The literature on the tear film is rich in articles reporting the composition and production of tear proteins1–4 and inflammatory markers such as cytokines.5–8 However, an extensive literature review indicates that there are far fewer articles that report on lipids in the tear film and, in particular, their interaction with contact lens materials. This is partly because of difficulties encountered in sampling and analysis of lipids in a fluid film and also because proteins are historically known to interact with hydrogel materials in a much more profound and predictable fashion.9–14 The recent introduction of more hydrophobic silicone hydrogel materials, which have a greater interaction with hydrophobic lipids than that seen with conventional hydrogel materials,15,16 and the recent interest in producing artificial lubricants that stabilize the lipid layer of the tear film,17 has renewed interest in the lipid composition of the tear film and, particularly, its interaction with contact lens materials.
This article will review the structure and composition of the lipid layer of the tear film and its relationship to contact lens deposition of lipid. It will also suggest management strategies for clinicians that may help to reduce clinically significant lipid deposition on hydrogel lens materials, particularly silicone hydrogels.
Lipid Composition and Structure of the Tear Film
The tear film is a highly structured film that lies on top of the conjunctiva and the cornea, provides many specialized functions and needs to be strictly maintained in terms of composition. Historically, the tear film was considered to be a fairly rigidly structured film, consisting of three layers, with an outermost lipid layer, middle aqueous layer, and a mucin layer that lies closest to the ocular surface.18,19 Most early studies suggest that the outermost lipid layer accounts for about 1% to 1.5% of the total thickness of the tear film (<100 nm), whereas the aqueous layer makes up 98% (7 μm), and the mucin layer 0.5% (0.02–0.05 μm).18–21 This model has more recently been revised to reflect a more complex structure of the tear film, which suggests that the mucin layer is a more complex gel-like structure and the lipid layer is far more complex than previously proposed. This updated tear film model proposes that the tear film has many more “layers,” comprising a superficial oily layer against the air interface, polar lipid layer, absorbed mucoid, an aqueous layer, and mucoid layer “glycocalyx” on top of the corneal epithelium.22–24
The lipid layer is produced by the meibomian glands, which are holocrine glands that secrete lipids onto the ocular surface through an opening in the eyelid margin. The actual glands are withdrawn into the tarsal plate, with 20 to 25 individual glands in the lower lid and 30 to 40 glands in the upper lid.25–27 Individual glands are composed of acinar cells that open into a central duct running through the entire gland.27 These acini produce both nonpolar and polar lipids25–28 and then release them into the central duct, a process called “acinar cell degeneration.”27 The exact mechanism controlling the secretion of lipids from the meibomian glands is incomplete, but it is thought that the glands respond to neuronal, hormonal, and vascular controls.27,29 Neural stimulation is suggested by the fact that the meibomian glands are surrounded with vessels that are richly innervated.30,31 This regulation may be direct, through innervations of the acini, or indirect through the vasculature.29 In addition, many of the tear secreting glands, including the meibomian glands, glands of Moll, and glands of Zeis, have vasoactive intestinal polypeptide (VIP) innervation.32 The fact that both the lacrimal and meibomian glands have VIP innervation suggests that they may form a unit where secretion is controlled by the same neurotransmitter.31 Hormonal control is also suspected, as the meibomian gland acini express both estrogen and androgen receptors.33–35 Considerable research has been completed examining androgen influence on meibomian glands in animal and human tissues.36–41 Androgen influence on the meibomian glands does not appear to influence the structure of the meibomian glands; however, the meibomian glands are an androgen target organ.33,34,40 Research has shown that androgens regulate meibomian gland function and affect the pattern of lipids that are expressed.40 Lipid secretion patterns from the meibomian glands are changed when the amount of androgens in a system decreases.36 This commonly occurs in women when they are going through menopause. During menopause, there is a drastic decrease in overall sex hormone levels, and therefore androgens.42 Postmenopausal women are therefore more likely to experience changes in lipid expression, which appear to contribute to symptoms of dry eye. Specifically, differences in neutral and polar meibum lipid profiles seem to be linked to dry eye.36 In older subjects wearing contact lenses, this could potentially result in decreased wearing times caused by reduced tear film stability.
