Recurrent Epithelial Erosions Research Articles

Corneal epithelial-stromal constructs to study differences associated with diabetes mellitus

Diabetes mellitus (DM) is a common metabolic disease associated with severe macrovascular and microvascular complications that influence nearly every tissue in the body, including the anterior and posterior segments of the eye. In the cornea, DM is associated with recurrent epithelial erosion and reduced wound-healing capacity, which increases the risk of corneal scarring. We previously developed a co-culture model of the cornea consisting of immortalized human corneal epithelial cells (hCE-TJ) overlaying a self-assembled stromal layer generated by human corneal fibroblasts (hCFs) over a 4-week period. In this study, we investigated epithelial-stromal constructs generated from hCFs derived from subjects with Type 1 (T1DM) or 2 diabetes (T2DM) compared to controls. We found that T2DM constructs exhibited a disrupted epithelium and a thicker, stratified stromal layer compared to controls or T1DM. Both T1DM and T2DM stromal constructs expressed lower expression of thrombospondin-1 in isolated extracellular vesicles (EVs) compared to controls with no significant difference observed in the presence of epithelial cells, suggesting that reduced provisional matrix secretion in the corneal stroma may be a factor that promotes delayed corneal wound healing in diabetes. The tetraspanins are established extracellular vesicle (EV) markers and include CD63, CD81, and CD9, and were highly expressed by EVs in all three cell types. Control corneal stromal fibroblasts produced more and larger EVs when compared to T1DM and T2DM hCF-derived EVs, supporting a role for altered cell-cell communication in the context of DM. Further characterization of EVs and their cargo is expected to aid in the development of targeted treatments to improve corneal wound healing.

IC3D Classification of Corneal Dystrophies-Edition 3.

The International Committee for the Classification of Corneal Dystrophies (IC3D) was created in 2005 to develop a new classification system integrating current information on phenotype, histopathology, and genetic analysis. This update is the third edition of the IC3D nomenclature. Peer-reviewed publications from 2014 to 2023 were evaluated. The new information was used to update the anatomic classification and each of the 22 standardized templates including the level of evidence for being a corneal dystrophy [from category 1 (most evidence) to category 4 (least evidence)]. Epithelial recurrent erosion dystrophies now include epithelial recurrent erosion dystrophy, category 1 ( COL17A1 mutations, chromosome 10). Signs and symptoms are similar to Franceschetti corneal dystrophy, dystrophia Smolandiensis, and dystrophia Helsinglandica, category 4. Lisch epithelial corneal dystrophy, previously reported as X-linked, has been discovered to be autosomal dominant ( MCOLN1 mutations, chromosome 19). Classic lattice corneal dystrophy (LCD) results from TGFBI R124C mutation. The LCD variant group has over 80 dystrophies with non-R124C TGFBI mutations, amyloid deposition, and often similar phenotypes to classic LCD. We propose a new nomenclature for specific LCD pathogenic variants by appending the mutation using 1-letter amino acid abbreviations to LCD. Pre-Descemet corneal dystrophies include category 1, autosomal dominant, punctiform and polychromatic pre-Descemet corneal dystrophy (PPPCD) ( PRDX3 mutations, chromosome 10). Typically asymptomatic, it can be distinguished phenotypically from pre-Descemet corneal dystrophy, category 4. We include a corneal dystrophy management table. The IC3D third edition provides a current summary of corneal dystrophy information. The article is available online at https://corneasociety.org/publications/ic3d .

Corneal Epithelial Thickness Mapping: A Major Review.

