**1. Introduction**

Dry eye disease is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles [1].

Historically, dry eye was mostly considered to be caused by a simple tear deficiency. According to the current definition of the disease, proposed by the Tear Film and Ocular Surface Society (TFOS) International Dry Eye Workshop (DEWS) in 2017, inflammation is one of the major features of the disease accompanied by tear film instability and hyperosmolarity, ocular surface damage, and neurosensory abnormalities. The proposed mechanism of the disease is the self-perpetuating vicious cycle, in which the loss of homeostasis of the tear film plays a major role. The mechanism was broadly introduced in 2007, further adopted by the TFOS DEWS II committee, and remains the leading concept of DED pathophysiology

[2, 3]. Meibomian gland dysfunction (MGD) is at the center of the vicious cycle of DED. As shown in **Figure 1**, MGD is a key trigger of tear film instability, inflammation, ocular surface apoptosis, and neurosensory abnormalities. Understanding the pathophysiology of DED has significant implications for the methods of diagnosis and methods of treatment. Anti-inflammatory therapies are already available in DED treatment, but understanding their role and differences among them is crucial in successful patient management.
