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Form and Function of the Cornea
The cornea is the clear, outermost layer of the eye that overlays the anterior chamber, iris, and pupil. It functions primarily as (1) a protective barrier to the rest of the eye by shielding against dust, bacteria, and other foreign agents, and (2) an exterior lens that helps focus entering light onto the retina. Additionally, the cornea serves to filter out certain harmful UV rays. Absolute transparency is a critical feature of the cornea and so it is an avascular region that relies on tears around its anterior face and aqueous humor around its posterior face for nourishment and protection against infection. Furthermore, because of its lack of blood vessels, oxygen is directly absorbed by the cornea rather than delivered through hemoglobin. Each of the five layers (in order from outermost to innermost) of the cornea serves an essential function.

Epithilium – Blocks entry of foreign particles such as dust, debris, and bacteria. Absorbs and distributes oxygen and nutrients from tears to the rest of the cornea. The epithelial cells attach to and organize themselves around a basement membrane.

Bowman’s Layer – Primarily composed of collagen, which helps the cornea maintain its shape. Stroma – Comprises of 90% of the cornea’s thickness. Its main components are water and collagen and it helps maintain the cornea’s shape and elasticity. The arrangement of collagen within the stroma plays an important role in maintaining transparency and assisting in light conduction.

Descemet’s Membrane – Composed primarily of collagen fibers and protects against injury and infection.

Endothelium – Extremely thin, innermost layer that is essential for maintaining corneal transparency. It pumps excess fluid out of the corneal stroma to prevent swelling, which would interfere with the clarity of vision.

Contact Lens Types
Contact lenses can be roughly classified under two main categories: soft contact lenses and hard contact lenses. Soft contact lenses are generally made using a flexible polymer-plastic material with water, allowing for oxygen permeability. Additionally, some are capable of providing UV protection. Soft contact lenses often come in the form of daily disposables or extended wear disposables (made of silicone hydrogel and usable for up to 30 days). In contrast, rigid gas permeable contact lenses are much more durable than their soft counterparts and may require daily wear in order to adjust to. Today, rigid gas permeable lenses are primarily made of silicone polymers, which are conducive to oxygen circulation. PMMA lenses (polymethyl methacrylate) are another form of rigid contact lenses that are impermeable to oxygen. When PMMA lenses are worn, oxygen is delivered to the eye only after being dissolved into tears. Developed in the 1960’s, PMMA lenses are rarely prescribed today because of the ubiquity of both soft and hard contact lens alternatives that offer greater comfort. Nevertheless, they are still favored by some people for their durability and cheap price. Other subcategories of contact lenses include bifocal (for correcting presbyopia), toric (for correcting astigmatism), and corneal reshaping contact lenses.

Summary
Long-term contact lens use leads to alterations in corneal thickness, stromal thickness, curvature, corneal sensitivity, cell density, and epithelial oxygen uptake, etc. Other changes include the formation of epithelial vacuoles and microcysts (containing cellular debris) as well as the emergence of polymegatheism in the corneal endothelium. Decreased corneal sensitivity, vision loss, and photophobia have also been observed in patients who have worn contact lens for an extended period of time. Surprisingly, many contact lens-induced changes in corneal structure are reversible if contact lenses are removed for an extended period of time.

Changes in Function and Morphology
The effects of extended contact lens wear on the cornea have been studied extensively and are well-documented. When determining the effects of long-term contact lens use on the cornea, many studies do not differentiate between users of hard and soft contact lenses, while studies that have made this differentiation have found similar results. This is probably because most contact lens-induced changes to the cornea are caused by hypoxia, which occurs as long as any physical barrier to the surface of the cornea is present. In certain instances, hard contact lenses were shown to cause the same changes in corneal structure as soft contact lenses, though these changes were more dramatic because rigid lenses are capable of inflicting greater trauma on the eyes.

Structural Damage
Long-term use of soft hydrogel contact lenses has been shown to alter the following in the cornea: epithelial oxygen uptake, epithelial thickness, stromal thickness, and corneal endothelial morphology. Furthermore, the formation of epithelial vacuoles and microcysts has been observed following long-term contact lens wear. Vacuoles are fluid-filled chambers that begin to appear one week after extended contact lens use begins; their number increases over time with extended contact lens wear. Microcysts tend to appear three months after contact lens wear begins and increase in number over time as long as contact lens wear resumes. On average, over five times as many epithelial microcysts than normal have been observed in long-term contact lens wearers.

