Putting a Lid on Epitheliopathy

The eyelids play an important role in the dynamic movement of the lacrimal functional unit across the ocular surface. Korb et al proposed that this action is primarily performed by a special portion of the palpebral conjunctiva known as the lid wiper region.¹ But what role does this tissue, and its interactions with the ocular surface, play in the setting of dysfunction in tear production, inflammation, hyperosmolarity, and loss of homeostasis, as seen in ocular surface disease (OSD)?^1,2

LID WIPER EPITHELIOPATHY

The lid wiper region is the marginal eyelid conjunctiva that makes close contact with the globe during a blink. Thus, lid wiper epitheliopathy (LWE) refers to epithelial disruption and damage to this area. Although the relationship between LWE and OSD is not completely understood, two factors that may accompany LWE are dry eye and contact lens wear (Figure).

LWE is revealed with the classic staining pattern of the palpebral conjunctiva and is best seen using vital dyes, particularly lissamine green,¹ which is generally more apparent on the upper lid than the lower lid, as the upper lid traverses more of the ocular surface with each blink. However, LWE can be easier to visualize on the lower lid due to better access during an ocular examination.

CELL-ON-CELL FRICTION

The presumed root cause of LWE and the mechanism of damage to these cells is friction, which can lead to apoptosis and, potentially, keratinization of conjunctival tissues.³ It’s easy to imagine how this epithelial disruption may exasperate OSD signs and symptoms, as the damaged, irregular lid wiper becomes less and less capable of performing its function. The damaged cells release cytokines and chemokines, triggering an inflammatory cascade, resulting in further damage to epithelial cells of the conjunctiva and goblet cells on the ocular surface, and, ultimately, perpetuating the vicious cycle of OSD.

STOP THE CYCLE

In addition to ocular surface staining, it is critical to examine the conjunctiva, including the palpebral conjunctiva, when assessing patients with OSD. The treatment of LWE centers on reducing the mechanical stress and friction between the lid-eye interface, allowing these tissues to heal and return to their normal structure and function. Hallmarks of such therapy include treating inflammation and increasing lubrication. Corticosteroids may be used to decrease inflammation in the acute phase, as well as artificial tears, punctal plugs, and a bandage contact lens to reduce cell-on-cell friction.

A NEW OPTION FOR THE TREATMENT TOOLBOX

In May, the FDA approved perfluorohexyloctane ophthalmic solution (Miebo, Bausch + Lomb), which is specifically designed to reduce evaporation and decrease surface tension. We are excited to explore this option for treating frictional OSD and LWE, as the properties of this drop may have potential to reduce the friction and shearing forces that occur with each blink in patients with LWE.