6.1 Contact lenses
Contact lens wear increases the risk of developing dry eye from between 2.01 and 2.96 times [580–582]. Contact lenses compartmentalize the tear film into two layers; the outer pre-lens tear film layer in front of the lens, and the inner post-lens tear film layer, which lies between the lens and the cornea [583,584]. With lens wear, the tear film undergoes extensive biophysical and biochemical changes, which have the potential to influence tear function and/or contact lens tolerance.
In 2013 TFOS published the outcomes of a workshop on Contact Lens Discomfort, including a subcommittee report of Contact Lens Interactions With the Tear Film [54]. The following were associated with worsening of comfort during lens wear: increases in the rapidity of tear film breakup time on the cornea or over the surface of a contact lens; higher contact lens water content; the grade of tear ferning (grade 0 vs. grades 1 or 2); increased tear evaporation rate during contact lens wear; reduced tear flow rate and tear volume; impaired tear film lipid layer; mucin degradation on contact lenses; increases in the concentrations of lipocalin-1, secretory phospholipase A2 (and activity), and lipid aldehyde products. The following section will concentrate on references published since that report.
In cross-sectional studies there are no statistically significant differences in tear film osmolarity between contact lens wearers and non-lens wearers [131,585]. The concentration of phospholipase A2 levels in tears has been associated with an increased concentration of malondialdehyde, which is also a by-product of phospholipid degradation and shorter TBUT over a contact lens [586].
The limited thickness of the post-lens tear film (1–2 μm) has clinical implications, as the stagnation of tears beneath a contact lens is believed to be one of the major causes of complications seen with contact lens wear, including mucin ball formation and ocular surface staining [587]. Technological limitations have not allowed for the accurate and non-invasive determination of fluid circulation between the pre- and post-lens tear film, a phenomenon commonly referred to as tear exchange or tear turnover. Fluorophotometry studies on tear exchange have demonstrated that tear exchange occurs in 30 min with soft lenses [588,589], which is longer than that with rigid lenses or no lens wear [590]. This large difference probably relates to lens size and material stiffness, and therefore lens movement with the blink. Silicone hydrogel materials were reported to improve tear exchange by 5% compared to hydrogels [589] due to the slightly higher modulus, which improves lens movement. Good tear exchange may minimize the risk of adverse sequelae via timely flushing of debris and metabolic by-products from the ocular surface. Innovations in soft lens designs, in an attempt to increase tear exchange, have not proven clinically effective thus far [587].
A thicker lipid layer during contact lens wear is associated with increased stability of the tear film, increased interblink period and decreased tear evaporation rate [586]. Using interferometry, the lipid layer thickness over soft contact lenses was estimated to be around 15 nm [586]. Reduced pre-lens TBUT values have been associated with increased symptoms of discomfort in hydrogel contact lens wearers [586]. A prospective, randomized, crossover study, showed that a daily disposable silicone hydrogel contact lens manufactured from delefilcon A permitted significantly longer NIBUT compared to lenses made from narafilcon A and filcon II-3, in addition to inducing significantly less corneal staining after 16 h of wear [595]. However, the study found no improvement in comfort with any particular contact lens [595]. Use of a liposomal eye spray has been reported to improve pre-lens TBUT [586]. Recently, a prospective, randomized, double blind study reported a favorable effect of Omega 3 fatty acid supplements in improving tear film stability, tear film breakup time and wear comfort in contact lens wearers [596].
The hypothesis that inflammation may be involved in contact lens discomfort has not been supported by two studies examining levels of cytokines in tears of contact lens wearers. One study examining tear cytokine concentrations of symptomatic and asymptomatic lens wearers found no difference in the concentration of 11 cytokines in tears, including IL-1β, IL-6 and IL-8 [597]. The other study found no change in the concentration of 14 cytokines in tears over the course of a day wearing contact lenses, even though comfort was significantly reduced [440]. The latter study did find the concentration of VEGF was correlated with ocular comfort, but the change in VEGF concentration was more pronounced when contact lenses were not worn rather than during lens wear.
Although previous studies evaluating transmembrane mucins during contact lens wear reported conflicting results, using fluorescein-labeled wheat germ agglutinin (F-WGA) as a marker, Fukui et al. [598] reported less fluorescence intensity in soft contact lens wearers. Observing a positive correlation between tear film breakup time and F-WGA fluorescence, the authors suggested that a decrease or compositional alteration of ocular surface glycocalyx could be a factor in contact lens-induced dryness. Disturbance of the glycocalyx during contact lens wear may be due to slower epithelial turnover and consequently decreased quality of surface mucin, contact lens-induced friction and resultant inflammation, or restricted tear exchange resulting in restricted delivery of secreted mucins on the corneal surface [598].
What is still unclear is the natural history of contact lens discomfort. Are people who experience contact lens discomfort normal before lens wear and at risk of developing symptoms of dry eye even on contact lens removal entirely as a result of wearing lenses? Or are those people predisposed to dry eye (perhaps having subclinical signs or symptoms) and contact lens wear tips them towards dry eye?
