MEIBOMIAN GLAND DYSFUNCTION

ADDRESSING MGD IN CONTACT LENS WEARERS

Proactively managing and treating meibomian gland dysfunction allows for more comfortable lens wear.

MELANIE FROGOZO, OD

Currently, there are more than 150 million contact lens wearers worldwide, and up to 50% of wearers report symptoms of dryness. Dry eye causes intolerance and discomfort in contact lens wearers and is thought to be a major contributor to dropout in patients under the age of 45 years old (Richdale et al, 2007). Although dry eye is multifactorial in etiology, there is a strong consensus that meibomian gland dysfunction (MGD) is the most common cause of evaporative dry eye (Schaumberg et al, 2011). Therefore, proactively managing and treating MGD will allow patients to continue to wear contact lenses comfortably.

WHAT IS MGD?

The meibomian glands are located at the margins of the upper and lower eyelids. Meibomian glands are large specialized sebaceous glands in the tarsal plates of the eyelids. Their function is to excrete lipids onto the ocular surface that form on the outermost layer of the tear film. There are about 30 to 40 glands located in the upper lid and 20 to 30 glands located in the lower lid. The glands follow the length of the tarsus; they are 5.5mm to 10.0mm long in the upper lids and 2.0mm to 5.0mm long in the lower lids (Knop et al, 2011; Greiner et al, 1998). Each gland contains 10 to 15 acini that constantly secrete sebum (Knop et al, 2011). The acini empty into a central duct via holocrine secretion. Finally, the secretions exit through the gland orifice at the upper and lower eyelid margins just anterior to the mucocutaneous junctions.

Meibum delivery onto the lid margin occurs with muscular contraction during lid movement (Nichols, 2011). The glandular secretions consists of a complex mixture of more than 45 various polar and nonpolar lipids (Lorentz and Jones, 2007). Healthy function of these lipids provides a smooth optical surface for the cornea at the air-lipid interface, reduces tear film evaporation, enhances stability and spreading of the tear film, prevents spill over of tears from the lid margin, prevents contamination of the tear film by sebum, and seals the lid margins during sleep (Knop et al, 2011).

The exact mechanism for controlling secretion of the meibomian glands is not fully understood; however, it is thought that androgens, estrogens, progestin, retinoic acid, growth factors, and possibly neurotransmitters regulate secretion. A decrease in overall sex hormones, such as during menopause, causes MGD by altering lipid secretions and creating tear film instability in older patients (Knop et al, 2011).

Reduced lipid secretion caused by MGD contributes to tear film instability and ultimately leads to dry eye disease (Baudouin et al, 2016). MGD is defined as “a chronic, diffuse abnormality of the meibomian glands, commonly characterized by terminal duct obstruction, and/or qualitative/quantitative changes in glandular secretion. This may result in alteration of the tear film, symptoms of eye irritation, clinically apparent inflammation, and ocular surface disease.” (Nelson et al, 2011; Nichols, 2011).

The main cause of MGD is thought to be due to non-inflammatory obstruction of the gland orifice and main duct by hyperkeratinization of the epithelium. Although there is terminal obstruction of the orifice, the acini cells continue to generate meibum, which causes dilation of the central duct and eventual dilation of the acini and connecting ductules. Clinically detectable meibomian gland dropout is thought to be the shrinkage and atrophy of acini due to obstructive pressure from dilation. In late stages, the whole duct is replaced with stratified squamous cornified epithelium. This obstruction reduces or completely inhibits the amount of meibum delivered to the lid margins. Insufficient lipids may cause increased tear evaporation and subsequent dry eye disease, hyperosmolarity and instability of the tear film, increased bacterial growth on the lid margin, and ocular surface inflammation and damage (Knop et al, 2011).

