CONTACT LENS INTERACTIONS WITH THE TEAR FILM

In evaluating contact lens interactions with the tear film and how those interactions might result in discomfort, the workshop considered the biophysical and the biochemical effects of contact lens wear on the tear film and their influence on discomfort.
The physical presence of a contact lens in situ divides the tear film into a pre- and postlens tear film, creating new interfaces with the ocular environment. Tear film changes occur upon lens application and during subsequent wear. In addition, biochemical differences are likely to exist between the pre- and postlens tear film layers. Partitioning of the tear film upon contact lens application and wear causes a series of compositional changes that result in a less stable tear film on the front surface of the lens and less well-defined changes to the postlens tear film layer. The resulting prelens tear film has reduced lipid layer thickness, reduced tear volume, and increased evaporation rate compared to the normal tear film. While the direct impact of these tear properties on discomfort has not been elucidated fully, the evidence to date specifically suggests that decreased tear film stability, increased tear evaporation, reduced tear film turnover, and tear ferning are associated with CLD. Further evidence is needed to support the associations between tear volume, surface tension, osmolarity, pH, and ocular surface temperature and CLD.
With respect to biochemical changes in tear film composi- tion associated with contact lens wear, there appears to be no relationship between total protein, lactoferrin, and lysozyme with CLD. Current evidence suggests that levels of tear lipocalin-1, levels and activity of sPLA2, and levels of degraded lipids may be increased, and phospholipids decreased in CLD, which may be consistent with biochemical and functional changes in the tear lipid layer. Certain polar lipids, specifically the (O-acetyl)-omega-hydroxy fatty acids and their esters, have been associated with symptom reporting and may be important in CLD. Further evidence is needed to establish links between MUC5AC and other changes in the tear proteome with CLD. Given the potential evidence for frictional wear and lid wiper epitheliopathy in the pathophysiology of CLD, it may be expected that tissue and tear proteases, and inflammatory mediators would be increased in the tear film; however, such changes have not yet been demonstrated consistently.

There are significant gaps in our understanding of the extent to which tear film changes in contact lens wear are responsible for CLD. There is good evidence for associations between changes in tear lipids likely in the prelens tear film and CLD, although it is not clear if these changes are causal, or that they are present before contact lens wear. To understand these relationships better, it is important to use the definition of CLD as defined herein in future research and to study relevant subject groups using an appropriate study design. The lack of evidence for the postlens tear film in CLD likely relates to the current difficulties in evaluating this layer, in addition to the fact that this layer is relatively stagnant, as it largely is trapped and stagnant behind the contact lens.
Evidence also suggests that the parameters of the prelens tear film are interrelated and, therefore, it is difficult to identify a single component as being responsible for CLD. Tear film stability (via evaporation), however, is recognized as a key factor in CLD, and it appears to be a consequence of multiple tear film characteristics and their interactions. Given the relevance of prelens tear film stability in CLD, future research should focus on the development of novel materials or surface treatments to resist tear evaporation during wear, and on the development of wetting agents in care products to promote long-term contact lens wettability.