Diabetes-associated dry eye disease(DDED)is a common ocular surface complication in patients with diabetes mellitus. It is characterized by lacrimal gland dysfunction, corneal neuropathy, meibomian gland dysfunction, and ocular surface barrier impairment,with the accumulation of reactive oxygen species(ROS)and the disruption of ocular surface homeostasis driven by positive ROS-inflammatory feedback as its key pathogenesis. Chronic hyperglycemia induces excessive production of ROS via activation of the polyol pathway, accumulation of advanced glycation end products(AGEs), protein kinase C(PKC)activation, and mitochondrial dysfunction. Through the interplay among the ROS-inflammation positive feedback loop, autophagy dysfunction, and endoplasmic reticulum(ER)stress, excess ROS triggers corneal nerve degeneration, reduced tear secretion, abnormal meibum, and systemic disruption of multiple ocular surface barriers, thereby forming a “hyperglycemia-oxidative stress-ocular surface injury” vicious cycle. In addition to artificial tears, anti-inflammatory agents, and physical therapies, treatment should include multi-target strategies such as stringent glycemic control, antioxidant therapy, neuroprotective therapy, secretagogue therapy, and integrative traditional Chinese and Western medicine. This review proposes an oxidative stress-centered pathophysiological framework for DDED and outlines the intervention targets of traditional Chinese and Western medicine, aims to provide a reference for mechanistic research and precision interventions.