Dry eye disease is a multifactorial condition characterised by tear film instability, hyperosmolarity and ocular surface inflammation. Understanding the epidemiology of dry eye disease and recognising both modifiable and non-modifiable risk factors can assist eye care practitioners in assessing, treating, and managing patients with the condition. This review considers current knowledge surrounding its incidence and prevalence, as well as associated demographic, systemic, ocular, and iatrogenic, and lifestyle-related modifiable risk factors. Population-based prevalence estimates vary according to the diagnostic criteria used to define dry eye disease, as well as severity and demographic characteristics of the population. Considering recent data and variable population demographics, conservative prevalence estimates suggest that 10–20% of the population over 40 years of age report moderate to severe symptoms and/or seek treatment for dry eye disease. Individuals with specific non-modifiable demographic risk factors may be at increased risk of developing dry eye disease. Advanced age, female sex and East Asian ethnicity have been identified as key non-modifiable demographic features predisposing individuals to dry eye disease. Systemic conditions that have been associated with an increased risk of dry eye disease include migraine, Sjögren syndrome, connective tissue disorders, mental health disorders, diabetes mellitus and androgen deficiency. Medications that may contribute to this risk include antidepressants, antihistamines, and hormone replacement therapy. Ocular and iatrogenic risk factors of dry eye disease include blepharitis, Demodex infestation, ocular surgery, blink completeness, contact lens wear, and topical ophthalmic medications. A range of modifiable lifestyle factors that can increase the risk of dry eye disease have also been identified, including low humidity environments, digital screen use, quality of sleep, diet, and eye cosmetic wear. Dry eye is a common disease affecting millions globally. Increasing knowledge regarding its associated risk factors can better prepare the eye care practitioner to successfully manage patients with this ocular surface disease.

Meibomian gland dysfunction (MGD) is a leading cause of non-aqueous deficient dry eye disease. Meibomian glands are responsible for the production of meibum, a lipid-rich secretion that coats the surface of the tear film, inhibiting evaporation of the underlying aqueous tear fluid. MGD can arise due to numerous extrinsic and intrinsic factors that drive changes in meibum quality or obstruction of gland orifices and can result in tear film instability, hyperosmolarity, epithelial damage and downstream ocular surface inflammation. Despite the high disease prevalence, management is not standardised, with a wide range of pharmacological and naturally derived therapies available. Potential pharmacological agents include anti-inflammatories (antibiotics, immunosuppressants and topical integrin antagonists), perfluorohexyloctane and topical aqueous secretagogues. Natural therapies that may offer suitable long-term solutions include oral dietary supplements (polyunsaturated fatty acids, astaxanthin, bilberry, Chinese herbal formulations and Korean red ginseng) and naturally derived topical formulations (castor oil, manuka honey, tea tree oil, coenzyme Q10 and green tea extract). The rising prevalence of MGD has led to the development of several novel therapeutic strategies, expanding the range of management options available to clinicians. A thorough examination should precede the initiation of treatment to identify underlying pathophysiology and guide targeted interventions. Treatment efficacy, duration and safety profiles must also be considered.

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.

Clinical test utility for detecting inflammation in dry eye disease (DED) remains largely uninvestigated. This cross-sectional study explored relationships between clinical tests and molecular biomarkers of ocular surface inflammation to determine their diagnostic utility. Inflammation indicators including bulbar conjunctival hyperaemia (subjective and objective grading), InflammaDry® MMP-9 test, Ocular Surface Inflammation Evaluation® score (Tearcheck®) and ocular surface staining were assessed in individuals with and without DED. Conjunctival impression cytology samples underwent droplet digital PCR to quantify MMP-9, IL-8 and IL-1β gene expression. Receiver operating characteristic curves established clinical test utility for detecting elevated biomarker levels and optimal cut-off values. Of 47 participants (55 ± 18 years; 21% male), 79% met the TFOS DEWS II diagnostic criteria for DED, with 84% classified as lipid-deficient. Biological MMP-9 presence was associated with NIBUT 1.0 or Efron grading >1.5), positive InflammaDry results, positive symptom scores (DEQ-5 >9 or OSDI >33.3), and thinner tear film lipid layer grade (LLG ≤ 2; all p < 0.05). No significant clinical associations with IL-8 or IL-1β levels were found. Two or more positive assessments from hyperaemia (JENVIS), NIBUT and LLG offered within-sample diagnostic accuracy of 78.6% sensitivity and 78.8% specificity. A test battery comprising bulbar conjunctival redness (JENVIS >1.0), tear film instability (NIBUT <5.8 s) and lipid insufficiency (LLG ≤2) optimally identified individuals with detectable MMP-9 expression. Two or more clinical signs identified high-risk individuals and, while further validation is warranted, it suggests inflammatory marker detection is limited to those with higher DED symptom and clinical sign scores.