Dry eye disease (DED) is a multifactorial ocular surface disorder arising from numerous interrelated underlying pathologies that trigger a self-perpetuating cycle of instability, hyperosmolarity, and ocular surface damage. Associated ocular discomfort and visual disturbance contribute negatively to quality of life. Ocular surface inflammation has been increasingly recognised as playing a key role in the pathophysiology of chronic DED. Current readily available anti-inflammatory agents successfully relieve symptoms, but often without addressing the underlying pathophysiological mechanism. The NOD-like receptor protein-3 (NLRP3) inflammasome pathway has recently been implicated as a key driver of ocular surface inflammation, as reported in pre-clinical and clinical studies of DED. This review discusses the intimate relationship between DED and inflammation, highlights the involvement of the inflammasome in the development of DED, describes existing anti-inflammatory therapies and their limitations, and evaluates the potential of the inflammasome in the context of the existing anti-inflammatory therapeutic landscape as a therapeutic target for effective treatment of the disease.

Background: Corneal sensitivity is a key indicator of ocular surface health. This prospective, cross-sectional study evaluated agreement between corneal sensitivity thresholds obtained from equivalent stimulus settings on a contemporary, enhanced dual-temperature non-contact corneal aesthesiometer (NCCA) and a previously validated (standard) device. Methods: Central corneal sensitivity thresholds were measured in the right eyes of healthy participants using both devices. Participants with previous ocular surgery, laser treatment, trauma, contact lens wear, diabetes, or peripheral neuropathy were excluded. Sensitivity thresholds were determined using a forced-response, double-staircase protocol. Inter-device agreement was assessed using Bland–Altman analysis, and consistency was assessed using intraclass correlation coefficients. Results: Median corneal sensitivity thresholds in 51 healthy participants (32 female, 19 male; mean age: 33 ± 14 years) did not differ between enhanced (0.23 [0.18 to 0.38]) and standard (0.25 [0.15 to 0.35]) NCCA instruments (p = 0.73). Bland–Altman analysis demonstrated moderate inter-device agreement, with a mean difference of −0.01 mbar (95% limits of agreement: −0.41 to 0.39 mbar). Linear regression analysis identified greater measurement discrepancies at higher thresholds (p < 0.05), indicating greater variability in individuals with reduced corneal sensitivity. Conclusions: The enhanced NCCA yields reliable corneal sensitivity measures for a room-temperature stimulus and acceptable agreement with the existing (standard) model.