As a long-term contact lens wearer, one of the things I want to know is whether my contact lenses are adversely and irreversibly affecting my eyes. The recent Tear Film and Ocular Surface Society’s (TFOS) Dry Eye Workshop II (DEWS II) reported that contact lens wearers are four times more likely to experience dry eye disease during the contact lens-wearing experience compared to non-lens wearers (Stapleton et al, 2017), a fact that likely contributes to the propensity for up to 50% of contact lens wearers to drop out of lens wear within the first three years (Pritchard et al, 1999).
While contact lens discomfort dissipates upon lens removal, the question still remains—is it possible that contact lens wear causes permanent damage? For example, given the constant interaction between the eyelids and the contact lens surface, does this repetitive action impact the meibomian glands? If it does, contact lens wearers could be developing chronic dry eye disease—which could not only affect their potential to continue with contact lens wear, but also could result in symptoms down the line, even without lens wear.
Some Say “Yea”
Ideally, a study would fit a healthy group of non-contact lens wearers with soft contact lenses and monitor them over time for changes to their meibomian gland structure, function, and symptoms. In the absence of such a “natural history” study, researchers so far have examined this question cross-sectionally.
Take Alghamdi and his colleagues from Australia (2016), for example. These authors examined the meibomian glands of 100 people who were categorized into one of five groups: non-lens wearers, people who had been wearing lenses for 2 ± 1 years, those who had been wearing lenses for 5 ± 1 years, those who had worn lenses for 10 ± 2 years, and those who had dropped out of lens wear for at least six months. They used meibography to examine meibomian gland structure (Figure 1) and found a difference between groups. The position of Marx’s line (Figure 2) was also assessed as an indication of scarring of the lid margin resulting in displaced positioning of the meibomian gland orifice; again, a significant difference was noted between groups. When the meibomian gland function was examined, there was a difference between groups in expressibility of the meibomian glands, the number of glands that were expressible, non-invasive tear breakup time, and tear meniscus area.
For all variables assessed, the non-lens-wearing group was significantly different to all other groups. Furthermore, the changes were noted within the first two years of lens wear, indicating that even short exposure to lens wear can have an impact on meibomian gland structure and function. Continued exposure did not appear to cause further damage to the glands, and stopping lens wear altogether did not result in a return to pre-lens-wear status (Alghamdi et al, 2016).
These findings indicate that contact lens wear does impact both the morphology and the function of the meibomian glands, even within the first few years of lens exposure.
The finding that the gland morphology and function does not deteriorate beyond this point is reassuring, suggesting adaptation of the adnexa to lens wear, akin to that seen in the biochemistry of the tear film during the early phase of contact lens wear (Markoulli et al, 2013).
Concerningly, those who drop out of lens wear do not appear to return to their original status prior to lens wear. A caveat of this study is its cross-sectional nature, whereby it is difficult to ascertain the status of the ocular surface and adnexa prior to lens wear.
In support of the affirmative argument relating to the impact of contact lens wear on the adnexa, others have similarly found poor meibomian gland expressibility (Henriquez and Korb, 1981; Ong and Larke, 1990; Machalińska et al, 2015) and greater meibomian gland dropout with contact lens wear (Arita et al, 2009).
More recently, these morphological changes of the meibomian glands have been associated with contact lens discomfort (Arita et al, 2017; Siddireddy et al, 2017). At the cellular level, in vivo confocal microscopy has been used to assess the morphology of the acini, the lipid-producing part at the end of the grape-like structure that is the meibomian gland (Figure 3) (Villani et al, 2011).
When contact lens wearers were compared to non-lens wearers, the former had reduced acinar diameter, indicating possible gland dropout (Villani et al, 2011). Moreover, this particular study reported a decrease in the density of the epithelial cells that surround the meibomian gland orifice, potentially a result of mechanical damage (Villani et al, 2011).
Unlike Alghamdi and colleagues (2016), both Arita et al (2009) and Villani and colleagues (2011) found that longer contact lens wearing experience resulted in poorer meibomian gland morphology.
A study of children wearing overnight orthokeratology over a three-year period reported distortion of the meibomian glands in two of the 58 children observed during this period (Na et al, 2016). These findings are of interest and would benefit from further examination with the inclusion of a control group to compare these changes to the natural history of the meibomian glands over a similar period.
Some Say “Nay”
On the other side of the debate as to whether contact lenses damage the meibomian glands are arguments from multiple studies showing no association between contact lens wear and poor meibomian gland function (Hom et al, 1990; Marren, 1994; Ong, 1996) or morphology (Pucker et al, 2015).
Still Looking for Answers
So, the debate goes on. A major limitation of the studies to date is their cross-sectional nature—it is therefore difficult to tell the order of events. Does reduced meibomian gland expressibility precede meibomian gland dropout, or is it the other way around? Do those who drop out of lens wear do so because of the change to their meibomian glands, or was that a precursor that ultimately contributed to their contact lens discontinuation? Moreover, how is it that contact lens wear affects the meibomian glands?
Hypotheses include mechanical irritation due to constant friction between the eyelids and contact lens surface (Ong and Larke, 1990) as well as obstruction of the glands by desquamated epithelial cells (Korb and Henriquez, 1980). More importantly, can we overcome this by the way in which we fit or design contact lenses? New substances such as lubricin hold some promise for the future in terms of reducing ocular surface friction (Lambiase et al, 2017).
Given that dysfunction of the meibomian glands is responsible for up to 80% of dry eye disease cases (Lemp et al, 2012), identifying and ameliorating factors that contribute to this is important. While the debate as to whether contact lens wear does, or does not, cause meibomian gland dysfunction continues, we need to routinely assess our contact lens-wearing patients for meibomian gland dysfunction and manage them sooner rather than later. CLS
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