Breaking the vicious circle of DED
Redefining the DED treatment
Dry Eye is a multifactorial disease characterized by an unstable tear film causing a variety of symptoms and/or visual impairment, potentially accompanied by ocular surface damage (Tsubota K, Yokoi N, Shimazaki J et. al., Ocul. Surf. 2017 65 – 76).
To develop topical strategies for treating DED the typical tear film model with its different layers has to be enriched with lacrimal and meibomian glands and the epithelium as a layer for the ocular surface damage and the corneal somatosensory pathway.
The modified “vicious circle of DED” considers the pathology of DED and highlights the key drivers of the disease (of Baudouin et al.):
Literature supports the role for inflammation in DED. Inflammation is, however, not the only cause. To understand DED beyond inflammation, patients’ signs and symptoms help to identify the respective root causes and treatment strategies.
Meibomian glands are the main source of lipids for the human tear film. The meibum spreads onto the tear film, promotes its stability, and prevents its evaporation.
Meibomian gland dysfunction (MGD) is a common and chronic disorder that has a significant adverse impact on patients’ quality of life. It is a leading cause of evaporative DED, as meibomian glands play an important role in providing lipids to the tear film, which helps to retard the evaporation of tears from the ocular surface.
DED further impacts visual function as an inadequate tear film and ocular surface damages result in visual disturbances. Recent publications highlight the correlation of ocular surface damage in dry eye patients and their difficulties with reading.