New thoughts on managing anterior segment disease are prompting opportunities for a healthier ocular surface. The eyelid margin has been the focus of much research, and clinically we are appreciating the delicate balance that a healthy lid margin provides for the ocular surface. This has implications for both contact lens and non-contact lens wearers.
Rynerson and Perry proposed a new theory regarding blepharitis and its long-term effects to the health of the ocular surface called “dry eye blepharitis syndrome“ (DEBS).1
Clinically, we refer to a patient as having blepharitis by the presence of collarettes or deposits at the base of the lashes (Figure 1). Interestingly, they are a manifestation of blepharitis; ODs are at times guilty of not diagnosing based on the inflammatory state. Blepharitis, by definition, is an inflammation of the eyelid margin, and, therefore, using lid debris as an identifier of blepharitis falls short.
Rynerson and Perry discuss the overpopulation of bacteria creating biofilms over the lid margin surface as the major contributor to much of the downstream inflammation and, therefore, dry eye.
Bacteria and biofilms
Our lid margins are naturally populated with bacteria that naturally live within biofilms. All bacteria living in a natural environment live within biofilms as means of survival. As these bacterial populations within a biofilm increase above certain threshold populations, they undergo quorum-sensing gene activation and begin to produce toxins known as virulence factors. It is these virulence factors, such as lipases, cytolytic toxins, and super antigens, that directly cause the inflammation that leads to blepharitis and, in some, the long-term sequelae of dry eye disease.2
This inflammation affects the ocular surface in phases based on the anatomical relationship of the structures within the lid. Logic would presume that smaller structures of the lid would initially be affected by the accumulation of biofilm within, and larger structures—or structures more distant to the lid margin—would be affected later.
Rynerson and Perry describe four stages of DEBS. These stages of DEBS are proposed as chronic long-term changes that occur over decades and manifest into the signs and symptoms that we know as dry eye disease.
Let’s review the order of the affected ocular structures along with the clinical manifestations that are evident at these phases.
1. Rynerson JM, Perry HD. DEBS – a unified theory for dry eye and blepharitis. Clin Ophthalmology. 2016 Dec 9;(10):2455-2467.
2. Knecht LD, O'Connor G, Mittal R, Liu XZ3, Daftarian P, Pasini P, Deo SK, Daunert S. Serotonin activates bacterial quorum sensing and enhances the virulence of Pseudomonas aeruginosa in the host. EBioMedicine. 2016 Jul;9:161-169.
3. Connor CG, Choat, C, Narayanan S, Kyser K, Rosenberg B, Mulder D. Clinical effectiveness of lid debridement with blephex treatment. Invest Ophthalmol Vis Sci. 2015 June;56(9):440. Available at: https://iovs.arvojournals.org/article.aspx?articleid=2334385&resultClick=1. Accessed 9/11/18.
4. Epitropoulous A, et al. Blephex – A Retrospective Analysis of Data Pre and Post Treatment. Available at: https://simovision.com/assets/Uploads/Study-A-retrospective-Analysis-of-.... Accessed 9/14/18.
5. Connor CG, Narayanan S, Miller W. Reduction in inflammatory marker matrix metalloproteinase-9 following lid debridement with BlephEx. Invest Ophthalmol Vis Sci. 2017 June;58(9):448. Available at: https://iovs.arvojournals.org/article.aspx?articleid=2638666&resultClick=1. Accessed 9/11/18.
6 Siddireddy JS, Tan-Showyin J, Vijay AK, Willcox M. A Comfortable Eye Needs Fats. Thesis competition at the University of South Wales, Sydney, 2015.