Keratoconus is a condition where the cornea, the clear front surface of the eye, gradually becomes thinner and bulges outward into a cone-like shape. This change in shape distorts vision, causing blurriness, sensitivity to light, and difficulty seeing clearly, especially at night. Understanding what causes keratoconus involves looking at a combination of genetic, environmental, and cellular factors that affect the cornea’s structure and strength.
At its core, keratoconus results from a weakening of the corneal tissue. The cornea is made up of layers of collagen fibers arranged in a precise pattern that gives it strength and shape. In keratoconus, this collagen matrix becomes disrupted. The collagen fibers lose their normal organization and the natural cross-links that hold them tightly together are reduced. This leads to a loss of tensile strength, making the cornea less able to maintain its normal dome shape. Instead, it thins and bulges outward under the pressure inside the eye.
The exact cause of this weakening is not fully understood, but several factors are known to contribute:
**Genetic predisposition:** Keratoconus often runs in families, suggesting a hereditary component. People with a family history of keratoconus are at higher risk. Researchers believe that certain genes involved in collagen production and corneal structure may be altered, making the cornea more vulnerable to weakening.
**Biochemical changes:** Studies show that in keratoconus, there is an imbalance in enzymes and molecules that maintain the cornea’s collagen. For example, enzymes that break down collagen (called matrix metalloproteinases) may be overactive, while natural inhibitors of these enzymes are reduced. This imbalance leads to gradual degradation of the corneal collagen.
**Oxidative stress:** The cornea is exposed to ultraviolet (UV) light and environmental toxins that can cause oxidative damage. Normally, the cornea has antioxidant defenses to protect against this damage, but in keratoconus, these defenses may be weaker. Oxidative stress can damage collagen fibers and cells in the cornea, contributing to its weakening.
**Mechanical factors:** Frequent eye rubbing is strongly linked to keratoconus. Rubbing the eyes applies mechanical trauma to the cornea, which can accelerate collagen breakdown and thinning. People with allergies or chronic eye irritation often rub their eyes more, increasing their risk.
**Inflammation:** Although keratoconus was once thought to be a non-inflammatory condition, recent research suggests low-grade inflammation may play a role. Inflammatory molecules found in the tears and corneal tissue of keratoconus patients can promote tissue remodeling and collagen degradation.
**Hormonal influences:** Some evidence indicates that hormones, especially during puberty or pregnancy, may affect corneal structure and contribute to keratoconus progression. This may explain why keratoconus often begins or worsens during adolescence or early adulthood.
**Environmental factors:** Exposure to UV light, eye allergies, and chronic eye irritation can all contribute to the development or worsening of keratoconus. UV light can induce oxidative damage, while allergies can lead to eye rubbing and inflammation.
In summary, keratoconus arises from a complex interplay of genetic susceptibility, biochemical imbalances, oxidative damage, mechanical trauma, and possibly inflammation and hormonal changes. These factors collectively weaken the corneal collagen matrix, causing the cornea to thin and bulge into a cone shape. This structural change distorts vision and can progressively worsen if untreated.
Because the cornea’s strength depends heavily on the integrity of collagen fibers and their cross-linking, treatments like corneal collagen cross-linking have been developed. This procedure uses riboflavin (vitamin B2) and ultraviolet light to create new chemical bonds between collagen fibers, strengthening the cornea and halting progression. However, understanding the root causes of keratoconus remains an activ
