Fuchs Endothelial Corneal Dystrophy

Fuchs endothelial corneal dystrophy (FECD) is a bilateral abnormality of corneal endothelial cells, characterized by the appearance of guttae in the central cornea, gradually spreading to the periphery.
When the barrier and pump functions of endothelial cells decline, edema of the corneal stroma and epithelium occurs, eventually leading to bullous keratopathy.
Autosomal dominant inheritance is predominant, and CTG trinucleotide repeat expansion in the TCF4 gene is one of the main causes (26–79% of patients, varying by ethnicity) ^1,8).
More common in women (female-to-male ratio 4:1), with symptoms manifesting in the 5th to 6th decades. In Japanese individuals, onset tends to be later than in Caucasians due to higher endothelial cell density.
Curative treatment is corneal endothelial transplantation (DMEK or DSAEK). In Japan, DSAEK has been covered by insurance since 2009, and DMEK since 2016.
The combination of Descemetorhexis (DSO) with selective removal of Descemet membrane and ROCK inhibitor eye drops (ripasudil) is gaining attention as a new option ¹⁴⁾.
It is one of the most common causes of corneal transplantation worldwide ^1,6).

1. What is Fuchs Endothelial Corneal Dystrophy?

Fuchs endothelial corneal dystrophy (FECD) is a progressive disease in which corneal endothelial cells become abnormal bilaterally. In 1910, Ernst Fuchs first reported 13 cases as “dystrophia epithelialis corneae,” and it was later identified as an endothelial disease, leading to its current name ¹⁾.

Guttae (guttata) appear on the endothelial surface of the central cornea and gradually spread to the periphery. When the barrier and pump functions (Na⁺/K⁺-ATPase) of endothelial cells decline, corneal stromal edema develops, progressing to epithelial edema and bullae formation. Thickening and irregularity of Descemet membrane lead to loss of corneal transparency.

History and Classification

In the IC3D (International Classification of Corneal Dystrophies) 2nd edition (Weiss 2015), FECD is classified under the “Corneal Endothelial Dystrophies” category ¹⁵⁾. It is broadly divided into the following two types based on age of onset.

Early-onset type (FECD1): Onset in childhood to young adulthood. Mainly caused by point mutations (L450W, Q455K, etc.) in the COL8A2 gene (1p34.3-p32.3) encoding the collagen type VIII alpha 2 chain ¹⁾.
Late-onset type (FECD2 and later): Slowly develops in the 5th to 6th decades. The most common cause is a CTG trinucleotide repeat expansion in the TCF4 gene (79% in Western populations) ¹⁾.

Epidemiology (Japan and International Comparison)

Indicator	Value	Source
Frequency of guttae in preoperative cataract patients	1.2%	Domestic multicenter survey
Prevalence in Japan (Kumejima Study, age ≥40)	4.1%	Higa 2011⁷⁾
Prevalence in Japanese women (age ≥40)	5.8%	Higa 2011⁷⁾
Japan: Male prevalence (age 40+)	2.4%	Higa 2011⁷⁾
Iceland: Reykjavik Eye Study, age 55+	Women 11%, men 7%	Zoega 2006¹⁰⁾
Sex ratio (international)	2.5:1 to 3.5:1 (female predominance)	Matthaei 2019¹⁾
Frequency of TCF4 repeat expansion in Japanese	12 out of 47 cases (26%)	Nakano 2015⁸⁾

Japanese people, as a yellow race, tend to have a lower incidence of FECD compared to white and black races. However, with the aging of society in Japan, the number of cases is expected to increase further. Japanese people have a higher corneal endothelial cell density than white people, which is thought to delay the onset of the disease.

In Japanese people, who often have narrow angles, laser iridotomy (LI) frequently leads to a decrease in endothelial cells, so careful attention is needed for early detection of FECD.

Q How often does it occur?

In a population-based study conducted in Okinawa’s Kumejima Island (Kumejima Study), corneal guttae were detected in 4.1% of individuals aged 40 years or older. The prevalence was 5.8% in women and 2.4% in men ⁷⁾. There is also domestic data showing that 1.2% of patients undergoing preoperative cataract examination had cornea guttata. Although the frequency is reported to be lower in Japanese than in Western populations, it is increasing with the aging society.

2. Main Symptoms and Clinical Findings

Slit-lamp, specular, and AS-OCT images of Fuchs endothelial corneal dystrophy, showing corneal endothelial guttae and hyperreflective findings on the posterior surface.