Recent literature suggests that atrophy of acini seen in MGD could be influenced by reasons other than obstruction via hyperkeratinization of the epithelium (Yamaguchi et al, 2006; Jester et al, 2015; Qazi et al, 2015). In both aging mice and humans, there is an anterior displacement of the mucocutaneous junction unrelated with hyperkeratinization. This anterior displacement of the Marx line has been associated with meibomian gland dropout in older subjects (Yamaguchi et al, 2006).

Additionally, meibomian glands up-regulate cell proliferation in response to desiccating stress. Response to this environmental stress causes the cells to create high levels of proteins in comparison to lipids, which alters the fluidity and stiffness of secretion, thus contributing to obstruction (Jester et al, 2015).

Finally, meibomian gland secretion may be altered by inflammatory cells found in the palpebral conjunctiva via confocal microscopy in patients who have symptomatic dry eye complaints without clinically apparent eye inflammation (Qazi et al, 2015).

EVALUATING MGD

Anatomical changes of the meibomian glands and surrounding lids seen during biomicroscopy are used to make a diagnosis of MGD. The clinical signs of MGD include changes in lid morphology, meibomian gland secretions, and meibomian gland dropout.

Lid Morphology Thickening of the lid margins is a common clinical feature often observed in MGD. As MGD progresses, the lid margin thickens and becomes more rounded, especially at the posterior margin. This rounding interferes with how the lid sits next to the globe. Telangiectasia of the lid margins is also seen frequently in MGD (Figure 1). Cutaneous hyperkeratinization and telangiectasia increase with age and are more commonly seen in the lower lids (Tomlinson et al, 2011). Irregularity of the lid margin can be seen when the orifice of a meibomian gland is destroyed and in cases of cicatricial and ulcerative lid disease (Tomlinson et al, 2011).

Figure 1. Lid margin showing signs of thickening, rounding, and telangiectasia characteristic of MGD.

The mucocutaneous junction is displaced anteriorly in MGD, causing the gland orifices to appear to lay in the mucosal tissue. Additionally, the mucocutaneous junction and the area between the orifices can appear ridged with progression of MGD (Tomlinson et al, 2011). This can be viewed by either specular reflection or through vital staining of the Marx line using lissamine green.

The orifices of the meibomian glands also change with disease progression. Capping of an orifice appears as a dome of oil with a trough. This can be seen in otherwise normal patients, although it may indicate that the underlying orifice is ulcerated and the cap is epithelialized.

Plugging or pouting may be an early sign of MGD and may eventually lead to destruction of the orifice as well as to meibomian gland loss. The affected orifices express minimal oil, and the surface appears uneven with the rest of the lid margin. Additionally, the inability to express meibum can occur in narrowed or obliterated orifices (Tomlinson et al, 2011).

The acini of the meibomian gland can also be altered by MGD. Concretions are deposits of lime salts within the acini (Tomlinson et al, 2011). These deposits follow the line of the meibomian main duct. In the presence of concretions, the central duct is dilated and the orifice is occluded, with no oil being expressible.

Larger chalazia also may be deposited within the lid in MGD. Chalazia represent a granuloma of the meibomian gland and are typically found under the upper lids (Tomlinson et al, 2011).

Meibomian Gland Secretions The meibomian gland secretions can be assessed by compressing the tarsal plate at the site at which the group of orifices is located. Meibum may be expressed from the orifices in this fashion using the pressure from your finger, a cotton swab, a pair of flat blunt forceps, or a device designed for meibomian gland expression. Expressed oil in those who have MGD can be graded as cloudy, granular, or inspissated. The expressed oil is clear in normal individuals who do not have MGD. Cloudy (Figure 2) and granular (Figure 3) expressions are both turbid fluid secretions; however, the latter contains particulate matter. An inspissated expression is a semi-solid plug or a substance with a toothpaste-like consistency that may extrude out as a curled thread. Inspissated secretions contain keratinized epithelial cells (Tomlinson et al, 2011).

Figure 2. Cloudy expressions from meibomian gland orifices in an MGD patient.

Figure 3. Granular expressions from meibomian gland orifices in an MGD patient. Courtesy of Christine Sindt, OD.