The composition of the meibum has a marked impact on both tear film stability and contact lens deposition. To determine what specific lipids are found in the meibomian secretions, the glands can be compressed, forcing the lipid to be excreted onto the lid margin, where it can be collected for analysis.43–45 Subsequent analysis by various forms of chromatography has determined the lipid types and relative amounts (Table 1).46–50
About 45 differing lipids have been identified in human meibum,23,44,47,51–54 with the individual lipid composition, in terms of both percentage of individual lipid and lipid types, varying greatly between individuals.55,56 Table 2 describes in greater detail the variety of lipids found within these lipid classes.23,44,46–48,51–54,56,57
If an individual has an altered concentration of a particular lipid in the tear film, the whole tear film may become unbalanced, resulting in complications such as contact lens intolerance and dry eye.58 Furthermore, diet, systemic medications, age, gender, environment, work atmosphere and the presence of contact lenses can also alter the final composition of the lipid within the tear film.59–62
Historically, lipids are considered to be only found within the outermost layer of the tear film. However, this is not the case and lipids are found throughout the tear film, including the base of the tear film adjacent to the outermost corneal epithelium.63 The superficial lipid layer actually comprises two different lipid phases, with the innermost layer being a polar-surfactant phase and the outermost phase being nonpolar (Fig. 1).23
The nonpolar phase contains a large amount of nonpolar lipids, including wax esters, cholesterol esters, triglycerides, and hydrocarbons. The nonpolar phase is larger than the polar phase and therefore, it is these lipids that are found in the greatest quantities.23 The hydrocarbons found in the nonpolar phase are much longer and therefore decrease the water vapor transmission rate of the lipid layer.64 The function of the nonpolar phase is that it regulates the transmission rate of water vapor, carbon dioxide, oxygen, and ions. Additionally, the nonpolar layer is a storage unit for triglycerides, wax esters, and other nonpolar lipids.23 The stability of the lipid layer relies on the chemical bonds that form between specific lipid types. Hydrogen bonds form between polar molecules, between water molecules and polar molecules, and between other lipid types such as triglycerides, wax esters, and sterol esters. Polar molecules can also bond with ionic bonds. The final type of bond is the van der Waals forces that form between fatty acids and fatty alcohol carbon chains.29
The polar phase of the lipid layer of the tear film is abundant in short-chain saturated fatty acids, which provide it with enhanced stability. However, the presence of unsaturated fatty acids or long branching chains of fatty acids contribute to instability and increased fluidity in the layer. There are a number of different types of polar lipids found in this phase, especially phosphatidylethanolamine, phosphatidylcholine, sphingomyelin, ceramides, cerebrosides plus many other specific phospholipids.23,47,52 The polar layer of the lipid tear film contains an estimated 3% to 5% of triglycerides.65 If there is a shortage of triglycerides it is possible that wax esters can supplement the triglycerides, but cannot replace them totally.23 The wax esters and triglycerides are not always strictly found in the polar phase but can bridge over to the nonpolar phase. Not all “normal” patients contain cholesterol esters in their tear film, but if they are present, and they bridge between the two lipid phases, the stability of the layers can be compromised.66 Additionally, free fatty acids, short-chain fatty alcohols, monoglycerides and diglycerides with short fatty acid chains are common in the polar phase.46 Some short-chained hydrocarbons may be found in the polar phase, and these hydrocarbons function to stabilize this phase.23 The overall stability of the polar lipid phase depends on the balance of polar lipids in the layer, the presence of ions, and the pH.23 Increases in pH, possibly caused by calcium, can affect the nature of internal phospholipid bonding and therefore jeopardize the stability of the polar phase of the tear film. The polar layer acts as a surfactant and a base for the more superficially located nonpolar phase.23
There are many factors that can result in alterations in lipid composition and in which lipid composition can play a significant etiological role. These include the development of lipid-related dry eye, such as that seen because of blepharitis or meibomian gland dysfunction. Another important consideration is that related to the interaction of contact lens materials with lipids within the tear film.
