Dry Eye Disease (DED) is the most common condition seen by eye care professionals. The disease has a significant impact on quality of life, with symptoms such as foreign body sensation, pain, blurry vision, dryness or watery eyes. Risk factors include, among others, skin pathologies, immunological imbalances, hormonal changes, environmental conditions, and poor hygiene.
In its evaporative form, Dry Eye Disease is mainly caused by meibomian gland dysfunction (MGD). In MGD, the meibomian glands are inflamed, blocked, displaced, or atrophied. As a result, meibum is not adequately secreted, thereby destabilizing the tear film and increasing the rate of evaporation of the aqueous layer. This exposes the cornea to pathogens, hyperosmolarity, nutrient depletion, and dehydration, which in turn leads to even more inflammation. This vicious cycle is the basis of the chronic inflammation that underlies Dry eye disease.11
Dry Eye
Key Facts
The prevalence of DED symptoms ranges from 5% to 50%.1
25% of Dry Eye Disease sufferers in the United States are undiagnosed.2
Women are twice as likely as men to have Dry Eye Disease.3
Refractive surgery can trigger and aggravate Dry Eye Disease 4, 5
85% of Dry Eye Disease patients have signs of MGD.7
80% of skin rosacea patients show signs of MGD.8
Rosacea is a Major Contributor to Meibomian Gland Dysfunction (MGD) and Dry Eye Disease
One of the major risk factors of MGD and Dry Eye Disease is skin rosacea.8 Several mechanisms of action have been proposed to explain the relationship between Rosacea and MGD. First, in Rosacea, abnormal blood vessels (telangiectasia) release pro-inflammatory mediators, which can easily propagate to the eyelids via the orbital vasculature. Second, demodex thrive on skin affected with Rosacea. These parasites play a major role in causing eyelid inflammation.9
In addition, demodex mites are infested with bacteria, especially Bacillus olerinus.10 Proliferation of this bacterium not only contributes directly to inflammation, but also increases the melting temperature of the meibum, thus causing thickened meibum to block the meibomian glands. Thickened secretions and blocked glands, or MGD, result in inadequate lipid contribution to the tears, causing tear film instability and a further increase in inflammation of the ocular surface.11
1. Stapleton F, Alves M, Bunya V, et al. TFOS DEWS II Epidemiology Report. Ocul Surf. 2017;15(3):334-65. 2. Farrand K, Fridman M, Stillman I, Schaumberg D. Prevalence of diagnosed Dry Eye Disease in the United States among adults aged 18 years and older. Am J Ophthalmol.. 2017;182:90-8. 3. Sullivan D, Rocha E, Aragona P, et al. TFOS DEWS II Sex, Gender, and Hormones Report. Ocul Surf.. 2017;15(3):284-333. 4. De Paiva C, Chen Z, Koch D, et al. The incidence and risk factors for developing dry eye after myopic LASIK. Am J Ophthalmol. 2006;141(3):438-45. 5. Solomon R, Donnenfeld E, Perry H. The effects of LASIK on the ocular surface. Ocul. Surf. 2004;2(1):34-44. 6. Shtein R. Post-LASIK dry eye. Expert Rev Ophthalmol. 2011;6(5):575-82. 7. Lemp M, Crews L, Bron A, Foulks G, Sullivan B. Distribution of aqueous-deficient and evaporative dry eye in a clinic-based patient cohort. Cornea. 2012;27:472-8. 8. Viso, E, Rodríguez-Ares M, D, Oubiña B, Gude F. Prevalence of asymptomatic and symptomatic meibomian gland dysfunction in the general population of Spain. IOVS. 2012;53(6):2601-6. 9. Liu J, Sheha HTS. Pathogenic role of Demodex mites in blepharitis. Curr Opin Allergy Clin Immunol.. 2010;10(5):505-10. J 10. armuda S, McMahon F, Zaba R, et al. Correlation between serum reactivity to Demodex-associated Bacillus oleronius proteins, and altered sebum levels and Demodex populations in erythematotelangiectatic rosacea patients. J Med Microbiol. 2014;63(Pt 2):258-62. 11. Baudouin C, Messmer E, Aragona P, et al. Revisiting the vicious circle of dry eye disease: a focus on the pathophysiology of meibomian gland dysfunction. Br J Ophthalmol. 2016;100(3):300-6