DEBS – a unification theory for dry eye and blepharitis

For many years, blepharitis and dry eye disease have been thought to be two distinct diseases, and evaporative dry eye distinct from aqueous insufficiency. In this treatise, we propose a new way of looking at dry eye, both evaporative and insufficiency, as the natural sequelae of decades of chronic blepharitis. Dry eye is simply the late form and late manifestation of one disease, blepharitis. We suggest the use of a new term in describing this one chronic disease, namely dry eye blepharitis syndrome (DEBS). Bacteria colonize the lid margin within a structure known as a biofilm. The biofilm allows for population densities that initiate quorum-sensing gene activation. These newly activated gene products consist of inflammatory virulence factors, such as exotoxins, cytolytic toxins, and super-antigens, which are then present for the rest of the patient’s life. The biofilm never goes away; it only thickens with age, producing increasing quantities of bacterial virulence factors, and thus, increasing inflammation. These virulence factors are likely the culprits that first cause follicular inflammation, then meibomian gland dysfunction, aqueous insufficiency, and finally, after many decades, lid destruction. We suggest that there are four stages of DEBS which correlate with the clinical manifestations of folliculitis, meibomitis, lacrimalitis, and finally lid structure damage evidenced by entropion, ectropion, and floppy eyelid syndrome. When one fully understands the structure and location of the glands within the lid, it becomes easy to understand this staged disease process. The longer a gland can resist the relentless encroachment of the invading biofilm, the longer it can maintain normal function. The stages depend purely on anatomy and years of biofilm presence. Dry eye now becomes a very easy disease to understand. We feel that dry eye should be treated and prevented by early and routine biofilm removal through electromechanical lid margin debridement.