Among patients who have worn soft hydrogel contact lenses for over a year, significant reductions in epithelial oxygen uptake, epithelial thickness, and stromal thickness have been recorded, while an increase in endothelial polymegathism was found. In patients who had worn contact lenses for approximately five years or more, a 30 to 50 μm reduction in central and peripheral corneal thickness has been recorded. Furthermore, the reduction was more pronounced in patients wearing hard contact lenses than in patients wearing soft contact lenses. Increased corneal curvature is also known to arise from long-term contact lens wear; this increase in corneal curvature can be as much as 0.5 diopters greater than normal. Corneal surface irregularity and asymmetry are also caused by long-term contact lens wear; these problems are sometimes correlated with astigmatism in contact lens wearers and are thought to be caused by hypoxia, surface molding, and chronic and mild trauma to the cornea from contact lens use. Long-term use of PMMA or thick hydrogel contact lenses have been found to cause corneal warpage (shape distortion).

Functional Damage
Corneal sensitivity is significantly diminished after extended contact lens wear (five or more years). However, this difference in sensitivity is not correlated with a change in the number of nerve fiber bundles in the subbasal plexus of the cornea. Long-term use of PMMA or thick hydrogel contact lenses have been found to cause increased eye irritability, photophobia, blurred vision, and persistent haloes.

Unchanged Variables
The number of corneal keratocytes in the epithelial stroma has not been found to change with long-term contact lens wear. Endothelial cell density also does not change with long-term contact lens wear. No strong relationship has been found between long-term contact lens wear and corneal astigmatism.

Reversibility of Damage
Many of the observed changes appear to be reversible.

Epithelial oxygen uptake has been found to return to normal levels one month after cessation of contact lens wear. Epithelial thickness has been found to return to a normal level as soon as one week following the cessation of contact lens wear. Stromal thickness has been shown to subside two days after contact lens wear is halted. However, endothelial polymegathism does not seem to return to normal levels even long after the cessation of contact lens wear. Even after a six month period in which contact lenses are not warn, polymegathism seems to remain. The density of microcysts also remains as long as one month after contact lenses are removed, and microcysts do not disappear completely until two to three months after contact lens wear is completed halted. Reductions in epithelial oxygen uptake and thickness are thought to be caused by long-term contact lens wear-induced hypoxia, which hinders epithelial metabolism and mitosis. Recovery of normal epithelial oxygen uptake can be recovered if contact lens wear is completely halted for one month. Because long periods of contact lens wear are correlated with extended hypoxia, the resurgence of cellular growth and epithelial metabolism following contact lens removal (and hence, improved oxygen circulation) leads to an initial, increased resurgence of microcysts containing cellular debris. Over time, microcysts will disappear if contact lenses are not worn.

Corneal sensitivity has been found to be significantly diminished following long-term contact lens wear. However, this difference in sensitivity is not correlated with a change in the number of nerve fiber bundles in the subbasal plexus of the cornea, suggesting that diminished corneal sensitivity following extended periods of contact lens wear is not caused by a reduction in nerve fiber bundles but possibly a change in functionality. One of two years of hard contact lens wear has not been shown to affect corneal sensitivity, but real changes are observed following five years of hard contact lens wear. However, this significant decrease in corneal sensitivity appears to be reversible. Following cessation of hard contact lens usage, corneal sensitivity has been shown to be fully regained after several months: patients who had worn hard contact lenses for a decade or longer were able to regain normal corneal sensitivity after four months of not wearing contact lenses at all. It is thought that constant adhesion of contact lenses to the cornea may lead to adaptation to mechanical stimuli, thus decreasing corneal sensitivity to tactile stimuli. A proposed explanation for the reduced sensitivity is the induced quiescence of free nerve endings following long term corneal exposure to contact lenses.

Long-term use of PMMA or thick hydrogel contact lenses have been found to cause corneal warpage (shape distortion), increased eye irritability, photophobia, blurred vision, and persistent haloes. Collectively, these symptoms constitute Corneal Exhaustion Syndrom (CES), which is associated with corneal endothelium abnormalities including edema, polymegathism, irregular mosaic, and pigment deposition. Patients with CES suffer from compromised corneal endothelium resulting from chronic hypoxia and acidosis. These problems can be alleviated by providing a patient with lenses that allow for greater oxygen permeability.

Etiology
Increases in corneal curvature are thought to be caused by corneal thinning-induced ectasia. Another proposed explanation is that impairments in oxygen delivery caused by long-term contact lens wear can lead to epithelial edema and stromal thickening, which subsequently increase corneal curvature. Two explanations have been proposed for contact lens-induced stromal thinning. It is thought that contact lens-induced edema may inhibit stroma tissue synthesis. Alternatively, contact lens-induced hypoxia may trigger a lactic acid buildup that leads to the erosion of stromal tissue. The mechanism behind contact lens-induced polymegathism is unknown, though it is also thought to be a byproduct of corneal edema and epithelial hypoxia.