Effects of long-term contact lens wear on the cornea

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Long-term contact lens use can lead to alterations in corneal thickness, stromal thickness, curvature, corneal sensitivity, cell density, and epithelial oxygen uptake. Other structural changes may include the formation of epithelial vacuoles and microcysts (containing cellular debris), corneal neovascularization, as well as the emergence of polymegethism in the corneal endothelium. Functional changes from long-term contact lens use include decreased corneal sensitivity, vision loss, and photophobia. Many contact lens-induced changes in corneal structure are reversible if contact lenses are not used for an extended period of time.

Contents

Knowledge about the form and function of the cornea and the various types of contact lenses and their common complications is important to understanding this article.

Changes in function and morphology

Layers of the Cornea (1) Epithelium (2) Anterior elastic lamina (3) Substantia propria (4) Posterior elastic lamina (5) Endothelium of the anterior chamber Vertical section human cornea-Gray871.png
Layers of the Cornea (1)  Epithelium (2)  Anterior elastic lamina (3)  Substantia propria (4)  Posterior elastic lamina (5)  Endothelium of the anterior chamber
Disposable, soft contact lenses. ColorContactLens.JPG
Disposable, soft contact lenses .
Keratitis, or an inflammation of the cornea Clare-314.jpg
Keratitis , or an inflammation of the cornea

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. [1]

Structural change

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. [2] 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. [3] On average, over five times as many epithelial microcysts than normal have been observed in long-term contact lens wearers. [2] The hypoxic environment the cornea experiences when hydrogel contact lenses are worn is conducive to forming microcysts and vacuoles, most likely due to suppression of corneal endothelium metabolism. [4] [5]

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 polymegethism (the variation in the size of corneal endothelial cells) was found. [2] The cause is unclear, but is thought to be related to chronic corneal hypoxia. [4] 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. Contact lens-induced hypoxia triggers the cornea to undergo anaerobic respiration, resulting in a buildup of lactic acid that osmotically draws water into corneal cells, causing edema. [6] Two explanations have been proposed for contact lens-induced stromal thinning. It is thought that this edema may inhibit stromal tissue synthesis. [4] Alternatively, the lactic acid buildup may lead to the erosion of stromal tissue. [4]

Increased endothelial polymegethism is also found in long-term wearers of rigid gas permeable lenses as soon as one week after contact lens wear begins. This change is indicated by significant increases in Max/Min cell size ratio in contact lens wearers. [7] The mechanism behind contact lens-induced polymegethism is unknown, though it is also thought to be a byproduct of corneal edema and epithelial hypoxia. [2] Endothelial pleiomorphism is another factor that arises from long-term use of rigid gas permeable lenses; significant decreases in 6-sided cells are noted after one year, accompanied by increased numbers of 7-sided cells. [7]

Increased corneal curvature is yet another change known to arise from long-term contact lens wear; [1] this increase in corneal curvature can be as much as 0.5 diopters greater than normal. [8] This is thought to be caused by corneal thinning-induced ectasia. [1] 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. [1]

Long-term use of contact lenses has been associated with an increased risk of corneal neovascularization, an irreversible sight threatening condition in which new blood vessels grow in the avascular cornea as a response to prolonged hypoxia. [9] Contact lenses cause corneal neovascularization because they restrict oxygen diffusion to the corneal epithelium. In the short term, the cornea responds to oxygen deprivation by increasing blood flow to the corneal limbus, the narrow circular border between the cornea and sclera. Over time, this chronic limbal hyperemia can progress to corneal neovascularization. [10]