Lipid Deposition on Contact Lenses
Contact lens wear causes changes in the structure of the tear film, particularly within the lipid layer.67 Contact lenses lie within the aqueous layer of the tear film and therefore create a much thinner aqueous layer for the anterior lipid layer to cover. The presence of a contact lens also eliminates the smooth ocular surface over which the eyelid moves during a blink and also acts as a physical obstacle to destabilize the tear film. It is therefore much more difficult to reconstruct the tear film over this interface.68 Because of these factors, there is only a thin lipid layer on the outer surface of a soft hydrogel lens and no lipid layer covering a rigid lens.69 To remain “totally” biocompatible while being worn, the contact lens must form an overlying tear film that is structured similarly to that seen with no lens in place, which remains the ultimate goal in contact lens material research.
With little or no lipid layer present, the tear film easily becomes destabilized69,70 and the lipids come into direct contact with the lens material. Although their interaction with rigid lenses may interfere with surface wetting, a further problem exists with hydrogel lenses in that the materials are essentially semipermeable membranes, which have an ability to both adsorb and absorb lipids, resulting in varying degrees of lipid deposition. Although data on protein deposition on contact lens materials and its subsequent impact have been widely published,71–79 there is a relative dearth of information on the interaction of lipid with contact lenses. The deposition of lipid is primarily driven by the hydrophobic lipids adhering to hydrophobic sites on the lens surface and the specific chemistry of the underlying lens material.
Some of the earliest observations of the interaction of lipid with hydrogel contact lenses was that of Hart and co-workers,62,80,81 who examined lenses from both daily and overnight wearers, before the introduction of frequent replacement lenses. In one study,80 Hart reported that 15% of hydrophilic extended wear contact lens wearers needed to replace their lenses because of obvious deposition, with the rate of deposition ranging from a few weeks to a few months and was highly subject-dependent. The deposition pattern commonly seen was a central deposition of “oily bumps,” which Hart termed “jelly-bumps,” “mulberry spots” or “lens calculi,” as shown in Fig. 2.80 Hart demonstrated by various forms of microscopy and histochemical staining analysis that lipid was present in all deposits and was the prime component, with the principal lipid type being cholesteryl esters.80 Scanning and scanning transmission electron microscopy found small amounts of calcium within the deposits, at much lower levels than the lipid. This was an important finding, as calcium was previously considered to be a major component of these nodular deposits,82–88 which often are white in appearance. Hart also found that lipid deposits formed in an in vitro model were morphologically and histochemically similar to those formed in vivo.
In a later study,81 Hart determined that the jelly bump deposits had a fairly consistent composition of long and intermediate sized cholesteryl esters, triglycerides, and waxy esters. This composition is similar to the composition of lipids found in meibomian gland secretions. It was also found that individuals with higher deposition rates may have a lipid-rich tear film and a decreased tear flow, potentially resulting in “greasy” deposits on the front surface of their lenses (Fig. 3). These lipids are insoluble in aqueous mediums and therefore showed some resistance to cleaning products.81 Hart also examined lifestyle choices and their effect on lipid deposition of contact lenses.62 Individuals who consumed larger amounts of alcohol, protein, and fat exhibited increased lipid deposition on their lenses. Patients with diabetes who were medicated with diuretics, anticholinergic, or sympathomimetic drugs were found to have lower potassium levels in the tear film and this correlated with increased lipid deposition.62 This was one of the first times that attention was drawn to the marked intersubject variability in lipid deposition patterns. Hart proposed that the reason such nodular deposits occurred were caused by localized spots of drying, resulting in hydrophobic areas that attracted lipids, which then soaked into the lens material.80 This area then acted as a larger nonwetting area, which acted as a nidus for more lipid deposition. This continuous cycle of dewetting and lipid deposition resulted in a lipid-based nodule forming.