The corneal epithelium (CE) is the outermost layer of the cornea with constant turnover, relative stability, remarkable plasticity, and compensatory properties to mask alterations in the underlying stroma. The advent of quantitative imaging modalities capable of producing epithelial thickness mapping (ETM) has made it possible to characterize better the different patterns of epithelial remodeling. In this comprehensive synthesis, we reviewed all available data on ETM with different methods, including very high-frequency ultrasound (VHF-US) and spectral-domain optical coherence tomography (SD-OCT) in normal individuals, corneal or systemic diseases, and corneal surgical scenarios. We excluded OCT studies that manually measured the corneal epithelial thickness (CET) (e.g., by digital calipers) or the CE (e.g., by confocal scanning or handheld pachymeters). A comparison of different CET measuring technologies and devices capable of producing thickness maps is provided. Normative data on CET and the possible effects of gender, aging, diurnal changes, refraction, and intraocular pressure are discussed. We also reviewed ETM data in several corneal disorders, including keratoconus, corneal dystrophies, recurrent epithelial erosion, herpes keratitis, keratoplasty, bullous keratopathy, carcinoma in situ, pterygium, and limbal stem cell deficiency. The available data on the potential role of ETM in indicating refractive surgeries, planning the procedure, and assessing postoperative changes are reviewed. Alterations in ETM in systemic and ocular conditions such as eyelid abnormalities and dry eye disease and the effects of contact lenses, topical medications, and cataract surgery on the ETM profile are discussed.

The newest IC3D classification of corneal dystrophies

In the year 2015, the International Committee for the Classification of Corneal Dystrophies (IC3D) incorporated new clinical, histopathologic, and genetic information into the former 2008 classification. To this end, the IC3D sighted and evaluated worldwide peer‐reviewed articles for new information on corneal dystrophies published between 2008 and 2014. Using this information, corneal dystrophy templates including categories 1 to 4 and anatomic classification were updated. New clinical, histopathologic, and confocal photographs were added.On the basis of revisiting the cellular origin of corneal dystrophies, a modified anatomic classification was proposed consisting of (1) epithelial and subepithelial dystrophies, (2) epithelial‐stromal TGFBI dystrophies, (3) stromal dystrophies, and (4) endothelial dystrophies. The entity “Epithelial recurrent erosion dystrophies ERED” actually includes a number of potentially distinct epithelial dystrophies (Franceschetti corneal dystrophy, Dystrophia Smolandiensis, and Dystrophia Helsinglandica) but must be differentiated from dystrophies such as TGFBI‐induced dystrophies, which are also often associated with recurrent epithelial erosions. The chromosome locus of Thiel‐Behnke corneal dystrophy is only located on 5q31. The entity previously designated as a variant of Thiel‐Behnke corneal dystrophy on chromosome 10q24 may represent a novel corneal dystrophy. Congenital hereditary endothelial dystrophy (CHED, formerly CHED2) is most likely only an autosomal recessive disorder. The so‐called autosomal dominant inherited CHED (formerly CHED1) is insufficiently distinct to continue to be considered a unique corneal dystrophy. On review of almost all of the published cases, the description appeared most similar to a type of posterior polymorphous corneal dystrophy linked to the same chromosome 20 locus (PPCD1). Anterior segment OCT has emerged as a helpful tool to reveal in vivo features of several corneal dystrophies that previously required histopathologic examination in order to definitively diagnose them.This revision of the IC3D classification includes an updated anatomic classification of corneal dystrophies that more accurately classifies TGFBI dystrophies affecting multiple layers rather than being confined to one corneal layer. At this time, a 3rd edition of the IC3D classification of corneal dystrophies is under way.

Heterozygous COL17A1 variants are a frequent cause of amelogenesis imperfecta

BackgroundCollagen XVII is most typically associated with human disease when biallelic COL17A1 variants (>230) cause junctional epidermolysis bullosa (JEB), a rare, genetically heterogeneous, mucocutaneous blistering disease with amelogenesis imperfecta (AI),...

Classic lattice corneal dystrophy: a brief review and summary of treatment modalities.

To provide a brief summary and comparison of the most recent literature on available and theorized treatment modalities for classic lattice corneal dystrophy (LCD). This paper aims to support practitioners in their management of this disease. A search was carried out on available literature through PubMed and Google Scholar of English language articles up to January 2023 that relate to the treatment of LCD. Due to scarcity of literature regarding specific novel therapies for LCD, results from other corneal pathologies (granular corneal dystrophy, corneal scarring) are sometimes included for contrast, which is clearly denoted. LCD is a slowly progressive disease that leads to recurrent epithelial corneal erosions, stromal haze, corneal opacification, substantial discomfort, and visual impairment. Due to its autosomal-dominant inheritance pattern, this disease can persist throughout ancestral lines and requires consistent treatment and follow-up. An optimal management plan is necessary to (1) prolong years of life with best achievable visual acuity; (2) treat painful recurrent corneal erosions as they occur; (3) ensure proper follow-up throughout the life of a patient, as well as monitor at-risk offspring; and (4) monitor efficacy of treatment. This paper addresses (1) treatment for early disease including corneal epithelial debridement, photo therapeutic keratectomy (PTK), femtosecond laser-assisted lamellar keratectomy (FLK), and others; (2) treatment for late disease including full thickness keratoplasties and anterior lamellar keratoplasties; and (3) potential future treatment considerations including a wide variety of topical/systemic, genetic, and regenerative approaches.