Contact lens wear increases the risk of developing dry eye from between 2.01 and 2.96 times [580–582]. Contact lenses compartmentalize the tear film into two layers; the outer pre-lens tear film layer in front of the lens, and the inner post-lens tear film layer, which lies between the lens and the cornea [583,584]. With lens wear, the tear film undergoes extensive biophysical and biochemical changes, which have the potential to influence tear function and/or contact lens tolerance.
In 2013 TFOS published the outcomes of a workshop on Contact Lens Discomfort, including a subcommittee report of Contact Lens Interactions With the Tear Film [54]. The following were associated with worsening of comfort during lens wear: increases in the rapidity of tear film breakup time on the cornea or over the surface of a contact lens; higher contact lens water content; the grade of tear ferning (grade 0 vs. grades 1 or 2); increased tear evaporation rate during contact lens wear; reduced tear flow rate and tear volume; impaired tear film lipid layer; mucin degradation on contact lenses; increases in the concentrations of lipocalin-1, secretory phospholipase A2 (and activity), and lipid aldehyde products. The following section will concentrate on references published since that report.
In cross-sectional studies there are no statistically significant differences in tear film osmolarity between contact lens wearers and non-lens wearers [131,585]. The concentration of phospholipase A2 levels in tears has been associated with an increased concentration of malondialdehyde, which is also a by-product of phospholipid degradation and shorter TBUT over a contact lens [586].
The limited thickness of the post-lens tear film (1–2 μm) has clinical implications, as the stagnation of tears beneath a contact lens is believed to be one of the major causes of complications seen with contact lens wear, including mucin ball formation and ocular surface staining [587]. Technological limitations have not allowed for the accurate and non-invasive determination of fluid circulation between the pre- and post-lens tear film, a phenomenon commonly referred to as tear exchange or tear turnover. Fluorophotometry studies on tear exchange have demonstrated that tear exchange occurs in 30 min with soft lenses [588,589], which is longer than that with rigid lenses or no lens wear [590]. This large difference probably relates to lens size and material stiffness, and therefore lens movement with the blink. Silicone hydrogel materials were reported to improve tear exchange by 5% compared to hydrogels [589] due to the slightly higher modulus, which improves lens movement. Good tear exchange may minimize the risk of adverse sequelae via timely flushing of debris and metabolic by-products from the ocular surface. Innovations in soft lens designs, in an attempt to increase tear exchange, have not proven clinically effective thus far [587].
A thicker lipid layer during contact lens wear is associated with increased stability of the tear film, increased interblink period and decreased tear evaporation rate [586]. Using interferometry, the lipid layer thickness over soft contact lenses was estimated to be around 15 nm [586]. Reduced pre-lens TBUT values have been associated with increased symptoms of discomfort in hydrogel contact lens wearers [586]. A prospective, randomized, crossover study, showed that a daily disposable silicone hydrogel contact lens manufactured from delefilcon A permitted significantly longer NIBUT compared to lenses made from narafilcon A and filcon II-3, in addition to inducing significantly less corneal staining after 16 h of wear [595]. However, the study found no improvement in comfort with any particular contact lens [595]. Use of a liposomal eye spray has been reported to improve pre-lens TBUT [586]. Recently, a prospective, randomized, double blind study reported a favorable effect of Omega 3 fatty acid supplements in improving tear film stability, tear film breakup time and wear comfort in contact lens wearers [596].
The hypothesis that inflammation may be involved in contact lens discomfort has not been supported by two studies examining levels of cytokines in tears of contact lens wearers. One study examining tear cytokine concentrations of symptomatic and asymptomatic lens wearers found no difference in the concentration of 11 cytokines in tears, including IL-1β, IL-6 and IL-8 [597]. The other study found no change in the concentration of 14 cytokines in tears over the course of a day wearing contact lenses, even though comfort was significantly reduced [440]. The latter study did find the concentration of VEGF was correlated with ocular comfort, but the change in VEGF concentration was more pronounced when contact lenses were not worn rather than during lens wear.
Although previous studies evaluating transmembrane mucins during contact lens wear reported conflicting results, using fluorescein-labeled wheat germ agglutinin (F-WGA) as a marker, Fukui et al. [598] reported less fluorescence intensity in soft contact lens wearers. Observing a positive correlation between tear film breakup time and F-WGA fluorescence, the authors suggested that a decrease or compositional alteration of ocular surface glycocalyx could be a factor in contact lens-induced dryness. Disturbance of the glycocalyx during contact lens wear may be due to slower epithelial turnover and consequently decreased quality of surface mucin, contact lens-induced friction and resultant inflammation, or restricted tear exchange resulting in restricted delivery of secreted mucins on the corneal surface [598].
What is still unclear is the natural history of contact lens discomfort. Are people who experience contact lens discomfort normal before lens wear and at risk of developing symptoms of dry eye even on contact lens removal entirely as a result of wearing lenses? Or are those people predisposed to dry eye (perhaps having subclinical signs or symptoms) and contact lens wear tips them towards dry eye?
