Contact lens wear and the diabetic corneal epithelium: A happy or disastrous marriage?

Abstract

Diabetes mellitus is an epidemic in the US and abroad. With the advent of new contact lens technology, the use of contact lenses as glucose sensors in lieu of the traditional finger stick is quickly becoming realized. This has the potential to rapidly expand the contact lens market into this growing patient population. The independent cellular and physiological effects of contact lens wear and diabetes on the corneal epithelium have been described. However, little evidence exists to date to support whether there is increased risk associated with contact lens wear in diabetes. The focus of this review is to discuss what is known about the cellular effects of contact lenses on the corneal epithelium, the pathophysiological changes in the corneal epithelium that occur in diabetes, and whether an increased risk for corneal epithelial damage and/or infection may negatively impact safety in diabetic contact lens wearers. Available data indicates that there are inherent risks associated with contact lens wear in diabetics. Importantly, eye care practitioners fitting contact lenses in the diabetic patient need to carefully consider the duration of disease, the level of glycemic control, the presence of retinopathy, and the patient's overall health.

Keywords: Contact lens; Cornea; Diabetes; Epithelium; Infectious keratitis.

Figure 1:

Schematic of corneal epithelial renewal. (A) Stem cells reside in the basal layer of the limbus. (B) Following departure from the limbus, basal epithelial cells become transient amplifying cells and exhibit a high proliferative capacity. (C) Cells continue to migrate to the central cornea, losing proliferative capacity as they go. After the final round of cell division, the paired cells move towards the corneal surface. (D) At the corneal surface, cells are shed or desquamated into the precorneal tear film. Figure taken from Ladage et al. Contact Lens Ant eye 2002.

Figure 2:

In vivo confocal microscopy confirms loss of the human subbasal nerve plexus in diabetes. (A) A representative image of the subbasal nerve plexus in a patient with T2DM. (B) A representative image of the subbasal nerve plexus in a non-diabetic control. Scale bar: 100 μm. Figure taken from Stuard et al. Invest Ophthalmol Vis Sci 2018.

Figure 3:

Distribution of basal epithelial cell proliferation and surface cell shedding in the rabbit cornea. 5-bromo-2’-deoxyuridine (BrdU) labeling of mitotic cells across the limbal and corneal epithelium (dotted line). Calcein-ethidium live/dead staining showing a central peak in non-viable cells in the surface epithelium (solid line). Figure taken from Ladage et al, Contact Lens Ant Eye 2002.

Figure 4:

Epithelial thinning is associated with loss of the subbasal nerve plexus in a Type 1 streptozotocin diabetic mouse model. (A) Three-dimensional surface rendering of the subbasal nerve plexus and associated terminal epithelial nerves in a control mouse. β-tubulin III staining in green. (B) Three-dimensional surface rendering of a Type 1 diabetic mouse. Scale bar: 10 μm. (C – D) Nerve modeling and segmentation using IMARIS Filament. Representative images showing the subbasal nerve plexus is shown in red, terminal epithelial nerves in blue (C, normal; D diabetic). Scale bar: 10 μm. Loss of the subbasal nerve plexus in (D) was associated with significant thinning of the corneal epithelium after 12 weeks of diabetes, 34.0 μm ± 3.0 μm (diabetes) compared to 38.6 μm ± 3.8 μm (control). Figure taken from Cai et al. Am J Pathol 2014.

Figure 5:

Corneal ulcers reported in diabetic patients. (A) Corneal ulcer caused by Prototheca wickerhamii. Numbers as described as detailed in the original case report. 1: central ulcer; 2: region of corneal thinning; 3: large infiltrate surrounding the ulcer; 4: lenticular changes. Image taken from Narayanan et al. Indian J Ophthalmol 2018. (B) Corneal ulcer caused by Roussoella solani. Image taken from Mochizuki et al. J Infect Chemo 2017. (C) Corneal ulcer caused by Corynebacterium propinquum. Image taken from Todokoro et al. J Clin Microbiol 2015. (D) Corneal ulcer caused by Stenotrophomonas maltophilia. Image taken from Holifield et al. Eye Contact Lens 2011.