Iovino C, et al. Corneal endothelium features in Fuchs’ Endothelial Corneal Dystrophy: A preliminary 3D anterior segment optical coherence tomography study. PLoS One. 2018. Figure 2. PMCID: PMC6264151. License: CC BY.

Composite image showing corneal endothelial abnormalities in Fuchs endothelial corneal dystrophy. Slit-lamp reveals a beaten metal appearance, while specular microscopy and AS-OCT show endothelial cell loss and hyperreflective spots on the posterior corneal surface.

Subjective Symptoms

Typically, patients under 50 years of age are asymptomatic. Symptoms progress slowly, correlating with the degree of edema.

Morning blurring: Corneal edema worsens during eyelid closure at night, leading to the lowest visual acuity upon waking. With eyes open during the day, edema improves, and vision recovers by evening, a characteristic pattern ¹⁾.
Persistent decreased vision: When edema is severe, vision remains reduced throughout the day ²⁾.
Photophobia and glare: Exacerbated by light scattering from an irregular Descemet’s membrane ¹⁾.
Eye pain and tearing: Severe epithelial edema leads to bullae formation; their rupture causes intense eye pain and tearing ¹⁾.

Clinical Findings (Findings Confirmed by Physician Examination)

Slit-lamp microscopy is fundamental. Observation is performed using a combination of direct illumination, retroillumination, and specular reflection.

Grade 0-1 (None to Mild)

Findings: 12 or fewer central guttae (Grade 0) or more than 12 non-confluent guttae (Grade 1)

Symptoms: Usually asymptomatic. Detected as dark spots on specular microscopy.

Grade 2-3 (Moderate)

Findings: Confluent guttae in the central 1–5 mm. Mild beaten-metal appearance.

Symptoms: Morning blurring. Endothelial image becomes unclear on specular microscopy.

Grade 4 (Severe)

Findings: Extensive confluent guttae >5 mm centrally. Beaten-metal appearance with pigmentation.

Symptoms: Persistent blurring and photophobia from morning through the day.

Grade 4+ Edema (Very Severe)

Findings: Stromal edema, epithelial edema, and bullae formation. Marked corneal opacity.

Symptoms: Severe vision loss, eye pain, and tearing throughout the day. Quality of life significantly reduced.

This clinical staging is based on the modified classification by Krachmer et al. (1978)⁵⁾.

Details of slit-lamp findings:

Corneal guttae: Abnormal collagen-like material produced by degenerated endothelial cells protrudes hemispherically from the posterior Descemet membrane into the anterior chamber. Appears as gray-white or brownish deposits on the posterior corneal surface.
Beaten-metal appearance: A characteristic appearance resulting from the confluence and increase of guttae combined with pigmentation. Best observed with specular reflection.
Corneal edema: Progresses in order from Descemet membrane irregularity → stromal swelling (stromal edema) → subepithelial fluid accumulation (epithelial edema).

Q Why is vision worse in the morning and better during the day?

In a healthy cornea, endothelial cells constantly pump water out to the anterior chamber to maintain transparency. In FECD, because the endothelial pump function is reduced, evaporation of water also stops while sleeping (with eyes closed), so the cornea is most edematous in the morning and foggy vision is worse. When the eyes are open, water evaporates from the corneal surface, and during the day the edema improves to some extent, so vision recovers. As the disease progresses, this diurnal variation disappears and foggy vision persists all day.

3. Causes and Risk Factors

Genetic Factors

FECD is mainly autosomal dominant, but there is variability in penetrance and expressivity, and some cases have no clear family history.

Major causative genes:

TCF4 gene (18q21.2): Expansion of CTG trinucleotide repeat (CTG18.1) is the most common cause. More than 50 repeats is considered pathological, detected in about 79% of FECD patients in Western countries^1,9). In 47 Japanese FECD patients, 12 cases (26%) had this expansion, lower than in Western populations⁸⁾. It correlates with severity in Western patients but shows poor correlation in Japanese patients¹⁾.
COL8A2 gene (1p34.3-p32.3): Encodes the alpha-2 chain of type VIII collagen. Point mutations such as L450W, Q455K, Q455V cause early-onset FECD (FECD1)¹⁾.
Other candidate genes: SLC4A11, TCF8/ZEB1, AGBL1, LOXHD1, TGFBI, CLU have been reported¹⁾.

In Japanese patients, the frequency of TCF4 repeat expansion is lower than in Western populations, so other genetic backgrounds need to be elucidated⁸⁾.

