What is meibomian gland dysfunction (MGD)?

Meibomian gland dysfunction, almost always shortened to MGD, is a long-running problem with the oil glands set into your eyelids. The international workshop that produced the standard definition in 2011 called it "a chronic, diffuse abnormality of the meibomian glands, commonly characterized by terminal duct obstruction and/or qualitative/quantitative changes in the glandular secretion". In plainer language: the glands that should oil your tear film are blocked, making oil of the wrong consistency, or both.

That oil is what stops your tears evaporating. When it thins, thickens or stops arriving, the tear film breaks up too quickly between blinks and the eye dries in patches. The same workshop concluded that MGD "may well be the leading cause of dry eye disease throughout the world". It builds quietly over years, without the redness and crusting people associate with an eyelid problem, and is often well advanced before anyone looks for it.

What the meibomian glands do

They sit in a single vertical row inside the tarsal plate that stiffens each eyelid — roughly 25 to 40 glands in the upper lid, 20 to 30 in the lower. Each opens through a tiny pore just behind the lashes, visible as a faint line of pale dots along the rim.

They are holocrine sebaceous glands: the secreting cells fill with lipid and then break down completely, so the cells themselves become the oil. That oil is meibum, and it forms the outermost layer of the tear film — the layer the workshop describes as protecting the watery tears against evaporation and stabilising the film by lowering surface tension. Our guide to the layers of the tear film has more.

Blinking is the delivery mechanism: the orbicularis muscle compresses the tarsal plate with each blink, squeezing meibum onto the lid margin for the next blink to draw up over the film. At any moment only about 45% of gland openings are actively delivering, and the number of active glands falls by roughly half between the ages of 20 and 80.

What "dysfunction" actually means

The workshop split MGD by how much meibum reaches the lid margin: low-delivery states and high-delivery states. Low-delivery is subdivided into hyposecretory, where the glands make too little, and obstructive, where they make it but cannot get it out.

Obstructive MGD is the form most people have. The terminal duct — the last stretch before the pore — narrows as its lining thickens with keratin, the meibum behind it stiffens, and pressure builds back along the gland. The anatomy report describes obstructed glands becoming dilated and then atrophic, with fewer secretory acini. That order matters: the blockage comes first and the tissue loss comes later.

Blackie and colleagues argued that the commonest form of obstructive MGD is the one that shows the least. They called it nonobvious obstructive MGD: inflammation and the classic signs may be absent unless the examiner deliberately expresses the glands. Their review described it as very common and significantly underdiagnosed, and treating it succeeds only if the obstruction is relieved. Our article on the signs of MGD covers the examination.

Why blocked glands dry the eye out

The TFOS DEWS II definition puts loss of tear film homeostasis at the centre of dry eye disease, with instability, hyperosmolarity, surface inflammation and damage, and neurosensory abnormalities as the key mechanisms. The pathophysiology report describes the engine as a vicious circle: evaporative water loss concentrates the tears, hyperosmolarity damages the surface directly and by provoking inflammation, epithelial and goblet cells are lost, the surface becomes less wettable, the film breaks up sooner, and evaporation concentrates the tears further. MGD feeds that circle at the first step.

That report explains two things patients find puzzling. Discomfort comes not only from dryness but from hyperosmolarity, lost lubrication, inflammatory mediators and nerve changes, which is why eyes can feel dreadful and look unremarkable. Visual symptoms come from irregularity of the tear film and surface, which is why vision smears and clears for a second after each blink. The classification report also puts aqueous-deficient and evaporative dry eye on a continuum rather than in separate boxes; our comparison of evaporative and aqueous-deficient dry eye covers where the line falls.

How common it is, and who gets it

Reported prevalence varies enormously, much of it down to differing definitions rather than real differences. Asian population studies reported MGD in 69.3% of the Beijing Eye Study and 60.8% in the Shihpai Eye Study; a Bangkok study gave 46.2%, though the subcommittee flagged its sampling as not truly population-based. Largely Caucasian populations gave far lower figures, 3.5% in the Salisbury Eye Evaluation and 19.9% in the Melbourne Visual Impairment Project. For dry eye disease overall, the TFOS DEWS II epidemiology report gives a range of 5% to 50%, rising with age and higher in women.

The most telling figure comes from a clinic. Lemp and colleagues assessed 299 people across ten sites in Europe and the United States. Of the 224 classified as having dry eye disease, 159 fell into a category: 79 had MGD alone, 57 had both MGD and aqueous deficiency, and only 23 were purely aqueous deficient. Overall, 86% showed signs of MGD.

