Effects of long-term contact lens wear on the cornea

Last updated August 13, 2023

Long-term contact lens use can lead to alterations in corneal thickness, stromal thickness, curvature, corneal sensitivity, cell density, and epithelial oxygen uptake, etc. Other changes may include the formation of epithelial vacuoles and microcysts (containing cellular debris) as well as the emergence of polymegethism in the corneal endothelium. Decreased corneal sensitivity, vision loss, and photophobia have also been observed in patients who have worn contact lenses for an extended period of time. 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.^[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]

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 was found.^[2] 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 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.^[4] Endothelial pleiomorphism is another factor that arises from long-term use of rigid gas permeable lenses; significant decreases in hexagonal cells are noted after one year, accompanied by increased numbers of cells of other than six sides.^[4]

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.^[5] 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 PMMA or thick hydrogel contact lenses have been found to cause corneal warpage (shape distortion).^[6]

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,^[7] suggesting that the latter may slow the progression of myopia by flattening the cornea.

Functional change

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.^[8] Long-term use of PMMA or thick hydrogel contact lenses have been found to cause increased eye irritability, photophobia, blurred vision, and persistent haloes.^[6]

Long-term use of rigid gas permeable contact lenses has been associated with slower myopic progression.^[7]

Unchanged variables

The number of corneal keratocytes in the epithelial stroma has not been found to change with long-term contact lens wear.^[8] 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.^[8] 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.^[9]

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 Syndrom (CES), which is associated with corneal endothelium abnormalities including edema, polymegethism, 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.^[6]

Cause

Increases in corneal curvature are thought to be caused by corneal thinning-induced ectasia.^[1]

Two explanations have been proposed for contact lens-induced stromal thinning. It is thought that contact lens-induced edema may inhibit stroma tissue synthesis.^[2] Alternatively, contact lens-induced hypoxia may trigger a lactic acid buildup that leads to the erosion of stromal tissue.^[2] 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]

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.^[9]

Related Research Articles

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.

LASIK or Lasik, commonly referred to as laser eye surgery or laser vision correction, is a type of refractive surgery for the correction of myopia, hyperopia, and an actual cure for astigmatism, since it is in the cornea. LASIK surgery is performed by an ophthalmologist who uses a laser or microkeratome to reshape the eye's cornea in order to improve visual acuity. For most people, LASIK provides a long-lasting alternative to eyeglasses or contact lenses.

$<span class="mw-page-title-main">Radial keratotomy</span> Refractive surgical procedure to correct myopia (nearsightedness$

Radial keratotomy (RK) is a refractive surgical procedure to correct myopia (nearsightedness). It was developed in 1974 by Svyatoslav Fyodorov, a Russian ophthalmologist. It has been largely supplanted by newer, more accurate operations, such as photorefractive keratectomy, LASIK, Epi-LASIK and the phakic intraocular lens.

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.

Orthokeratology, also referred to as Night lenses, Ortho-K, OK, Overnight Vision Correction, Corneal Refractive Therapy (CRT), Accelerated Orthokeretology, Cornea Corrective Contacts, Eccentricity Zero Molding, and Gentle Vision Shaping System (GVSS), is the use of gas-permeable contact lenses that temporarily reshape the cornea to reduce refractive errors such as myopia, hyperopia, and astigmatism.

Fuchs dystrophy, also referred to as Fuchs endothelial corneal dystrophy (FECD) and Fuchs endothelial dystrophy (FED), is a slowly progressing corneal dystrophy that usually affects both eyes and is slightly more common in women than in men. Although early signs of Fuchs dystrophy are sometimes seen in people in their 30s and 40s, the disease rarely affects vision until people reach their 50s and 60s.

<span class="mw-page-title-main">Recurrent corneal erosion</span> Medical condition

Recurrent corneal erosion is a disorder of the eyes characterized by the failure of the cornea's outermost layer of epithelial cells to attach to the underlying basement membrane. The condition is excruciatingly painful because the loss of these cells results in the exposure of sensitive corneal nerves. This condition can often leave patients with temporary blindness due to extreme light sensitivity (photophobia).