The work by Hart and colleagues in the United States was closely mirrored by that of Bowers and Tighe in the United Kingdom. They focused on analyzing the gross morphology, chemical composition, and arrangement of “white spot deposits” that form on different contact lens materials.89,90 In their first experiment, they examined the occurrence, location, and gross morphology of elevated white spot deposition which formed on contact lenses taken from a controlled contact lens trial and randomly from a clinical setting.90 Deposits were analyzed using several microscopy techniques including phase contrast, light, dark-field, and scanning electron microscopy. Additionally, stereomicroscopy was used to examine deposit occurrence. It was determined that there are three interactive sublayers to the morphology of an elevated white spot deposit and that differences in lens material and wearing protocol do not affect this morphology. In contrast, the rate of deposition was markedly influenced by the lens materials and patient variability.90 In their second experiment, Bowers and Tighe continued their previous white spot deposit analysis by examining their chemical composition and geological arrangement.89 The deposits were found to have a well-formed trilayer structure of lipid, where the primary or basal layer was composed of unsaturated lipids, whereas the secondary and tertiary layers were predominantly cholesterol and their esters.89 Other tear components, like proteins, were present in the deposits, but were not found to play a role in the morphology of the deposits. The wearing schedule, lens material chemistry and individual differences in tear film structure did not influence the composition or location of these deposits.89 They concluded from these results that it was the primary layer of unsaturated lipids that altered the biological surface of hydrogel lens materials and thus cause decreased biocompatibility with the surrounding ocular environment.89
Throughout the 1990s, Tighe, Franklin and colleagues set out to further their exploration into lipid deposition on contact lenses. They published a series of articles examining the influence that calcium, lens materials, and surfactant cleaners has on lipid deposition.91–94 In their first article, Bowers and colleagues examined the formation of white surface films and the importance of the role of calcium.94 Various contact lenses were collected, from a controlled clinical study and other clinical settings. During the controlled clinical study, the care solutions used were modified to increase the calcium concentration in the lens material in order to see the influence calcium has on deposit formation. They determined that these white surface films were morphologically different from elevated white spots, as these films have a heterogeneous structure where the lipid components are easily separated from the calcium portion. The lipid components were mainly cholesterol and cholesterol esters. The lens materials that were subjected to artificially raised calcium levels did not exhibit increased formation of elevated white spots. These results suggest that calcium may only have a secondary role in stabilizing lipids that have already been immobilized.94 Franklin and colleagues next examined lipid and protein deposition on human worn lenses after 1 week and studied the effect of surfactant cleaning on these deposits.93 Lipid and protein deposition was assessed using fluorescence spectroscopy at their respective wavelengths of emission and optimal excitation. This technique revealed that lipid deposition was largely influenced by an individual’s life-style, tear film composition and surrounding environment, whereas protein deposition was driven by the composition, charge and water content of the contact lens material. Individual tear film chemistry also influenced the effectiveness of surfactant cleaners on lipid deposition, making them only moderately helpful, especially within the first week of lens wear.93 Other studies have indicated that some surfactant cleaners are more efficient are removing lipid and protein deposits than others, and that these cleaners are important in reducing reactive lipids that can accumulate further along in the deposition process.92 Franklin and colleagues also examined the deposition of lipids onto a contact lens surface and the subsequent penetration into the lens matrix.92 This experiment demonstrated that there is a marked range of lipid types that deposit on lenses, from polar to nonpolar species and that this deposition is highly patient dependent. Surfactant cleaners are relatively helpful in minimizing lipid deposition and autooxidation of the lipids, but this is only temporary, as the lipid layer of the tear film is being constantly replenished.92 One further study around this time period by Tighe and his group examined the different types of cleaners available on the market and their efficiency at removing in vitro doped lipid from the surface of a contact lens.91 Soft contact lens surfactant cleaning solutions were compared with traditional chlorine-based and peroxide-based disinfectant systems. Surfactant cleaning solutions were found to vary widely in their ability to remove lipid from lens surfaces and disinfectant systems alone were found to remove virtually no lipid.91
