The Glenn A. Fry Award lecture 1988: the ocular response to contact lens wear.

Contact lens materials over the last 20 years have progressed from polymethyl methacrylate (PMMA) through hydrogels to high Dk rigid and semi-soft lenses. Our understanding of how and why contact lenses affect the eye has also advanced considerably. We now know that: (1) the oxygen demands of the eye are high and (2) carbon dioxide accumulates and corneal acidosis occurs with most current contact lenses, especially with extended wear (EW). The effects of these perturbations on the epithelium include decreased metabolic rate, thinning, microcysts, and reduced adhesion. In addition, stromal edema and thinning and, with pressure, distortion occur with the long-term use of low to moderate oxygen transmissible lenses. Endothelial polymegethism also occurs and is a relatively permanent effect of inadequate oxygen permeability (Dk). The major consequence of chronic hypoxia and acidosis is, for a significant number of patients, corneal intolerance and discontinuation of lens wear. High permeability materials (100 Dk) that provide adequate gaseous exchange for daily wear and minimal changes in EW are now available and should be used where possible. The more obvious problems of contact lens-induced chronic inflammation, e.g., contact lens-induced papillary conjunctivitis (CLPC), and acute inflammation, e.g., acute red eye (ARE), are less well understood. Protein deposits, lens ageing, occlusion, mechanical effects, and bacterial contamination have all been implicated. The remaining frontiers include understanding and avoiding the stimuli to low grade irritation and inflammation by making contact lenses more comfortable and improving their compatibility with the ocular surfaces.