Contact Lens Interactions with the Ocular Surface and CLD
BY MARIA MARKOULLI, PHD, MOPTOM, GRADCERTOCTHER, FBCLA, FAAO
It is the ultimate nuisance to clinicians, patients, and industry alike that despite the investment into contact lens technology, 10% to 50% of wearers drop out of lens wear within three years of commencement, most commonly because of discomfort (Pritchard et al, 1999). Dry eye symptoms are the most common (Riley et al, 2006), with 70% of people reporting symptoms late in the day (Begley et al, 2001).
To understand this conundrum, the Tear Film and Ocular Surface Society (TFOS) commissioned the TFOS International Workshop on Contact Lens Discomfort (CLD), which came to a consensus regarding the definition of CLD as being “a condition characterized by episodic or persistent adverse ocular sensations related to lens wear,” and that this resulted from “reduced compatibility between the contact lens and the ocular environment,” (Nichols KK et al, 2013). Given the outcome of reduced wearing time and ultimate contact lens discontinuation, it is important to understand the impact that contact lenses have on the ocular surface and what can be done about it.
The Role of Lens-Ocular Surface Interactions in CLD
During contact lens wear, the lens interacts with many aspects of the ocular surface. It separates the tear film into the pre- and post-lens tear film. This affects the tear film lipid layer spread, tear film stability, and tear evaporation, which in turn contributes to CLD (Craig et al, 2013). Reduced tear film stability and impaired lipid layer function result in less lubrication and greater friction between the contact lens and the ocular surface (Jones et al, 2013). If we review the features of the ocular surface that have been associated with CLD—for example, conjunctival staining, conjunctival folds, and lid wiper epitheliopathy—we can see a further link with friction.
CLD and the Conjunctiva Contact lens interaction with the conjunctiva can result in changes visible at both a cellular and a clinical level. At the cellular level, contact lens wear can result in conjunctival metaplasia in which the epithelial cells flatten and increase in shape, and goblet cell density decreases (Doughty, 2011), indicating mechanical friction. These cellular changes relate to CLD (Efron et al, 2013) and are reversible with lens wear cessation (Knop and Brewitt, 1992).
On a more clinical level, the TFOS workshop identified lid parallel conjunctival folds (LIPCOFs) as being associated with CLD (Efron et al, 2013). LIPCOFs can be identified using slit lamp biomicroscopy and white light, with the patient in primary gaze. Most recently, optical coherence tomography has also been used to quantify the degree of LIPCOFs (Tapasztó et al, 2011). Using routine slit lamp biomicroscopy, the number of conjunctival folds above the inferior lid are assessed relative to the height of the tear meniscus (Németh et al, 2012). Of note, LIPCOFs disappear when the lower eyelid is retracted and then reappear after a few blinks.
Tapasztó et al (2011) further showed that the very presence of a contact lens contributed to the presence of LIPCOFs and that removing the lens could significantly alter the appearance of this clinical phenomenon, contributing to the theory that they are mechanically induced. LIPCOFs are thought to represent elastic fiber degradation as a result of inflammation (Meller and Tseng, 1998) or due to mechanical friction influencing lymphatic flow (Watanabe et al, 2004).
While their etiology is not well understood, their presence can be a good positive predictive value for dry eye disease (Németh et al, 2012). Their role in both CLD and dry eye disease is thought to be due to the displacement of the tear meniscus (Meller and Tseng, 1998; Murube, 2005; Pult and Riede-Pult, 2015).
Unlike the controversial role of corneal staining in CLD, there is evidence to suggest that conjunctival staining as a result of contact lens wear is linked with CLD (Efron et al, 2013). Conjunctival staining can be assessed clinically by instilling sodium fluorescein and using the cobalt blue light of a slit lamp biomicroscope with a Wratten #12 filter. It can also be assessed using lissamine green and white light (Korb et al, 2008). It is not clear what conjunctival staining means at a cellular level; research needs to be conducted to understand this. As with the other conjunctival changes in contact lens wear, given the circumlimbal location coinciding with the edge of the contact lens, it is thought that this is again a result of increased friction between the lens and the ocular surface.
CLD and the Lid Wiper The term “lid wiper” was coined by Korb et al (2002) and describes a region that extends from the tarsal conjunctiva to the posterior lid border (Knop et al, 2012), with an area of 2.7mm ± 2.0mm (Navascues-Cornago et al, 2015). Lid wiper epitheliopathy is defined as staining of the lid wiper with fluorescein or lissamine green.
The role of the lid wiper is to distribute the tear film between blinks, analogous to a windshield wiper. Because it is presumed to be the only part of the eyelid that is in constant apposition with the globe, and hence with the contact lens, it is subjected to the friction that results from this interaction, ultimately impacting comfort (Korb et al, 2002) and, more specifically, leading to CLD. Lid wiper epitheliopathy is thought to result from the sheer stress of this mechanical interaction, a theory supported by reports that greater eyelid pressure is associated with greater lid wiper epitheliopathy (Yamamoto et al, 2015).
Given that friction is linked to CLD as well as to the clinical signs of lid wiper epitheliopathy, conjunctival staining, and LIPCOFs, it would seem fitting that a good place to begin to minimize CLD would be to reduce the amount of friction between the ocular surface, the lid margin, and the contact lens.
In an attempt to do this, Guthrie et al (2015) used an oil-in-water emulsion in symptomatic lens wearers, which improved symptoms and reduced the presence of lid wiper epitheliopathy. Another approach advocated lubricin, a product of the proteoglycan 4 gene, as a means to reduce friction and epitheliopathies of the ocular surface (Schmidt et al, 2013). This glycoprotein is secreted by synoviocytes, specialized cells located within the joints; its presence protects cartilage tissue against friction-related damage. Schmidt et al (2013) were able to identify ocular surface expression of lubricin; they suggest that a deficiency in this protein may result in ocular surface staining that is indicative of sheer stress and friction-related damage.
Important Directions for Future Research
The TFOS CLD workshop recommended that more needs to be done to understand the interactions between the ocular surface and the contact lens as well as how these relate to CLD. The association between friction and CLD and the signs of lid wiper epitheliopathy, LIPCOFs and conjunctival staining indicate that we need to look clinically for these signs as an indication of friction. These may be a “marker” of sorts of a patient at risk of CLD.
Taking action to then minimize friction is required to reduce this risk and the subsequent risk of dropping out of lens wear. Papas et al (2013) recommend careful, individual assessment, establishing the current status of the lens and its interactions with the ocular surface and adnexa. Once this has been ascertained, changing lens type and care solution, or eliminating the latter altogether by implementing a daily disposable schedule, is advised (Papas et al, 2013) to minimize lens-ocular surface interaction. Where this does not suffice, instigating tear supplementation with preservative-free supplements is recommended.
While in the future we may see the contact lens industry incorporating lubricin or other measures to reduce friction between the ocular surface and the contact lens, current evidence-based measures need to be implemented to overcome CLD. Importantly, each patient needs to be evaluated for the risk factors of CLD, with these being addressed as early as possible to minimize the number of people resorting to contact lens discontinuation. CLS
For references, please visit www.clspectrum.com/references and click on document #244.
Dr. Markoulli is a lecturer at the School of Optometry & Vision Science at the University of New South Wales in Sydney.