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This may seem to be an odd question to be asking, but please hear me out. Back in the early 1970s, when studying General Physiology 101, I was taught that the five cardinal signs of inflammation, expressed classically in Latin, were dolor (pain), calor (heat), rubor (redness), tumor (swelling) and functio laesa (loss of function). This ‘rule of thumb’ worked fine when considering inflammatory reactions of the skin, but I soon learnt that it was of less assistance when considering ocular inflammation. For example, being avascular, the cornea cannot display rubor. Further to this, in Ocular Physiology 101, I was taught that the eye enjoys ‘immune privilege’—an evolutionary adaptation that provides protection from the potentially damaging effects of an inflammatory immune response.
These concepts have been playing on my mind throughout my academic career when trying to understand adverse ocular reactions to contact lens wear. I have authored a book on this very topic.1 More than a quarter of a century ago, I asked whether contact lens-induced corneal oedema is inflammatory,2 and at that time concluded that it is not.3 A related question of contemporary interest is whether contact lenses, in addition to inducing an occasional frank inflammatory response, stimulate the eye to be in a constantly elevated inflammatory status, albeit sub-clinical.
Fast forward to the 21st century. Researchers and clinicians are now able to assess the inflammatory response to contact lens wear across a broad spectrum—ranging from the classical macroscopic perspective of signs and symptoms according to the five cardinal signs outlined above,1 to the emerging microscopic, sub-clinical world of inflammatory cells and biochemical mediators. As I shall outline below, phenomena at the microscopic end of this spectrum can now be investigated …
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