Meibomian Gland Dropout Meibomian gland dropout refers to the complete or partial loss of acinar tissue observed with meibography (Figure 4). Gland dropout is normal with increased age and is not necessarily associated with obstructive MGD. Nonetheless, dropout is a feature of MGD and increases with the severity of progression (Tomlinson et al, 2011). Additionally, loss in meibomian glands is not necessarily correlated with dry eye symptoms unless the tear film is disrupted (Pult and Riede-Pult, 2012).

Figure 4. Meibography of early gland dropout of the inferior lid (circled).

MANAGING MGD AND CONTACT LENSES

As mentioned earlier, MGD is the leading cause of evaporative dry eye, which in turn is the most common form of dry eye disease. Dryness is one of the main ocular symptoms that causes discontinuation of contact lens use (Richdale et al, 2007). Therefore, MGD should be managed and addressed in all contact lens patients so that they may wear their lenses comfortably.

Whether or not contact lens wear causes MGD is unclear. There are some early reports of an association between contact lens wear and decreased meibomian gland expressibility (Henriquez and Korb, 1981) and meibomian gland loss (Arita et al, 2009). Nevertheless, other studies show no increased risk of MGD or meibomian gland loss with contact lens wear (Hom et al, 1990; Nichols and Sinnott, 2006).

The inconsistency in findings most likely reflects the lack of consensus regarding the definition and diagnosis of MGD before the International Workshop on Meibomian Gland Dysfunction in 2011 (Knop et al 2011; Nelson et al, 2011). A recent study by Alghamdi et al (2016) found that there are changes in meibomian gland morphology with contact lens wear, including gland loss and blocked orifices. Nonetheless, these changes occur early in contact lens wear and do not seem to progress after two years of wear.

Because contact lens wear increases the risk of blocked meibomian gland orifices (Alghamedi et al, 2016; Nichols and Sinnott, 2006), it is reasonable to treat against these changes by recommending lid hygiene to patients. Blocked orifices lead to decreased and altered meibomian gland expression, which in turn can cause tear film instability. Ultimately, this can decrease the wettability of the contact lens surface (Figure 5), thus leading to discomfort and blurry vision.

Figure 5. Scleral lens showing decreased wettability due to lipid deposits in a patient who has MGD.

The mainstay of lid hygiene in MGD consists of applying heat and massage to the eyelids (Geerling et al, 2011). Heating the lids improves MGD by melting the altered meibomian gland secretions. This can be accomplished by using a warm compress (e.g., hot wet cloth and heated dry rice bag), heated masks, and commercially available devices that emit heat to the lids (Figure 6). Heating the lid margins improves obstructive meibomian gland disease and improves blocked gland orifices, tear film evaporation, and ocular surface epithelial damage (Goto et al, 2002; Mori et al, 2003). Additionally, heating along with scrubs that contain cleansing solutions for the eyelashes and lid margin is a common combination treatment for MGD that can improve tear breakup time as well as dry eye symptoms.

Figure 6. Patient being treated for MGD with device that emits heat to meibomian glands.

Meibomian gland loss can occur with contact lens wear (Arita et al, 2009; Alghamedi et al, 2016); however, loss is also normal with advanced age (Tomlinson et al, 2011) and with other eye conditions, such as ocular rosacea (Machalińska et al, 2016). Monitoring meibomian glands for signs of dropout is valuable in managing dry eyes in contact lens wearers. As gland loss increases, lipid layer thickness decreases and tear breakup becomes more rapid (Pult and Riede-Pult, 2012). One study found that the threshold for gland loss at which dry eye symptoms occur is about 17% in the upper lid and 29% in the lower lid (Arita et al, 2012). The meibomian glands can be observed by applying a transilluminating light source to the skin side of an everted lid and viewing the disposition of the glands on the mucosal side. Additionally, there are now instruments that use infrared technology to document tissue loss (Tomlinson et al, 2011).