The epidemiology subcommittee sorted risk factors into three groups. Ophthalmic: chronic blepharitis, Demodex infestation, contact lens wear, floppy eyelid syndrome. Systemic: ageing, androgen deficiency, menopause, rosacea, Sjögren syndrome. Medicines: isotretinoin, antiandrogens, antihistamines and postmenopausal hormone therapy. Contact lenses deserve a caveat: the meta-analysis found MGD in 37.7% of wearers against 32.1% of non-wearers, not a statistically significant difference. Age is the clearest signal: gland abnormalities were uncommon at 50 and under, rising sharply above it.

What people report is not "dry" but grittiness, heavy or tired eyes, burning, and vision that blurs and clears with a blink, worse late in the day. Watering confuses people; our article on why dry eyes water explains the reflex.

How MGD is treated

The management subcommittee set out a staged algorithm, a ladder rather than a menu. At stage 1 the patient is informed about the condition and about environmental and dietary factors, with lid hygiene, warming and expression offered as options; at stage 2 warming becomes an instruction rather than a suggestion — a minimum of four minutes, once or twice daily, followed by massage and expression — alongside lubricants and topical azithromycin; stage 3 adds oral tetracycline derivatives and ointment at bedtime; and stage 4 makes anti-inflammatory therapy central. Running across every stage is what the report calls "plus" disease, comorbidities such as chalazion or Demodex-related anterior blepharitis that need treating in their own right. Our guide to the stages of MGD sets out what each looks like.

Heat sits at the bottom of that ladder for a reason: meibum has to be warm enough to flow before anything else can work. The report specifies continuous 45 °C compresses for at least four minutes, replaced every two minutes with a preheated one to hold the temperature. Reaching the right eyelid temperature and staying there is the practical difficulty, covered in what temperature a warm compress needs to be and whether heated eye masks work.

If you have an active eye infection, have had eye surgery recently, have glaucoma, or notice any change in your vision, speak to your optometrist or ophthalmologist before starting heat therapy or continuing with it.

Holding an eyelid at a useful temperature for ten minutes is harder than it sounds, which is where a purpose-made electric mask earns its place. The Meibocare E-Heated Eye Mask is designed to bring the eyelids to about 42 °C on the recommended setting and timer, using a graphene heating element with flaxseed filling, and its three settings are each paired to a timer — 20 minutes on Low, 15 on Medium, 10 on High. It is notified to Medsafe on the New Zealand WAND database (240927-WAND-746QNT), a register that records notification rather than assessing the device, and is the test device in a registered randomised trial at the University of Auckland (ACTRN12625000997459).

Frequently asked questions

What is meibomian gland dysfunction in simple terms?

It is a chronic problem with the oil glands in the eyelids. The standard definition describes a diffuse abnormality of the meibomian glands, commonly involving blockage of the terminal ducts and changes in the quality or quantity of the oil they make. Because that oil stops tears evaporating, MGD is the usual cause of evaporative dry eye.

Is meibomian gland dysfunction the same as dry eye?

No, but they overlap heavily. MGD is a disorder of the eyelid oil glands; dry eye disease is the loss of tear film homeostasis that often follows. In one clinic-based study of 224 dry eye patients, 86% showed signs of MGD. Dry eye can also arise from insufficient tear production, and many people have both.

How common is meibomian gland dysfunction?

Estimates vary widely with population and definition. Asian population studies have reported figures from 46.2% in Bangkok to 69.3% in Beijing, while studies in largely Caucasian populations reported 3.5% in Salisbury and 19.9% in Melbourne. Age is the strongest pattern: notable gland abnormalities were uncommon at 50 and under and rose sharply above that.

Can meibomian gland dysfunction be fixed?

MGD is managed rather than resolved once and for all. The workshop treatment algorithm starts with eyelid warming, massage and expression, adding lubricants, topical or oral antibiotics and anti-inflammatory therapy as severity increases. Most people need to keep a daily routine going, because the obstruction returns when the routine stops.

Educational information only, not medical advice. References: Nichols KK, et al. Invest Ophthalmol Vis Sci. 2011;52:1922–1929; Knop E, et al. Invest Ophthalmol Vis Sci. 2011;52:1938–1978; Schaumberg DA, et al. Invest Ophthalmol Vis Sci. 2011;52:1994–2005; Geerling G, et al. Invest Ophthalmol Vis Sci. 2011;52:2050–2064; Craig JP, et al. Ocul Surf. 2017;15:276–283; Bron AJ, et al. Ocul Surf. 2017;15:438–510; Stapleton F, et al. Ocul Surf. 2017;15:334–365; Lemp MA, et al. Cornea. 2012;31:472–478; Blackie CA, et al. Cornea. 2010;29:1333–1345.