Tear Film and Ocular Surface in Keratoconus

Abstract

Keratoconus (KC) is an ectatic corneal disorder, characterised by progressive stromal thinning and structural weakening with apical cone-like protrusion, leading to progressive myopia, irregular astigmatism, scarring and decreased vision. It is a leading cause of corneal transplantation in the developed world. While keratoconus has been traditionally considered a predominantly degenerative, non-inflammatory disease of multivariate origin, the exact aetiology remains largely unknown. There is now evidence of genetic inheritance and possible association with systemic disease, as well as substantial evidence that certain environmental factors, such as ocular surface disease, atopy and contact lens wear, and behaviours, such as excessive eye rubbing, may play a key role. The factors that determine or affect the progression or stabilisation of the disease are not well characterised or understood.A number of studies suggest a pivotal role of inflammation in the pathogenesis and progression of KC, contradicting the dogma that traditionally classified keratoconus as a non-inflammatory condition. Elevated levels of inflammatory mediators, such as pro-inflammatory cytokines, tumour necrosis factor, interleukins, cell adhesion molecules, and matrix metalloproteinases (MMPs) have been detected in keratoconic eyes compared to normal, implying that chronic inflammatory events are involved in the manifestation and progression of the disease. Many studies have attempted to investigate in depth the pathogenesis of keratoconus. And while it is widely accepted that complex interactions between genetic and environmental factors, both mechanical and biochemical, influence the development and course of