Abstract
Dry Anophthalmic Socket Syndrome (DASS) is a multifactorial condition that affects roughly half of all prosthetic eye wearers and remains frequently underrecognized. It is characterised by symptoms such as dryness, discomfort, discharge, and inflammation of the socket surface. Diagnostic criteria include validated symptom questionnaires (e.g., OSDI, DEQ-5, SANDE) and at least one clinical sign such as conjunctival staining, blepharitis, or reduced tear meniscus height. This review describes the anatomical, cellular, and molecular changes associated with DASS. Meibomian gland dysfunction is common, with a significant reduction in gland density and structure. Goblet cell density is also often decreased, particularly in the tarsal and bulbar conjunctiva, although findings may be affected by topical treatments. Increased conjunctival inflammation-evidenced by immune cell infiltration and elevated markers such as MMP-9 and ICAM-1-is frequently observed, particularly in the posterior socket lining. Oxidative stress, mediated by dysregulated NOX4, KEAP1, and NRF2 expression, appears to play a contributory role. Additional factors influencing DASS include eyelid malpositions such as entropion and ectropion, prosthesis smoothness and amount of tear film production. Poor hygiene practices and environmental factors may exacerbate symptoms. Given its multifactorial aetiology, DASS requires a complex management strategy targeting inflammation, tear film instability, mechanical irritation, eyelid position and patient education. Increased awareness, standardised diagnostics, and evidence-based care protocols are critical to improving outcomes for prosthetic eye wearers.