Pathophysiology of Chalazion
Primary Mechanism – Meibomian Gland Dysfunction
- Meibomian gland dysfunction is the primary driver of chalazion formation, characterized by altered biochemical composition of the gland’s secretions. 1
- Obstruction of the meibomian orifices results in plugging with material that can range from turbid fluid to a thick, cheese‑like consistency. 1
Clinical Manifestations
- Typical eyelid findings of a chalazion include pouting or plugging of the meibomian orifices, thickening and scalloping of the eyelid margin, and prominent blood vessels crossing the mucocutaneous junction. 1
Secondary Inflammatory and Structural Changes
- Chronic lipogranulomatous inflammation may progress to atrophy and fibrosis of the meibomian glands within the affected area. 1
- Reduced delivery of normal meibum to the lid margin and tear film occurs as a consequence of meibomian gland dysfunction. 1
- The resulting tear‑film hyperosmolarity and instability promote increased bacterial colonization of the lid margin, evaporative dry eye, and ocular surface inflammation. 1
Associated Ocular Surface Conditions
- Chalazia exist on a continuum with blepharitis and meibomian gland dysfunction and are frequently observed in patients who also have rosacea or seborrheic dermatitis. 1