Contact lens wear is one of the primary risk factors for the development of ocular
surface inflammatory events. The purpose of this review is to examine and summarize
existing knowledge on the mechanisms of contact lens related ocular surface inflammation
and the evidence for the effectiveness of current objective methods to measure ocular
surface inflammation. Contact lens wear is postulated to trigger an inflammatory response
on the ocular surface due to mechanical, chemical, hypoxic stress, or by the introduction
of microbes and their toxins. Apart from the traditional signs of inflammation, such
as swelling, oedema, redness and heat, on the ocular surface, other methods to measure
ocular surface inflammation in sub-clinical levels include tear inflammatory mediator
concentrations, conjunctival cell morphology, and corneal epithelial dendritic cell
density and morphology. Tear inflammatory mediator concentrations are up- or down-regulated
during contact lens wear, with or without the presence of associated inflammatory
events. There is higher conjunctival cell metaplasia observed with contact lens wear,
but changes in goblet cell density are inconclusive. Dendritic cell density is seen
to increase soon after initiating soft contact lens wear. The long term effects of
contact lens wear on dendritic cell migration in the cornea and conjunctiva, including
the lid wiper area, require further investigation. Currently patient factors, such
as age, smoking, systemic diseases and genetic profile are being studied. A better
understanding of these mechanisms may facilitate the development of new management
options and strategies to minimize ocular surface inflammation related to contact
lens wear.