In the early 1990s, Mirejovsky et al. reported on an in vitro artificial tear solution that contained proteins, mucin and lipids.51 This was a significant advance over previous doping solutions, which were almost exclusively based on proteins dissolved in buffer. The updated artificial tear solution better represented the range of components found within the tear film and therefore improved the usefulness of in vitro doping studies. Her work looked at both in vitro doped lenses and also investigated the ability of two histochemical stains (Nile Red and Oil-Red-O) to stain lipids. Mirejovsky showed that the Nile Red stain was far superior at detecting lipids and that the in vitro model solution produced a lipid deposition pattern that was similar to that obtained from human worn lenses. She also demonstrated that lipids could deposit onto hydrogel lenses either in isolation or bound to tear film proteins.51
Some of the most widely cited studies on the interaction of lipids with hydrogel lenses were those performed during the early to mid 1990s by Rapp and colleagues, who completed a series of experiments examining lipid deposits on a variety of contact lens types.77,79,95–97 In Rapp’s first experiment, patient worn soft contact lenses were examined for lipid deposition and analyzed for various lipid types using thin layer chromatography, high-pressure liquid chromatography, and gas liquid chromatography. Rapp showed that wax esters, fatty sterols, fatty alcohols, free fatty acids, and diglycerides were all detectable on hydrophilic lenses, whereas cholesterol, cholesteryl esters and triglycerides were not detectable. He concluded that the more polar lipids will deposit preferentially on hydrophilic lenses when compared to nonpolar lipids and that not all available lipids present in the tear film appear to deposit on hydrogel lenses.97 Subsequent studies revealed that all lipid types interact with contact lens materials, but that the interaction is driven by both the lipid type and the chemical composition of the lens material.77,79,95,96 Rapp’s work with Bontempo77,79,95 was crucial in indicating that, within conventional hydrogel materials, FDA group II lenses deposit the most lipid, and FDA group III deposit the least. They also reported that nonionic materials deposited more lipid than ionic materials, and that high water lenses deposited more lipid than low water materials.95 These data led to the development of the “pull/push” theory of lipid deposition, in which the “pull” represents the polymer lens material adhering the lipid and the “push” represents the water in the lens material driving the lipid into the matrix.54,95 Further research has been undertaken to find the differences between monomeric compositions within the same FDA group,98 which show that FDA classification alone is insufficient to accurately describe the pattern of lipid deposition that can occur.
Rigid gas permeable (RGP) lenses were also examined by Rapp,95 and this work indicated that these materials generally deposit more lipid than many soft lens materials, probably because of the hydrophobicity of the lens. RGP lenses contain low amounts of water, and therefore the high lipid adherence is tied to the individual characteristics of the polymer. For instance, silicone-based RGP lenses deposit more lipid than fluorine-containing RGP lenses because the silicone addition increases the hydrophobicity of the lens, but the fluorine addition decreases the hydrophobicity and thus decreases lipid deposition.95 Bontempo and Rapp also analyzed the interactions between proteins and lipid on the surface of hydrophilic and rigid gas-permeable contact lenses in vitro.79,96 They reported specific interactions that occur on a hydrophilic contact lens surface when lipids and proteins are present concurrently. When a group IV lens undergoes protein deposition, the surface of the lens becomes less hydrophilic and therefore attracts increased lipids. For group II lenses, the proteins compete with more polar lipid deposited on the lens surface and displace them.79 When RGP lenses were examined for lipid and protein interactions on the lens surface, different interactions were found. The surface of an RGP lens