Meibomian Gland Dysfunction

Meibomian gland dysfunction (MGD) is the most common cause of evaporative dry eye disease and is present — to varying degrees — in the majority of dry eye patients. It results from obstruction of the meibomian gland terminal ducts and/or qualitative changes in meibum, leading to lipid layer deficiency, accelerated tear evaporation, and ocular surface inflammation. MGD is frequently underdiagnosed because its signs may be subtle and its symptoms overlap with aqueous-deficient dry eye.

MGD is extraordinarily prevalent — population-based studies report rates of 38–69% in adults, with higher rates in Asian populations and increasing prevalence with age. It is the dominant subtype of dry eye disease in clinical practice, present in the majority of patients presenting with dry eye symptoms.

The primary mechanism is obstruction of the meibomian gland terminal ducts by hyperkeratinization of the ductal epithelium and increased meibum viscosity. Obstructed glands accumulate inspissated secretions, leading to gland dilation, acinar atrophy, and ultimately permanent gland dropout (detectable on meibography). The resulting lipid layer deficiency accelerates tear evaporation, increases tear film osmolarity, and triggers inflammatory cascades on the ocular surface. Demodex infestation, bacterial colonization, and rosacea all contribute to MGD pathogenesis through distinct but overlapping mechanisms.

Symptoms include burning, foreign body sensation, fluctuating vision, and lid margin discomfort — often indistinguishable from aqueous-deficient dry eye. Clinical signs include lid margin irregularity, telangiectasia, plugged or capped meibomian gland orifices, turbid or toothpaste-like meibum on expression, and meibomian gland dropout on infrared meibography. Rapid tear breakup time and reduced lipid layer thickness on interferometry support the diagnosis.

Management is stepwise and targets both the gland obstruction and the resulting ocular surface inflammation. Warm compresses (10 minutes daily) and lid massage are foundational — heat liquefies inspissated meibum and facilitates expression. Lid hygiene with hypochlorous acid or surfactant-based cleansers reduces bacterial colonization and biofilm. Omega-3 supplementation (EPA/DHA) has evidence for improving meibum quality and reducing evaporative dry eye symptoms.

In-office procedures including thermal pulsation (LipiFlow®, iLux®) and intense pulsed light (IPL) therapy provide more sustained gland clearance than home therapy alone. Oral doxycycline (50–100 mg daily) has anti-inflammatory and lipase-inhibiting properties that improve meibum quality and reduce lid margin inflammation. Topical azithromycin (AzaSite®) delivers antibiotic and anti-inflammatory benefit directly to the lid margin.

Follow-up at 4–8 weeks after initiating therapy to assess symptom response and meibum quality. Meibography provides objective documentation of gland status and progression. Patients with significant gland dropout require long-term management to preserve remaining gland function.