Research Projects

Keratoconus is a bilateral corneal ectatic disease causing progressive corneal thinning and distortion. This disease commonly affects individuals between 10-30 years of age and causes progressive loss of vision. There are some risk factors for progression such as vernal keratoconjunctivitis, pregnancy, advanced disease at presentation etc. Currently, collagen crosslinking is the only known treatment to halt the progression of disease. This procedure, however, is not able to restore the corneal thickness or reverse the corneal distortion. It merely halts the disease progression by improving the biomechanical strength of the cornea. Consequently, most patients need spectacles or contact lenses for achieving good visual acuity affecting their overall quality of life. Patients who have too advanced a disease are not eligible for collagen crosslinking and are subjected to corneal transplantation. This not only adds to the burden on the eye bank for donor tissues, but also affects these individuals at a young age when the donor corneas are more likely to be rejected by the recipient. Patients are usually monitored regularly to detect progression. However, there are no predictive markers for progression of disease.?The pathophysiology of keratoconus progression is poorly understood. It has been shown that tear cytokine levels are altered in keratoconus as compared to normal eyes. Similarly, confocal microscopy has shown alterations in corneal nerves and keratocyte density in keratoconus as compared to normal eyes. In this study, we analyse and correlate the alterations in tear cytokine levels and confocal microscopic changes at cellular level to understand the pathophysiology of progressive disease as compared to non-progressive disease. This would help predict progression at an earlier stage potentially preserving good vision in these eyes. Secondly, understanding the pathophysiology behind keratoconus progression could help in developing a treatment modality alternate to collagen crosslinking.