneal pathophysiology during contact lens wear may be hypoxic, hypercapnic, allergic, toxic, mechanical or osmotic in origin. Of these, the most common etiological factors are hypoxia and hypercapnia. By inducing corneal hypoxia, contact lens wear suppresses corneal aerobic metabolism and stimulates anaerobic glycolysis. These changes have many important sequelae, including lowered epithelial metabolic rate, increased epithelial lactate production and an acid shift in stromal pH. A reduction in epithelial metabolic rate affects every aspect of epithelial physiology, including miotic rate, cellular functional integrity and the cellular reserves of glycogen.
In a histological study of monkeys, PMMA lenses or thick hydrogel lenses caused corneal epithelial thinning after only a few days of wear. Contact lens wear of duration may cause thinning of epithelium with the consequence of reduction of epithelial layers, for example, from seven to three. Ren et al examined 178 patients to determine the effects of different contact lens types with regard to central epithelial thickness. The thickness of the central corneal epithelium was determined by in vivo tandem scanning confocal microscopy (Tandem Scanning).
The results show significant central epithelial thinning with all tested contact lenses. The central epithelial thinning may result from an overall decrease in central basal proliferation associated with decreased upward movement to replace exfoliated cells. The investigations of Ren and colleagues could explain the contact lens-induced regression of epithelial opacities in the central cornea due to epithelial thinning in patients with Fabry’s disease, and Meesmann and Lisch corneal dystrophy.
Conclusions
The postulated contact lens thinning of the corneal epithelium, dependent on contact lens type and wearing time, may cause a diminished barrier function of the corneal epithelium against bacterial, mycotic and viral infections. The occurrence of a severe keratitis represents a relatively frequent ocular problem with regard to contact lens wearers.
Our reported contact lens-induced alterations of the corneal epithelium concern every one of the approximately 100 million contact lens wearers worldwide. At the moment, it is not possible to measure the epithelium’s exact thickness of the cornea. It would be desirable, with regard to the postulated contact lens-induced changes, if the measurements of the corneal epithelium’s thickness and the exact number of epithelial layers could be performed more precisely in the future.