Abstract
Ocular surface inflammation is one of the major features of dry eye disease (DED) according to the definition proposed by the Tear Film and Ocular Surface Society (TFOS) International Dry Eye Workshop (DEWS) in 2007 and 2017. This chapter discusses the potential pathomechanism of the DED vicious cycle and focuses on the role of chronic inflammation and flares in DED pathophysiology. Ocular inflammation may be regarded as both a cause and effect of DED. The current understanding of the mechanism responsible is that the repeating desiccating stress accompanied by hyperosmolarity induces the immune system reaction, leading to the chronic inflammation and apoptosis of ocular surface cells. On the cellular level, there is growing evidence from experimental, animal, and human studies that Th17 lymphocytes play a crucial role in DED pathogenesis. Also, potential methods of anti-inflammatory methods of treatment are discussed, such as eye lubricants, autologous serum eye drops, topical steroids, oral and topical immunomodulation drugs, and N-acetylcysteine (NAC). Understanding the role of inflammation on the cellular and molecular level may lead to improve treatment options for patients. A new approach to DED treatment should be focused to target not only symptoms but also break the pathological dry eye cycle.