References in this excerpt:
[54] Craig JP, Willcox MD, Argueso P, Maissa C, Stahl U, Tomlinson A, et al. The TFOS International Workshop on Contact Lens Discomfort: report of the contact lens interactions with the tear film subcommittee. Invest Ophthalmol Vis Sci 2013;54. TFOS123–56.
[131] Chen SP, Massaro-Giordano G, Pistilli M, Schreiber CA, Bunya VY. Tear osmolarity and dry eye symptoms in women using oral contraception and contact lenses. Cornea 2013;32:423–428.
[440] Willcox MD, Zhao Z, Naduvilath T, Lazon de la Jara P. Cytokine changes in tears and relationship to contact lens discomfort. Mol Vis 2015;21:293–305.
[580] Tan LL, Morgan P, Cai ZQ, Straughan RA. Prevalence of and risk factors for symptomatic dry eye disease in Singapore. Clin Exp Optom 2015;98:45–53.
[581] Paulsen AJ, Cruickshanks KJ, Fischer ME, Huang GH, Klein BE, Klein R, et al. Dry eye in the beaver dam offspring study: prevalence, risk factors, and health-related quality of life. Am J Ophthalmol 2014;157:799–806.
[582] Yang WJ, Yang YN, Cao J, Man ZH, Yuan J, Xiao X, et al. Risk Factors for Dry Eye Syndrome: A Retrospective Case-Control Study. Optom Vis Sci 2015;92:e199–205.
[583] Holly FJ. Tear film physiology and contact lens wear. II. Contact lens-tear film interaction. Am J Optom Physiol Opt 1981;58:331–341.
[584] Nichols JJ, King-Smith PE. The impact of hydrogel lens settling on the thickness of the tears and contact lens. Invest Ophthalmol Vis Sci 2004;45:2549–2554.
[585] Muselier-Mathieu A, Bron AM, Mathieu B, Souchier M, Brignole-Baudouin F, Acar N, et al. Ocular surface assessment in soft contact lens wearers; the contribution of tear osmolarity among other tests. Acta Ophthalmol 2014;92:364–369.
[586] Rohit A, Willcox MD, Brown SH, Mitchell TW, Stapleton F. Clinical and biochemical tear lipid parameters in contact lens wearers. Optom Vis Sci 2014;91:1384–1390.
[587] Muntz A, Subbaraman LN, Sorbara L, Jones L. Tear exchange and contact lenses: a review. J Optom 2015;8:2–11.
[588] McNamara NA, Polse KA, Bonanno JA. Fluorophotometry in contact lens research: the next step. Optom Vis Sci 1998;75:316–322.
[589] Paugh JR, Stapleton F, Keay L, Ho A. Tear exchange under hydrogel contact lenses: methodological considerations. Invest Ophthalmol Vis Sci 2001;42:2813–2820.
[590] Polse KA. Tear flow under hydrogel contact lenses. Invest Ophthalmol Vis Sci 1979;18:409–413.
[591] Luo L, Li DQ, Doshi A, Farley W, Corrales RM, Pflugfelder SC. Experimental dry eye stimulates production of inflammatory cytokines and MMP-9 and activates MAPK signaling pathways on the ocular surface. Invest Ophthalmol Vis Sci 2004;45:4293–4301.
[592] Heimer SR, Evans DJ, Mun JJ, Stern ME, Fleiszig SM. Surfactant protein D contributes to ocular defense against Pseudomonas aeruginosa in a murine model of dry eye disease. PLoS One 2013;8:e65797.
[593] Toshida H, Nguyen DH, Beuerman RW, Murakami A. Neurologic evaluation of acute lacrimomimetic effect of cyclosporine in an experimental rabbit dry eye model. Invest Ophthalmol Vis Sci 2009;50:2736–2741.
[594] Toshida H, Nguyen DH, Beuerman RW, Murakami A. Evaluation of novel dry eye model: preganglionic parasympathetic denervation in rabbit. Invest Ophthalmol Vis Sci 2007;48:4468–4475.
[595] Wolffsohn JS, Mroczkowska S, Hunt OA, Bilkhu P, Drew T, Sheppard A. Crossover evaluation of silicone hydrogel daily disposable contact lenses. Optom Vis Sci 2015;92:1063–1068.
[596] Bhargava R, Kumar P. Oral omega-3 fatty acid treatment for dry eye in contact lens wearers. Cornea 2015;34:413–420.
[597] Lopez-de la Rosa A, Martin-Montanez V, Lopez-Miguel A, Calonge M, Enriquez-de-Salamanca A, Gonzalez-Garcia MJ. Corneal Sensitivity and Inflammatory Biomarkers in Contact Lens Discomfort. Optom Vis Sci 2016;93:892–900.
[598] Fukui M, Yamada M, Akune Y, Shigeyasu C, Tsubota K. Fluorophotometric Analysis of the Ocular Surface Glycocalyx in Soft Contact Lens Wearers. Curr Eye Res 2016;41:9–14.