Non-genetic Risk Factors

Female sex: Higher risk of developing FECD; female-to-male ratio internationally is 2.5:1 to 3.5:1^1,2)
Aging: Symptoms become apparent in the 5th to 6th decades¹⁾
Family history: Having a first-degree relative with FECD increases risk²⁾
Smoking: Promotes onset through increased oxidative stress²⁾
Diabetes: Metabolic disorders affect endothelial cells²⁾
Ocular background conditions: Pseudoexfoliation syndrome (PEX), narrow-angle eyes, endothelial loss after laser iridotomy (LI)
Systemic comorbidities: Association with myotonic dystrophy type 1 (DM1) has been reported¹⁾

Q Is it hereditary? Will it affect my child?

FECD is mainly inherited in an autosomal dominant pattern. Theoretically, the probability of passing it to a child is 50%. However, there is great variability in the age of onset and severity (incomplete penetrance); many people who inherit the gene live their entire lives with only very mild symptoms. In particular, the proportion of TCF4 gene abnormalities, which is the most common cause in Western countries, is low in Japanese people⁸⁾, suggesting possible differences in genetic background. If you are concerned, we recommend consulting a genetic specialist.

4. Diagnosis and Examination Methods

Although there are no unified diagnostic criteria in Japan, clinical diagnosis is made by combining the following examinations.

Slit-Lamp Microscopy

Evaluate guttae and edema on the posterior corneal surface using direct illumination.
Specular reflection is most important and essential for confirming a beaten-metal appearance.
Assess the degree of stromal edema and opacity using retroillumination.
Note that Japanese people have higher corneal endothelial cell density than Caucasians, so symptoms may be less apparent even with similar endothelial loss.

Specular Microscope (Specular Reflection Endothelial Cell Imaging Device)

This is the most important examination for diagnosing and monitoring FECD.

Parameter	Normal Value	Abnormal Threshold
Endothelial cell density (neonatal period)	3,500–4,000 cells/mm²	—
Endothelial cell density (20s)	2,700 cells/mm²	—
Endothelial cell density (70 years and older)	Average 2,200 cells/mm²	—
Minimum for corneal transparency	—	400–500 cells/mm² or less
CV (coefficient of variation)	0.2–0.3	≥ 0.35
Hexagonality	60–70%	≤ 50%

Dark spot: The elevation of guttae deviates from the plane of specular reflection, appearing as a black circular area on the specular image. This does not indicate actual loss of endothelial cells; rather, the cells are not visible because they are not on the same plane due to the elevation.
In cases with severe edema or opacity, a contact specular microscope is more useful than a non-contact type, providing a wider and clearer image of the endothelium.
The normal annual endothelial cell loss rate is 0.5%/year. After cataract surgery, it accelerates to 2%/year, and after glaucoma surgery, to 10%/year.

Other Tests

Confocal microscopy: Allows observation of all layers of the cornea in a layered manner. The morphology of guttae and details of Descemet’s membrane can be evaluated¹⁾.
Anterior segment OCT: Can non-invasively quantify corneal thickness, Descemet’s membrane thickening, and subepithelial edema¹⁾.
Ultrasound pachymetry (corneal thickness measurement): Gold standard for preoperative evaluation. Central corneal thickness >640 μm is an indicator of increased risk of postoperative corneal decompensation¹⁾.
Scheimpflug imaging: Can evaluate the central-to-peripheral thickness ratio¹⁾.
Modified Krachmer classification (Krachmer et al. 1978)⁵⁾: Used for staging and determining surgical indications.

Differential Diagnosis

Disease	Key Points for Differentiation
Posterior polymorphous corneal dystrophy (PPCD)	AD inheritance, bilateral, band-like and vesicular opacities of Descemet’s membrane. Genes: PPCD1 (20p11.2-q11.2), PPCD2 (COL8A2), PPCD3 (ZEB1)
Congenital hereditary endothelial dystrophy (CHED)	AR inheritance (SLC4A11 mutation), onset at birth to infancy, corneal edema and opacity from birth
Pseudophakic bullous keratopathy (PBK)	Endothelial damage after cataract surgery. No guttae, history of surgery
Pseudoexfoliation syndrome keratopathy	PEX material deposition, elevated intraocular pressure, PEX material on the anterior lens capsule is key for differentiation
Iridocorneal endothelial (ICE) syndrome	Unilateral, with iris atrophy, anterior synechiae, and glaucoma. No guttae
Endothelial changes in narrow-angle eyes	May show cornea guttata-like findings. Differentiated by intraocular pressure and angle morphology

Q What is a specular microscope? What can it tell us?

