Abstract

The preocular tear film (POTF) is composed of a deep aqueous-mucin phase that supports a thin superficial lipid phase. The tear lipid layer (TLL), although thin, stabilizes the POTF providing a 25% surface-tension decrease and a 90-95% aqueous evaporation reduction. TLL is formed from lipids secreted by tarsal meibomian glands and spread onto the ocular surface by blinking. The TLL itself is composed of two phases. A thin and deep polar phase, adjacent to the aqueous-mucin layer, has a surfactant role. A thicker and superficial nonpolar phase has antievaporative properties. At the same time, tear lipocalins help the TLL spread and stabilize the lipid-aqueous interface. For clinical examination, TLL is directly observed with the Tearscope. POTF stability and the evaporation rate depend on the lipid layer pattern. When chronic, POTF qualitative trouble (evaporative syndrome) due to a TLL anomaly, leads to secondary ocular surface impairment with increased tear instability and self-propagation of ocular dryness. Meibomian gland dysfunction (MGD) results from local pathology, dermatologic disease (ocular rosacea) or iatrogenic etiology. Cosmetic use is the other principal cause of TLL destabilization. Lid hygiene is the mainstay of MGD treatment. Systemic antibiotics (cyclins) can be associated in cases of severe symptoms. Topical treatment is useful if there is marginal lid inflammation or infection.