Wearing a contact lens disturbs the lipid layer. The presence of a contact lens on the eye is associated with increased tear breakup time and altered meibum secretions (Rohit et al, 2013). An unstable tear film results in more localized spots of dehydration on the contact lens. This results in decreased surface wettability and also makes the lens more susceptible to lipid deposition, which further worsens contact lens wetting and increases discomfort. Clinical experience shows that frequently replacing contact lenses can help reduce the accumulation of deposits. Additionally, educating patients to rub lenses with a multipurpose cleaner will also lessen deposition. Finally, more resistant deposits may be removed with a surfactant cleaner (Lorentz and Jones, 2007).

Yamada et al (2006) reported that contact lens wear decreased cholesterol and increased pro-inflammatory enzyme phospholipase A₂, which is responsible for creating free-fatty acids in the tear film. The formation of unsaturated fatty acids results in inflammation around the eye and in the meibomian glands, which leads to decreased and altered secretion as well as to obstruction of orifices (Yamada et al, 2006) and ultimately to contact lens discomfort. Using artificial tears helps spread the lipid layer and may dilute debris and pro-inflammatory molecules within the tears (Geerling et al, 2011). Frequently replacing contact lenses will also decrease exposure to inflammatory deposits on the lenses (Lorentz and Jones, 2007). Furthermore, oral antibiotic treatment, such as minocycline, decreases free-fatty acids in tears (Geerling et al, 2011).

Progression in MGD causes lid anatomy changes, such as increased thickening, rounding, and obstructive-related inflammation of the lid margins. Not only does this cause the lid to sit differently next to the globe, it can also affect contact lens comfort (Tomlinson et al, 2011). My patients who have MGD often will complain of pressure or foreign body sensation on their lids while wearing contact lenses. Contact lenses act as a physical obstacle that lids have to stretch and blink over (Lorentz and Jones, 2007), more so in large-diameter and high-modulus lenses.

Patients who have inflamed lid margins from MGD may be more sensitive to the changes in lid posture that the extra bulk of a contact lens creates. In such cases, topical azithromycin (Foulks et al, 2010) and cyclosporine (Schechter et al, 2009; Perry et al, 2006) may be prescribed to decrease lid inflammation caused by MGD. Both medications improve meibomian gland plugging and quality of lid secretions, decrease lid margin redness, and provide patient-reported overall relief from MGD symptoms (Schechter et al, 2009; Perry et al, 2006).

Although contact lens wear is associated with MGD, scleral contact lenses may provide relief to patients who have severe MGD symptoms. A large-diameter rigid scleral lens reduces airflow across the corneal surface in patients who have lipid deficiency and reduces tear evaporation. In addition, the scleral lens may be used to hold lubricating tears over the ocular surface, augmenting corneal health and protecting it from further damage (Geerling et al, 2011; Jackson, 2009).

Because contact lens wear is associated with risks for MGD, treatment should be initiated in symptomatic patients; however, proactive treatment should be considered even in asymptomatic patients who have clinical signs. Proactively treating MGD should help keep contact lens wearers comfortable for longer and can potentially delay or decrease dropout rates. Table 1 shows the recommended treatment algorithm for MGD as defined by the 2011 International Workshop on Meibomian Gland Dysfunction (Geerling et al, 2011).

SUMMARY

Let’s recap: Dryness is the main ocular symptom associated with lens wear discontinuation. MGD is the leading cause of evaporative dry eye, the most common form of dry eye disease. Treating MGD with lid hygiene and anti-inflammatory regimens can guard against progressive disease. MGD can be treated proactively in all lens wearers so lens wear can be continued comfortably. CLS

For references, please visit www.clspectrum.com/references and click on document #253.

Dr. Frogozo specializes in adult and pediatric specialty contact lenses. She is the director of the Contact Lens Institute of San Antonio and the owner of Alamo Eye Care in San Antonio, Texas. She also is a consultant to CooperVision. You can contact her at contactlensinstitutesa@gmail.com.