Modern silicon hydrogel lenses pose very little risk for neovascularization, especially when compared to traditional hydrogel lenses, because they have much higher oxygen transmissibility (between 4 and 6 times higher) compared to older hydrogel formulations. [11] The oxygen transmissibility of contact lenses is measured in units of Dk/t, which is the oxygen permeability of the lens material (Dk) divided by the thickness of the lens (t). The industry standard is to report Dk/t values measuring lens thickness at the center of a -3.00 D lens. [12] [13] The higher a contact lens wearer's prescription is, the thicker their lens is overall, which decreases Dk/t. Minus lenses are thicker away from the center, while plus lenses are thicker at the center, which decreases Dk/t in those zones. [12] [13] Silicon hydrogel lenses were introduced in the late 1990s and their usage has steadily increased. In 2023, they made up almost 75% of all soft daily-wear contact lenses prescribed in a prescribing survey of 20 countries. [14] In fact, silicon hydrogel lenses have largely eliminated both short and long-term side effects of corneal hypoxia, like corneal reddening, edema, and neovascularization, except for contact lens wearers with high prescriptions. [15] Research subjects who wore silicon hydrogel contact lenses on an extended (overnight) basis for 9 months showed no signs of neovascularization, whereas subjects who wore hydrogel contact lenses showed signs of moderate neovascularization after only 3 months of extended wear. [16] Switching to silicon hydrogel lenses from lenses with lower oxygen permeability can cause limbal hyperemia and symptoms of corneal neovascularization to decrease by "emptying" the blood vessels, though they remain in the cornea and can refill under hypoxic conditions or if irritated. [17]

Long-term use of contacts made from polymethylmethacrylate (PMMA), a relatively rigid, oxygen-impermeable material, or thick hydrogel contact lenses have been found to cause corneal warpage (shape distortion). [18] PMMA contacts are rarely prescribed today. [19]

Long-term use of cosmetic contact lenses increases the risk of corneal infection, at least partially due to user habits like improper cleaning, overwearing, sleeping with lenses on, and borrowing others' lenses. [20] However, the physical composition of cosmetic contact lenses themselves also plays a role in increasing the risk of long-term corneal complications. The surface of cosmetic contact lenses are often rougher than their prescription counterparts, and this increases the risk of mechanical trauma to both the inside of the eyelid as well as the cornea. Surface roughness may also facilitate eye secretion buildup, microorganism proliferation, and corneal infection, especially if cosmetic contacts are stored unused in lens solution for prolonged periods. [21]

Functional change

Corneal sensitivity is significantly diminished after extended contact lens wear (five or more years). 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. 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. [22] A proposed explanation for the reduced sensitivity is the induced quiescence of free nerve endings following long term corneal exposure to contact lenses. [23]

Long-term use of PMMA or thick hydrogel contact lenses have been found to cause increased eye irritability, photophobia, blurred vision, and persistent haloes. [18]

There is some evidence to show that rigid gas permeable contact lenses are capable of slowing myopic progression after long-term wear. This same effect was not found in patients who had worn soft contact lenses for an extended period of time. Greater corneal steepening was found in patients wearing soft contact lenses than in patients wearing rigid gas permeable contact lenses, [24] suggesting that the latter may slow the progression of myopia by flattening the cornea.

Unchanged variables

The number of corneal keratocytes in the epithelial stroma has not been found to change with long-term contact lens wear. [22] Endothelial cell density also does not change with long-term contact lens wear. [2] No strong relationship has been found between long-term contact lens wear and corneal astigmatism. [1]

Reversibility of damage

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. However, endothelial polymegethism does not seem to return to normal levels even long after the cessation of contact lens wear. [2] Even after a six-month period in which contact lenses are not worn, polymegethism seems to remain. [3] Stromal thickness does not return to a normal level even after an entire month in which contact lens wear is halted. [3] The density of microcysts also remains as long as one month after contact lenses are removed, [2] and microcysts do not disappear completely until two to three months after contact lens wear is completely halted. [3]

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. [2] Recovery of normal epithelial oxygen uptake can occur if contact lens wear is completely halted for one month. [3] 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, however, microcysts will disappear if contact lenses are not worn. [2]

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. [22] One or 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. [23]