Corneal cross-linking (CXL) with riboflavin (vitamin B₂) and UV-A light is a surgical treatment for corneal ectasia such as keratoconus, PMD, and post-LASIK ectasia.

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.

Corneal dystrophy is a group of rare hereditary disorders characterised by bilateral abnormal deposition of substances in the transparent front part of the eye called the cornea.

George Jessen (1916–1987) was an optometrist who was an early pioneer of the contact lens. He is credited with being one of the first to employ the concept of orthokeratology, a direct attempt to reduce refractive error with the use of a contact lens, under the term orthofocus.

<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 corneal pathophysiology 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.

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.

Pre Descemet's endothelial keratoplasty (PDEK) is a kind of endothelial keratoplasty, where the pre descemet's layer (PDL) along with descemet's membrane (DM) and endothelium is transplanted. Conventionally in a corneal transplantation, doctors use a whole cornea or parts of the five layers of the cornea to perform correction surgeries. In May 2013, Dr Harminder Dua discovered a sixth layer between the stroma and the descemet membrane which was named after him as the Dua's layer. In the PDEK technique, doctors take the innermost two layers of the cornea, along with the Dua's layer and graft it in the patient's eye.

Neurotrophic keratitis (NK) is a degenerative disease of the cornea caused by damage of the trigeminal nerve, which results in impairment of corneal sensitivity, spontaneous corneal epithelium breakdown, poor corneal healing and development of corneal ulceration, melting and perforation. This is because, in addition to the primary sensory role, the nerve also plays a role maintaining the integrity of the cornea by supplying it with trophic factors and regulating tissue metabolism.

Ophthalmic drug administration is the administration of a drug to the eyes, most typically as an eye drop formulation. Topical formulations are used to combat a multitude of diseased states of the eye. These states may include bacterial infections, eye injury, glaucoma, and dry eye. However, there are many challenges associated with topical delivery of drugs to the cornea of the eye.

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

1 2 3 4 5 Liu, Z.; Pflugfelder, S. (January 2000). "The effects of long-term contact lens wear on corneal thickness, curvature, and surface regularity". Ophthalmology. 107 (1): 105–111. doi:10.1016/S0161-6420(99)00027-5. PMID 10647727.
1 2 3 4 5 6 7 8 9 10 11 Holden, B.A.; Sweeney, B.F.; Vannas, A.; Nilsson, K.T.; Efron, N. (November 1985). "Effects of long-term extended contact lens wear on the human cornea". Invest. Ophthalmol. Vis. Sci. 26 (11): 1489–1501. PMID 3863808.
1 2 3 4 5 Holden, BA; Vannas, A; Nilsson, K; Efron, N; Sweeney, D; Kotow, M; La Hood, D; Guillon, M (June 1985). "Epithelial and endothelial effects from the extended wear of contact lenses". Curr. Eye Res. 4 (6): 739–42. doi:10.3109/02713688509017678. PMID 2992884.
1 2 Esgin, H.; Erda, N. (January 2002). "Corneal Endothelial Polymegethism and Pleomorphism Induced by Daily-Wear Rigid Gas-Permeable Contact Lenses". CLAO Journal. 28 (1): 40–43. PMID 11838988.
↑ Miller, D. (October 1968). "Contact Lens-Induced Corneal Curvature and Thickness Changes". Arch. Ophthalmol. 80 (4): 430–432. doi:10.1001/archopht.1968.00980050432004. PMID 5674798.
1 2 3 Sweeney, D. (August 1992). "Corneal Exhaustion Syndrome with Long-Term Wear of Contact Lenses". Optometry and Vision Science. 69 (8): 601–608. doi:10.1097/00006324-199208000-00002. PMID 1513555. S2CID 42597709.
1 2 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.
1 2 3 Patel, S.; McLaren, J.; Hodge, D.; Bourne, W. (April 2002). "Confocal Microscopy In Vivo in Corneas of Long-Term Contact Lens Wearers". Invest. Ophthalmol. Vis. Sci. 43 (4): 995–1003. PMID 11923239.
1 2 Millodot, M. (July 1978). "Effect of Long-term Wear of Hard Contact Lenses on Corneal Sensitivity". Arch. Ophthalmol. 96 (7): 1225–1227. doi:10.1001/archopht.1978.03910060059011. PMID 666631.