A specular microscope (specular reflection endothelial camera) is a device that non-invasively photographs and measures the endothelial cells in the innermost layer of the cornea using special light reflection. The examination measures endothelial cell count (cell density), variation in cell size (CV value), and uniformity of shape (hexagonal cell ratio). In FECD, guttae appear as black spots (dark spots), helping to assess disease stage. The imaging takes a few minutes and is painless.

5. Standard Treatment

The goal of treatment is to restore corneal transparency and maintain vision. Depending on the stage of the disease, symptomatic therapy or surgical treatment is selected.

Symptomatic Therapy (Pharmacotherapy)

Aimed at symptom relief before surgery is indicated. It does not restore endothelial cell count or suppress disease progression.

5% hypertonic saline eye drops/ointment: Uses osmotic pressure difference to draw water out of the cornea, reducing edema. Mainly useful for relieving morning foggy vision.
Therapeutic contact lenses: Worn to reduce eye pain and tearing caused by ruptured bullae.
Corneal drying with a hair dryer: Warm air is directed at the closed eye to promote evaporation of moisture from the corneal surface ¹⁾. Provides temporary improvement of edema.

Surgical Therapy (Curative Treatment)

DMEK (Descemet Membrane Endothelial Keratoplasty)

Graft: Descemet membrane + endothelium only (thickness about 15 μm)

Features: First reported by Melles in 2006 ¹¹⁾. Rapid visual recovery, low rejection rate. Requires a skilled surgeon.

Insurance coverage in Japan: Since 2016

DSAEK (Descemet Stripping Automated Endothelial Keratoplasty)

Graft: Thin stroma + Descemet membrane + endothelium (thickness 50–150 μm)

Features: Ultrathin (UT-DSAEK <130 μm), nano-thin (<70 μm) achieve visual outcomes close to DMEK. Easier manipulation and shorter learning curve ^4,12).

Insurance coverage in Japan: Since 2009

PKP (Penetrating Keratoplasty)

Graft: Full-thickness cornea (diameter 7.0–8.5 mm)

Features: Classic option. Challenges include suturing, astigmatism management, and long-term rejection risk. In FECD, it is gradually being replaced by endothelial keratoplasty.

DSO (Descemetorhexis Without Endothelial Keratoplasty)

Procedure: Selective stripping of the central 4 mm of Descemet membrane only. No graft required.

Indications: Cases where residual peripheral endothelial cells can migrate and proliferate to the center. Approximately 75% achieve corneal clearance ¹⁴⁾.

ROCK inhibitor eye drops: Postoperative use of ripasudil promotes clearance even in non-responsive cases ¹⁴⁾.

DMEK vs UT-DSAEK Comparison

Parameter	DMEK	UT-DSAEK	Source
12-month BCVA (logMAR difference)	−0.06 (DMEK superior)	—	Sela 2023 meta-analysis ³⁾
Achievement rate of 20/25 or better	66%	33% (p=0.02)	Dunker 2020 RCT⁴⁾
OR of rebubbling	—	2.76 (favoring DSAEK)	Sela 2023³⁾
12-month ECD	No difference	No difference	Dunker 2020⁴⁾
Graft thickness <70 μm	—	No difference in visual acuity with DMEK	Sela 2023³⁾

In a meta-analysis by Sela et al. (2023) of 8 studies (376 eyes), BCVA at 12 months was significantly better with DMEK (−0.06 logMAR)³⁾. A multicenter RCT by Dunker et al. (2020) also showed a higher rate of achieving 20/25 or better with DMEK compared to UT-DSAEK (66% vs 33%, p=0.02)⁴⁾. However, for UT-DSAEK with graft thickness less than 70 μm, the difference from DMEK was reduced³⁾.

Cultured Human Corneal Endothelial Cell Injection Therapy (Kyoto Protocol)

The Kyoto University group (Kinoshita 2018) developed a treatment method in which cultured healthy donor corneal endothelial cells are injected into the anterior chamber together with a ROCK inhibitor (Y-27632)¹³⁾.

At 24 weeks postoperatively, cell density recovered to over 1,000 cells/mm² in 10 of 11 eyes (91%)
Corneal thickness improved to <630 μm in 10 of 11 eyes
No graft required; potential to treat many patients with a small number of donor cells

ROCK inhibitors exert their effect by promoting endothelial cell adhesion, suppressing apoptosis, and advancing the cell cycle¹³⁾.