Long-term use of PMMA or thick hydrogel contact lenses has been found to cause corneal warpage (shape distortion), increased eye irritability, photophobia, blurred vision, and persistent haloes. Collectively, these symptoms constitute corneal exhaustion syndrome, which is associated with corneal endothelium abnormalities including edema, polymegethism, irregular mosaic, and pigment deposition. Patients with corneal exhaustion syndrome 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. [18]

See also

Related Research Articles

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Contact lenses, or simply contacts, are thin lenses placed directly on the surface of the eyes. Contact lenses are ocular prosthetic devices used by over 150 million people worldwide, and they can be worn to correct vision or for cosmetic or therapeutic reasons. In 2010, the worldwide market for contact lenses was estimated at $6.1 billion, while the US soft lens market was estimated at $2.1 billion. Multiple analysts estimated that the global market for contact lenses would reach $11.7 billion by 2015. As of 2010, the average age of contact lens wearers globally was 31 years old, and two-thirds of wearers were female.

<span class="mw-page-title-main">Keratoconus</span> Medical condition involving the eye

Keratoconus (KC) is a disorder of the eye that results in progressive thinning of the cornea. This may result in blurry vision, double vision, nearsightedness, irregular astigmatism, and light sensitivity leading to poor quality-of-life. Usually both eyes are affected. In more severe cases a scarring or a circle may be seen within the cornea.

<span class="mw-page-title-main">Cornea</span> Transparent front layer of the eye

The cornea is the transparent front part of the eye that covers the iris, pupil, and anterior chamber. Along with the anterior chamber and lens, the cornea refracts light, accounting for approximately two-thirds of the eye's total optical power. In humans, the refractive power of the cornea is approximately 43 dioptres. The cornea can be reshaped by surgical procedures such as LASIK.

<span class="mw-page-title-main">Corneal endothelium</span> Single layer of endothelial cells on the surface of the cornea

The corneal endothelium is a single layer of endothelial cells on the inner surface of the cornea. It faces the chamber formed between the cornea and the iris.

<span class="mw-page-title-main">Orthokeratology</span> Corrective contact lenses

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<span class="mw-page-title-main">Fuchs' dystrophy</span> Medical condition

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<span class="mw-page-title-main">Recurrent corneal erosion</span> Separation of the cellular layers of the cornea of the eye

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<span class="mw-page-title-main">Corneal cross-linking</span> Surgical procedure

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<span class="mw-page-title-main">Scleral lens</span> Large contact lens resting on the sclera, creating a tear-filled vault over the cornea

A scleral lens, also known as a scleral contact lens, is a large contact lens that rests on the sclera and creates a tear-filled vault over the cornea. Scleral lenses are designed to treat a variety of eye conditions, many of which do not respond to other forms of treatment.

<span class="mw-page-title-main">Corneal dystrophy</span> Clouding of the transparent cornea of the eye

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<span class="mw-page-title-main">Corneal neovascularization</span> Medical condition

Corneal neovascularization (CNV) is the in-growth of new blood vessels from the pericorneal plexus into avascular corneal tissue as a result of oxygen deprivation. Maintaining avascularity of the corneal stroma is an important aspect of healthy corneal physiology as it is required for corneal transparency and optimal vision. A decrease in corneal transparency causes visual acuity deterioration. Corneal tissue is avascular in nature and the presence of vascularization, which can be deep or superficial, is always pathologically related.

<span class="mw-page-title-main">Pellucid marginal degeneration</span> Degenerative corneal condition

Pellucid marginal degeneration (PMD) is a degenerative corneal condition, often confused with keratoconus. It typically presents with painless vision loss affecting both eyes. Rarely, it may cause acute vision loss with severe pain due to perforation of the cornea. It is typically characterized by a clear, bilateral thinning (ectasia) in the inferior and peripheral region of the cornea, although some cases affect only one eye. The cause of the disease remains unclear.