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[The_effects_of_long-term_contact_lens_wear_on_corneal_thickness,_curvature,_and_surface_regularity-1] 1 2 3 4 5 Liu, Z.; Pflugfelder, S. (January 2000). "The effects of long-term contact lens wear on corneal thickness, curvature, and surface regularity". Ophthalmology. 107 (1): 105–111. doi:10.1016/S0161-6420(99)00027-5. PMID 10647727.

[Effects_of_long-term_extended_contact_lens_wear_on_the_human_cornea.-2] 1 2 3 4 5 6 7 8 9 10 11 Holden, B.A.; Sweeney, B.F.; Vannas, A.; Nilsson, K.T.; Efron, N. (November 1985). "Effects of long-term extended contact lens wear on the human cornea". Invest. Ophthalmol. Vis. Sci. 26 (11): 1489–1501. PMID 3863808.

[Epithelial_and_endothelial_effects_from_the_extended_wear_of_contact_lenses.-3] 1 2 3 4 5 Holden, BA; Vannas, A; Nilsson, K; Efron, N; Sweeney, D; Kotow, M; La Hood, D; Guillon, M (June 1985). "Epithelial and endothelial effects from the extended wear of contact lenses". Curr. Eye Res. 4 (6): 739–42. doi:10.3109/02713688509017678. PMID 2992884.

[Corneal_Endothelial_Polymegethism_and_Pleomorphism_Induced_by_Daily-Wear_Rigid_Gas-Permeable_Contact_Lenses-4] 1 2 Esgin, H.; Erda, N. (January 2002). "Corneal Endothelial Polymegethism and Pleomorphism Induced by Daily-Wear Rigid Gas-Permeable Contact Lenses". CLAO Journal. 28 (1): 40–43. PMID 11838988.

[Contact_Lens-Induced_Corneal_Curvature_and_Thickness_Changes-5] Miller, D. (October 1968). "Contact Lens-Induced Corneal Curvature and Thickness Changes". Arch. Ophthalmol. 80 (4): 430–432. doi:10.1001/archopht.1968.00980050432004. PMID 5674798.

[Corneal_Exhaustion_Syndrome_with_Long-Term_Wear_of_Contact_Lenses-6] 1 2 3 Sweeney, D. (August 1992). "Corneal Exhaustion Syndrome with Long-Term Wear of Contact Lenses". Optometry and Vision Science. 69 (8): 601–608. doi:10.1097/00006324-199208000-00002. PMID 1513555. S2CID 42597709.

[A_Randomized_Trial_of_the_Effects_of_Rigid_Contact_Lenses_on_Myopia_Progression-7] 1 2 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.

[Confocal_Microscopy_In_Vivo_in_Corneas_of_Long-Term_Contact_Lens_Wearers-8] 1 2 3 Patel, S.; McLaren, J.; Hodge, D.; Bourne, W. (April 2002). "Confocal Microscopy In Vivo in Corneas of Long-Term Contact Lens Wearers". Invest. Ophthalmol. Vis. Sci. 43 (4): 995–1003. PMID 11923239.

[Effect_of_Long-term_Wear_of_Hard_Contact_Lenses_on_Corneal_Sensitivity-9] 1 2 Millodot, M. (July 1978). "Effect of Long-term Wear of Hard Contact Lenses on Corneal Sensitivity". Arch. Ophthalmol. 96 (7): 1225–1227. doi:10.1001/archopht.1978.03910060059011. PMID 666631.

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