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.

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Cytokines are key cell signalling proteins in a number of immune and homeostatic pathways of the human body. In particular, they mediate intracellular mechanisms of allergy on the ocular surface by triggering cellular responses that result in typical physiological ocular allergy symptoms, such as itchiness, watery eyes, irritation, and swelling. Given the recent research focus in optometry on the aetiology of corneal ectasia subtypes like keratoconus, there is an increasing need for the development of new clinical diagnostic methods. An increasing trend is evident among recent publications in cytokine studies, whereby the concentrations of cytokines in healthy and disease states are compared to derive a specific cytokine profile for that disease referred to as ‘biosignatures’. Biosignatures have diagnostic applications in ocular allergy as a cheap, non-invasive alternative to current techniques like IgE antibody testing and skin prick tests. Cytokine detection from tear samples collected via microcapillary flow can be analysed either by enzyme-linked immunosorbent assays (ELISA), multiplex magnetic bead assays, or immunoblot assays. Characterising patient hypersensitivities through diagnostic tests is the first step to managing exposure to triggers. Investigating cytokine biosignatures in ocular allergy and their links to physiology are imperative and will be the focus of this systematic review article.

The F-60 method allows faster collection than F-20, but the latter results in better repeatability than both the F-60 and Schirmer sampling techniques. All three techniques return the same concentrations of TPC and Substance P. This indicates that tear collection using the F-20 may be more appropriate when conducting comparative analysis, whereas the F-60 may be more appropriate when more volume is required.

Correlation between the two instruments was better when compared on collected tear samples. Tear film osmolarity measurement is influenced by the sample collection technique with the osmolarity of on-eye tears being higher than that of collected tears. This highlights the importance of measuring tear film osmolarity directly on-eye. The in situ osmometer has good repeatability for conducting this measurement.