dry eye dx and tx

The New Dry Eye, Part 3: Ocular Surface Inflammation

BY KELLY K. NICHOLS, OD, MPH, PHD

In this final installment of a three-part series, I will conclude my discussion of the new dry eye definition, which published in April 2007 as part of the Report of the International Dry Eye Workshop (DEWS) in the journal The Ocular Surface. This column will focus on the last part of the definition — inflammation of the ocular surface (Table 1).

Inflammation Basics

The ocular surface can respond to acute and chronic insults only in a limited fashion, and most would consider the inflammatory cascade as the primary response mechanism. We can assess some clinical hallmarks of inflammation such as heat, edema and redness with slit lamp biomicroscopy. For example, when we clinically see bulbar injection in a contact lens wearer, we're likely looking at a low-grade inflammatory response.

Tears and the Tear Film

The ocular surface is bathed in a solution full of proteins and lipids of varying sizes and with many different roles. Mucins, which are proteins with carbohydrate chains attached, are significantly large molecules, while proteins are smaller and lipids are relatively tiny in comparison. Researchers have found more than 100 unique proteins in the normal ocular tear film, and many more are expected in the inflamed condition. Enzymes can be up-regulated or down-regulated in response to irritants and the inflammatory process. These complex biological processes are normal, and the resultant inflammatory mediators are detectable in the tear film in patients who have ocular surface disease as well as in patients wearing contact lenses.

What evidence supports the inclusion of inflammation in the definition of dry eye? Note that the definition states that dry eye is accompanied by inflammation of the ocular surface and not caused by. In the DEWS process, there were many somewhat heated debates over this issue, which is an indication of the status of our understanding in this area. There's compelling evidence of inflammatory mediators and proteins in the tear film of dry eye patients, as well as evidence that cyclosporine treatment can reduce some of these mediators. What remains unclear is whether inflammation initiates other processes on the ocular surface that result in symptoms or whether other processes create the inflammation. Either way, it's likely that this process potentates itself in a vicious cycle.

Can We Measure and Treat it?

Not all dry eye patients respond with a complete reduction of symptoms with the use of either topical cyclosporine or steroid drops. Dry eye is multifactorial; therefore, no two dry eye cases are exactly the same, either in presentation or in response to treatment. In addition, a clinician's ability to "see" inflammation is limited to the slit lamp as we have no clinical tests to detect inflammatory biomarkers. Finally, without understanding the true etiology of the disease and the interaction of the confounding factors, our ability to treat all patients effectively is limited.

Reducing inflammation, which we could potentially achieve with a topical immune-modulator or by stabilizing the tear film, is a worthy goal in managing this complex disease. CLS

Dr. Nichols is an associate professor at The Ohio State University College of Optometry in the area of dry eye research.