is hydrophobic and thus attracts more lipids than proteins. The polarity of some lipid molecules allow for binding with the matrix and attraction toward the aqueous. When lipids bind to the contact lens, the surface becomes less hydrophobic and this allows for subsequent protein deposition.96 In their final experiment, Bontempo and Rapp continued their protein and lipid interaction research by studying these interactions on group I and group IV lenses in vivo.77 They found that lysozyme was preferentially deposited on group IV lenses because of the available negative charges attracting the strongly positively charged protein. Group IV lenses showed deposition for both protein and lipids, but the specific deposition composition depended on the individual.77
Some of the more recent work on conventional hydrogel deposition with lipid was undertaken by Tighe and colleagues.14,78,98–101 In the first of these, an in vivo study was conducted to evaluate the deposition of protein and lipid on FDA group II lenses worn for various lengths of time.101 This was the first work to demonstrate that degree of deposition was influenced by frequency of replacement, with significantly increased deposition being noted for lenses worn for 3 months as opposed to 1 month. Overall lipid deposition increased with longer replacement schedules and 44% less lipid was detected for the shorter replacement time, with individual lipid deposition being shown to vary greatly.101 In a subsequent study,98 protein deposition was shown to be related to the degree of ionicity of the contact lens material, being greater in FDA group IV materials, whereas lipid deposition was strongly related to the monomeric composition, with increased lipid deposition being encountered in FDA group II materials, particularly those containing N-vinyl pyrrolidone (NVP). Group II lenses containing polyvinyl alcohol exhibited much less lipid deposition. Lipid deposition was also found to be dependent on the individual.98
Tighe and co-workers also examined both the effects of lens material and individual subject differences in lens spoilation.14 This controlled clinical study involved clinical and analytical techniques to analyze the deposition of tear film components on group II and IV lenses. Lipid analysis using fluorescence spectrophotofluorimetry determined that contact lenses containing NVP have the highest lipid deposition when compared with all other lens materials and that lipid deposition is greatly affected by patient-to-patient variations.14 In a further study,78 the progressive deposition of lipids was examined during a 1-month period in both group II and group IV lenses. Lipid deposition was found to be a cumulative process that does not plateau in a similar manner to that found in protein deposition on FDA group IV lenses. Once again, significant differences in individual lipid deposition were observed.78 A related study by Tighe and colleagues99 found corroborating evidence that increased lipid deposition was detected on contact lenses that contained NVP and that lipid deposition was found to slowly imbed itself into the polymer matrix.99
An overall review of the studies reported by Hart, Rapp, Tighe, and colleagues provide us with highly relevant information concerning the deposition of lipid into and onto hydrogel lenses. Their work shows that lipid deposition is more prominent on relatively hydrophobic substrates such as FDA group II materials, particularly those containing NVP, that large intersubject variations in lipid deposition commonly occur and that the deposition appears to be cumulative, with no plateau occurring. In addition, surfactant cleaning is required to adequately remove lipid and that cleaners vary in their ability to remove these lipid deposits.
The introduction of frequent replacement materials throughout the 1990s resulted in complications induced by deposition being largely eliminated. However, this retrospective review of the factors involved in lipid deposition is timely, as new silicone hydrogel lenses have very differing chemistries to that seen with traditional HEMA-based materials. Silicone hydrogels have exceptional oxygen transmissibility characteristics because of the incorporation of siloxane groups.102,103 However, these groups result in materials with an increased modulus to that seen in conventional HEMA-based materials102,104 and also result in surfaces that are significantly more hydrophobic.104–109 Given the known propensity for hydrophobic materials to deposit lipids, as described above, and also that hydrophobic substrates have a tendency to denature proteins,110–115 some knowledge of the deposition of both proteins and lipids on these novel materials would be valuable in understanding their clinical performance.
