12/02/2025
KERATOCONUS - An Inflammatory Disease in Disguise and the Importance of Treating Inflammation in Keratoconus
Traditionally, keratoconus has been considered a non-inflammatory disease driven primarily by mechanical, genetic, and biochemical factors, which contribute to the weakening and steepening of the cornea. As a result, clinical interventions have often focused on methods such as corneal crosslinking (CXL), rigid contact lenses, and, in some cases, corneal transplants. However, growing evidence from recent research suggests that keratoconus should not be classified as a purely non-inflammatory disease. Ocular inflammation plays a critical role in its pathogenesis, and the inflammatory processes involved may contribute significantly to the progression of the disease.
Traditionally, keratoconus has been considered a non-inflammatory disease driven primarily by mechanical, genetic, and biochemical factors, which contribute to the weakening and steepening of the cornea. As a result, clinical interventions have often focused on methods such as corneal crosslinking (CXL), rigid contact lenses, and, in some cases, corneal transplants. However, growing evidence from recent research suggests that keratoconus should not be classified as a purely non-inflammatory disease. Ocular inflammation plays a critical role in its pathogenesis, and the inflammatory processes involved may contribute significantly to the progression of the disease.
In addition to ocular inflammation, recent research has shown that other cofactors, such as reduced ocular blood flow, oxidative stress, ferroptosis, and excitotoxicity, have been shown to coexist and contribute to the progression of keratoconus.
This paper aims to explain how keratoconus involves ocular inflammation along with its associated cofactors and why the treatment of keratoconus should address inflammation and other cofactors.
By controlling and eliminating ocular inflammation and its associated cofactors, it is possible to stop disease progression, prevent further corneal damage, and reverse corneal ectasia in patients with keratoconus.