<span class="mw-page-title-main">Rigid gas permeable lens</span> Type of contact lens

A rigid gas-permeable lens, also known as an RGP lens, GP lens, or colloquially, a hard contact lens, is a rigid contact lens made of oxygen-permeable polymers. Initially developed in the late 1970s, and through the 1980s and 1990s, they were an improvement over prior 'hard' lenses that restricted oxygen transmission to the eye.

<span class="mw-page-title-main">Meesmann corneal dystrophy</span> Medical condition

Meesmann corneal dystrophy (MECD) is a rare hereditary autosomal dominant disease that is characterized as a type of corneal dystrophy and a keratin disease. MECD is characterized by the formation of microcysts in the outermost layer of the cornea, known as the anterior corneal epithelium. The anterior corneal epithelium also becomes fragile. This usually affects both eyes rather than a single eye and worsens over time. There are two phenotypes, Meesmann corneal dystrophy 1 (MECD1) and Meesmann corneal dystrophy 2 (MECD2), which affect the genes KRT3 and KRT12, respectively. A heterozygous mutation in either of these genes will lead to a single phenotype. Many with Meesmann corneal dystrophy are asymptomatic or experience mild symptoms.

<span class="mw-page-title-main">Corneal keratocyte</span>

Corneal keratocytes are specialized fibroblasts residing in the stroma. This corneal layer, representing about 85-90% of corneal thickness, is built up from highly regular collagenous lamellae and extracellular matrix components. Keratocytes play the major role in keeping it transparent, healing its wounds, and synthesizing its components. In the unperturbed cornea keratocytes stay dormant, coming into action after any kind of injury or inflammation. Some keratocytes underlying the site of injury, even a light one, undergo apoptosis immediately after the injury. Any glitch in the precisely orchestrated process of healing may cloud the cornea, while excessive keratocyte apoptosis may be a part of the pathological process in the degenerative corneal disorders such as keratoconus, and these considerations prompt the ongoing research into the function of these cells.

<span class="mw-page-title-main">Herpes simplex keratitis</span> Medical condition

Herpetic simplex keratitis is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in the cornea.

Post-LASIK ectasia is a condition similar to keratoconus where the cornea starts to bulge forwards at a variable time after LASIK, PRK, or SMILE corneal laser eye surgery. However, the physiological processes of post-LASIK ectasia seem to be different from keratoconus. The visible changes in the basal epithelial cell and anterior and posterior keratocytes linked with keratoconus were not observed in post-LASIK ectasia.

<span class="mw-page-title-main">Ophthalmic drug administration</span>

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Exposure keratopathy is medical condition affecting the cornea of eyes. It can lead to corneal ulceration and permanent loss of vision due to corneal opacity.

References

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  15. ↑ Sweeney, Deborah F. (January 2013). "Have Silicone Hydrogel Lenses Eliminated Hypoxia?". Eye & Contact Lens: Science & Clinical Practice. 39 (1): 53–60. doi:10.1097/ICL.0b013e31827c7899. ISSN   1542-2321.
  16. ↑ Dumbleton, K. A.; Chalmers, R. L.; Richter, D. B.; Fonn, D. (March 2001). "Vascular response to extended wear of hydrogel lenses with high and low oxygen permeability". Optometry and Vision Science: Official Publication of the American Academy of Optometry. 78 (3): 147–151. doi:10.1097/00006324-200103000-00006. ISSN   1040-5488. PMID   11327675.
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  21. ↑ Lim, Chris H. L.; Stapleton, Fiona; Mehta, Jodhbir S. (2019). "A review of cosmetic contact lens infections". Eye. 33 (1): 78–86. doi:10.1038/s41433-018-0257-2. ISSN   1476-5454. PMC   6328606 . PMID   30385879.
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  24. ↑ Walline, J.; Jones, L.; Mutti, D.; Zadnik, K. (December 2004). "A Randomized Trial of the Effects of Rigid Contact Lenses on Myopia Progression". Arch. Ophthalmol. 122 (12): 1760–1766. doi:10.1001/archopht.122.12.1760. PMID   15596577.
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