To date, very little work has been conducted on the deposition levels of silicone hydrogels, but what has been published appears to support what would be predicted from their relatively hydrophobic nature. Silicone hydrogels deposit minimal amounts of protein,15,72,74,116–120 which is largely denatured,15,74,120 and the degree of lipid deposition is higher than that seen with conventional hydrogels,15 although the exact amount of lipid deposited is under debate. Recently, Maziarz and colleagues compared two high-performance liquid chromatography techniques to quantify cholesterol, oleic acid, and oleic acid methyl ester on in vivo worn balafilcon contact lenses.121 Both methods found that oleic acid and its methyl ester were below the level of quantification. Cholesterol was the most commonly deposited lipid and had deposition quantities ranging from <1.50 to 37.0 μg per lens, which is substantially lower than the 300 to 600 μg per lens previously reported.15
What is unequivocal is that certain patients, when refitted from conventional HEMA-based materials into silicone hydrogels, exhibit clinically significant deposition on their silicone hydrogels that may not have been problematic with their HEMA-based materials (Fig. 4).16 One study reported this to occur in about 15% of silicone hydrogel wearers who use their care products using a “no-rub” regime and do not rub and rinse their lenses at the end of the day.122 When patients were advised to rub their lenses before disinfection, this level of clinically relevant deposition reduced to a negligible amount. As described above, the major type of deposition on silicone hydrogels is lipids, with some denatured proteins, both of which require a physical rub to maximize their removal from the surface of lenses. Based on the clinical data thus far, it would appear that silicone hydrogel wearers would benefit from being advised to use their care regimens with both a rub and rinse step being instigated before overnight soaking.123 Other methods to help minimize such deposition16 include replacing the lenses frequently, as lipids do progressively accumulate over time,78,101using a dedicated surfactant cleaner if merely rubbing with a multipurpose system fails, and treating any co-existing blepharitis or meibomian gland dysfunction in an attempt to produce a more stable, healthy lipid layer to the tear film.123–127
Ultimately, the degree of deposition remains irrelevant unless it results in symptoms or clinically significant signs, and the effects that lipid deposition has on either of these is not well documented. In fact, relatively few studies have directly linked deposition with alterations in symptoms and signs, and most of these have looked at deposition overall rather than the specific impact of lipid deposition alone. It is known that deposition of tear film components can reduce lens comfort,101,128–130 probably because of reduced lens wettability.131 As deposition occurs on the lens surface, the contact lens becomes progressively dewetted, resulting in poor wettability and subsequent sensations of dryness and discomfort. Poor vision is another negative affect of deposition.132,133 These symptoms can lead to discontinuation of lens wear129,130 and the more uncomfortable and irritating a contact lens becomes, the more likely the individual will remove the lens.130 Whether these symptoms result from lipid deposition, protein deposition, or a combination of both remains to be confirmed.
On reviewing the literature to-date, much work remains to be undertaken to further our understanding of the processes involved in lipid deposition, particularly on silicone hydrogels. Many of the studies thus far have used in vitro methodologies, which fail to take into account lens surface drying between blinks, which will result in increased hydrophobicity and enhance deposition, and the constant replenishment of the lipid within the surrounding fluid. Such studies need to be complemented and confirmed by ex vivo studies to ensure that the results are comparable to that found clinically. Other topics that have been inadequately examined are the degree to which lipid penetrates into the matrix of lens materials, the influence of various care regimens, the interaction between lipids and other constituents of the tear film, the kinetics of lipid deposition and the arrangement of lipid types on the surface. These are all subjects that require much greater understanding if our ability to further the development of lens materials, particularly siloxane-based materials, is to progress. What is clear from this literature review is that there are many factors that can affect the deposition process and dictate the ultimate amount of lipid on the contact lens, with material composition, replacement interval, care regimen and individual patient variability all playing significant roles. The future for lipid research on both the tear film and its relationship to contact lens deposition remains bright, but novel methodologies to examine the lipids involved in contact lens deposition and dry eye require significant intellectual input to unravel these complex interactions.
The authors of this manuscript do not have a financial interest in any of the products mentioned in this manuscript.
Centre for Contact Lens Research
School of Optometry
University of Waterloo
200, University Avenue West
Waterloo, ON N2L 3G1, Canada
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