Combination with Cataract Surgery

FECD is often associated with cataracts, and careful consideration is needed regarding the timing and method of surgery.

Preoperative central corneal thickness >640 μm indicates a high risk of corneal decompensation after cataract surgery alone, so simultaneous endothelial transplantation is recommended^1,16).
For Krachmer grade 2.5–4, about 20% of cases require endothelial transplantation after cataract surgery alone, so simultaneous surgery is recommended¹⁾.
Intraoperatively, endothelial protection techniques using viscoelastic materials such as the soft-shell technique are employed¹⁾.

Q Which should I choose: DMEK or DSAEK?

DMEK uses the thinnest graft (about 15 μm), offering faster visual recovery and fewer postoperative refractive changes. Meta-analyses also show superior BCVA at 12 months with DMEK³⁾. On the other hand, DSAEK graft manipulation is somewhat easier, with a shorter learning curve for surgeons, and it is widely performed in Japan. Ultra-thin DSAEK (<70 μm) has been reported to achieve visual outcomes nearly equivalent to DMEK³⁾. The choice is made based on a comprehensive assessment of the surgeon’s experience, the facility’s experience, and the patient’s corneal condition. Both procedures have been covered by insurance in Japan since 2016 (DMEK) or 2009 (DSAEK).

6. Pathophysiology and Detailed Mechanisms of Onset

Progressive Loss of Endothelial Cells and Descemet Membrane Changes

Normal corneal endothelial cells do not undergo cell division in the anterior chamber. When endothelial cells are lost, adjacent cells enlarge and migrate to cover the defect, causing cell density to irreversibly decrease with age. When it falls below 400–500 cells/mm², maintaining corneal transparency becomes difficult.

In FECD, degenerated endothelial cells produce and deposit abnormal collagen-like material on the posterior surface of Descemet membrane, forming guttae. Descemet membrane becomes thickened and irregular, creating a vicious cycle that further impairs endothelial function.

Vicious Cycle Model (Ong Tone 2021) ²⁾

Oxidative stress pathway: UV light, smoking, and aging lead to reactive oxygen species (ROS) production → mitochondrial dysfunction → further ROS production → DNA damage and apoptosis
Endoplasmic reticulum (ER) stress pathway: Accumulation of mutant proteins (e.g., COL8A2) in the ER → activation of the unfolded protein response (UPR) → promotion of apoptosis
Endothelial-to-mesenchymal transition (EndMT): Endothelial cells transform into fibroblast-like cells → abnormal extracellular matrix (ECM) deposition → promotion of guttae formation
Secondary stress from guttae: Mechanical disruption and contact stress from guttae → further apoptosis of remaining endothelial cells → acceleration of the vicious cycle

Aging, UV exposure, and smoking all increase oxidative stress and serve as entry points for the vicious cycle ²⁾.

Molecular Mechanism of TCF4 CTG Repeat Expansion ¹⁾

Nuclear RNA foci formation: RNA transcribed from expanded CTG repeats aggregates in the nucleus to form foci.
Sequestration of MBNL1 protein: RNA foci capture and sequester the splicing factor MBNL1.
mRNA missplicing: Loss of MBNL1 function leads to abnormal splicing of many mRNAs → endothelial cell dysfunction.
RAN translation: Repeat-Associated Non-ATG Translation (RAN translation) produces toxic peptides that damage endothelial cells.

Pump and Barrier Dysfunction

The pump function of the corneal endothelium depends on Na⁺/K⁺-ATPase. When endothelial cells are damaged, edema occurs through the following pathways.

Decreased endothelial pump function → water movement from aqueous humor to corneal stroma → stromal swelling (stromal edema)
Advanced stromal edema → fluid accumulation beneath the epithelium → epithelial edema → blister formation → pain due to rupture

If intraocular pressure rises (ocular hypertension) beyond the swelling pressure of the corneal stroma, epithelial edema may occur even if the endothelium is relatively healthy. Caution is required.

7. Latest Research and Future Prospects

Gene Therapy and Molecular Targeted Therapy

Antisense oligonucleotide (ASO) therapy: Targets TCF4 CTG repeat-derived RNA foci, aiming to eliminate nuclear foci, release MBNL1, and normalize missplicing (Hu 2018, Zarouchlioti 2018)¹⁾.
Oxidative stress reduction therapy: Antioxidants such as NAC (N-acetyl cysteine), lithium, and sulforaphane are being studied as candidates¹⁾.

