Dry eye disease (DED) is a multifactorial disorder of the ocular surface characterized by tear film instability, hyperosmolarity, inflammation, and neurosensory abnormalities. While the pathological effects of DED on the corneal epithelium and ocular surface have been extensively investigated, increasing evidence suggests that chronic ocular surface inflammation may also influence deeper corneal structures, including the corneal endothelium. The corneal endothelium plays a critical role in maintaining corneal transparency through regulation of stromal hydration. Alterations in endothelial cell density (ECD), coefficient of variation (CV), hexagonality (HEX), and central corneal thickness (CCT) have been reported in patients with varying severities of DED. This narrative review summarizes current evidence regarding the relationship between corneal endothelial cell characteristics and DED, explores potential pathophysiological mechanisms linking ocular surface inflammation to endothelial dysfunction, and discusses the clinical implications of these findings. Although available evidence remains limited and sometimes conflicting, chronic inflammation, oxidative stress, tear film instability, and neuroimmune interactions appear to contribute to subtle endothelial alterations in patients with moderate-to-severe DED. Further longitudinal studies are required to establish causality and determine the clinical significance of endothelial changes in DED management.