Contact lens wear is intrinsically inflammatory

Abstract

Eye‐care practitioners typically associate ocular inflammation during contact lens wear with serious complications such as microbial keratitis; however, more subtle mechanisms may be at play. This paper tests the notion that contact lens wear is intrinsically inflammatory by exploring whether uncomplicated contact lens wear meets the classical, clinical definition of inflammation – rubor (redness), calor (heat), tumor (swelling), dolor (pain) and functio laesa (loss of function) – as well as the contemporary, sub‐clinical definition of inflammation (cellular and biochemical reactions). It is demonstrated that all of these clinical and sub‐clinical criteria are met with hydrogel lens wear and most are met with silicone hydrogel lens wear, indicating that uncomplicated contact lens wear is intrinsically inflammatory. Consideration of both traditional and contemporary thinking about the role of inflammation in the human body leads to the perhaps surprising conclusion that the chronic, low grade, sub‐clinical inflammatory status of the anterior eye during contact lens wear, which may be termed ‘para‐inflammation’, is a positive, protective phenomenon, whereby up‐regulation of the immune system, in a non‐damaging way, maintains the eye in a state of ‘heightened alert’, ready to ward off any extrinsic noxious challenge. Characterisation of this inflammatory status may lead to the development of lens engineering or pharmacological strategies to modulate contact lens‐induced inflammation, so as to render lens wear more safe and comfortable.

Key words:

• conjunctiva
• cornea
• contact lens wear
• inflammation
• para‐inflammation

^a Professor Nathan Efron AC was awarded the H Barry Collin Research Medal by Optometry Australia in 2015. This paper is based on his award lecture presented at the Southern Regional Congress (hosted by Optometry Victoria) on 5 March 2016 in Melbourne, Australia.

^a Professor Nathan Efron AC was awarded the H Barry Collin Research Medal by Optometry Australia in 2015. This paper is based on his award lecture presented at the Southern Regional Congress (hosted by Optometry Victoria) on 5 March 2016 in Melbourne, Australia.

ACKNOWLEDGEMENTS

I wish to acknowledge and thank a number of mentors and colleagues who have been of great assistance during my career. Barry Cole and Leo Carney have been magnificent ‘career mentors’. I have published works with a total of 385 co‐authors and I thank all of these colleagues. It is obviously not possible to acknowledge them all; however, I do wish to single out a few who have been with me for the long haul. I have had the good fortune and very great pleasure to have worked with Noel Brennan since 1984, Phil Morgan since 1990, Rayaz Malik since 2000 and Nicola Pritchard since 2006. I thank the four of you for enriching my life in research. Suzi Fleiszig and I have enjoyed mentoring each other (if that is possible) for over 30 years. Thanks Suzi for your unfailing friendship. On a personal level, I thank my wife, Suzanne and children, Zoe and Bruce, for their wonderful support, encouragement, love and devotion. I also thank my mother, Elaine and late father Jack, who sacrificed much to provide me with my early educational opportunities.

Notes

^a Professor Nathan Efron AC was awarded the H Barry Collin Research Medal by Optometry Australia in 2015. This paper is based on his award lecture presented at the Southern Regional Congress (hosted by Optometry Victoria) on 5 March 2016 in Melbourne, Australia.