Regenerative Medicine and Cell Therapy Dissemination

Multicenter expansion of cultured human corneal endothelial cell injection therapy (Kyoto protocol)¹³⁾. It has the potential to treat many patients from a small number of donor corneas and is expected as a solution to donor shortage.
Expansion of indications for ROCK inhibitors (ripasudil, Y-27632) alone or as adjunctive therapy after DSO¹⁴⁾.

Early Diagnosis and Risk Stratification

Research on developing an early diagnosis scoring system combining genotype (TCF4 repeat number), sex, age, race, and smoking history¹⁾.
Elucidation of pathology and drug screening using UV-induced in vivo mouse models²⁾.

Since the contribution of TCF4 repeat expansion is relatively small in Japanese individuals⁸⁾, elucidating the genetic and environmental backgrounds unique to Japanese people is an important future issue.

8. References

Matthaei M, Hribek A, Clahsen T, Bachmann B, Cursiefen C, Jun AS. Fuchs Endothelial Corneal Dystrophy: Clinical, Genetic, Pathophysiologic, and Therapeutic Aspects. Annu Rev Vis Sci. 2019;5:151-175.
Ong Tone S, Kocaba V, Böhm M, Wylegala A, White TL, Jurkunas UV. Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis. Prog Retin Eye Res. 2021;80:100863.
Sela TC, Iflah M, Muhsen K, Zahavi A. Descemet membrane endothelial keratoplasty compared with ultrathin Descemet stripping automated endothelial keratoplasty: a meta-analysis. Br J Ophthalmol. 2023.
Dunker SL, Dickman MM, Wisse RPL, et al. Descemet Membrane Endothelial Keratoplasty versus Ultrathin Descemet Stripping Automated Endothelial Keratoplasty: A Multicenter Randomized Controlled Clinical Trial. Ophthalmology. 2020;127(9):1152-1159.
Krachmer JH, Purcell JJ Jr, Young CW, Bucher KD. Corneal endothelial dystrophy. A study of 64 families. Arch Ophthalmol. 1978;96(11):2036-2039.
Gain P, Jullienne R, He Z, et al. Global Survey of Corneal Transplantation and Eye Banking. JAMA Ophthalmol. 2016;134(2):167-173.
Higa A, Sakai H, Sawaguchi S, et al. Prevalence of and risk factors for cornea guttata in a population-based study in a southwestern island of Japan: the Kumejima study. Arch Ophthalmol. 2011;129(3):332-336.
Nakano M, Okumura N, Nakagawa H, et al. Trinucleotide repeat expansion in the TCF4 gene in Fuchs’ endothelial corneal dystrophy in Japanese. Invest Ophthalmol Vis Sci. 2015;56(8):4865-4869.
Wieben ED, Aleff RA, Tosakulwong N, et al. A common trinucleotide repeat expansion within the transcription factor 4 (TCF4) gene predicts Fuchs corneal dystrophy. PLoS One. 2012;7(11):e49083.
Zoega GM, Fujisawa A, Sasaki H, et al. Prevalence and risk factors for cornea guttata in the Reykjavik Eye Study. Ophthalmology. 2006;113(4):565-569.
Melles GR, Ong TS, Ververs B, van der Wees J. Descemet membrane endothelial keratoplasty (DMEK). Cornea. 2006;25(8):987-990.
Price MO, Feng MT, Price FW Jr. Endothelial Keratoplasty Update 2020. Cornea. 2021;40(5):541-547.
Kinoshita S, Koizumi N, Ueno M, et al. Injection of Cultured Cells with a ROCK Inhibitor for Bullous Keratopathy. N Engl J Med. 2018;378(11):995-1003.
Moloney G, Petsoglou C, Ball M, et al. Descemetorhexis Without Grafting for Fuchs Endothelial Dystrophy-Supplementation With Topical Ripasudil. Cornea. 2017;36(6):642-648.
Weiss JS, Møller HU, Aldave AJ, et al. IC3D classification of corneal dystrophies—edition 2. Cornea. 2015;34(2):117-159.
Seitzman GD, Gottsch JD, Stark WJ. Cataract surgery in patients with Fuchs’ corneal dystrophy: expanding recommendations for cataract surgery without simultaneous keratoplasty. Ophthalmology. 2005;112(3):441-446.

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