Immune Cells Localize to Sites of Corneal Erosions in C57BL/6 Mice.

Recurrent epithelial erosions develop in the cornea due to prior injury or genetic predisposition. Studies of recurrent erosions in animal models allow us to gain insight into how erosions form and are resolved. While slowing corneal epithelial cell migration and reducing their proliferation following treatment with mitomycin C reduce erosion formation in mice after sterile debridement injury, additional factors have been identified related to cytokine expression and immune cell activation. The relationship between recruitment of immune cells to the region of the cornea where erosions form and their potential roles in erosion formation and/or erosion repair remains unexplored in the C57BL/6 mouse recurrent erosion model. Here, high resolution imaging of mouse corneas was performed at D1, D7, and D28 after dulled-blade debridement injury in C57BL/6 mice. Around 50% of these mice have frank corneal erosions at D28 after wounding. A detailed assessment of corneas revealed the involvement of M2 macrophages in both frank and developing erosions at early stages of their formation.

Comparison of penetrating keratoplasty versus lamellar keratoplasty for macular corneal dystrophy: a retrospective study of a single-center experience

Background: Although penetrating keratoplasty (PK) still remains the dominant form of transplantation for macular corneal dystrophy (MCD) patients, many studies evaluating these new forms of selective lamellar keratoplasty (LK) now suggest equivalent or better visual outcomes. This study aimed to explore the difference in outcomes and complications that follows each type of these operations. Methods: A retrospective, single-center study was performed at King Abdulaziz medical city in 2022. The study included patients with a histological diagnosis of MCD who undergone either PK or LK. Data was collected from health records using a form that consisted of patient characteristic, type of operation and post-operative outcomes, including visual acuity, survival rate and complications. Results: The study included a total of 54 eyes of patients who have MCD. A best corrected visual acuity (BCVA) of 0.5 or better was achieved in 82.5% of eyes of PK group and 42.9% of eyes of LK group. Graft survival rate was 90% (36 eyes) and 85.7% (12 eyes) in PK and LK groups respectively. Regarding complications, four PK eyes (10%) and one LK eye (7.1%) had high intraocular pressure, three PK eyes (7.5%) and one LK eye (7.1%) developed rejection, one PK eye (2.5%) developed recurrent epithelial erosion, and another one PK eye (2.5%) developed Traumatic epithelial laceration. Conclusions: PK operations resulted in a better post-operative visual acuity compared to LK group. The graft survival rate was slightly better for the PK group. PK was associated with higher incidence of complications than LK group.

Epithelial recurrent erosion dystrophy (ERED) from the splice site altering COL17A1 variant c.3156C>T in families of Finnish-Swedish ancestry.

To describe four Finnish families with epithelial recurrent erosion dystrophy (ERED) caused by the pathogenic variant c.3156C>T in collagen type XVII alpha 1 chain gene (COL17A1). Eleven affected and two unaffected individuals underwent clinical ophthalmological examination, anterior segment photography, and corneal topography. Two of them underwent phototherapeutic keratectomy (PTK). Genetic analysis included both next-generation and Sanger sequencing. Specimens from the manual keratectomy of one patient were available for ophthalmic pathologic examination, including immunohistochemistry. The common splice-site altering synonymous variant c.3156C > T, p.(Gly1052=) in COL17A1 was confirmed in 15 individuals with ERED from the four families. Subepithelial corneal scarring grades varied and increased with age, leading to decreased best-corrected visual acuity. PTK improved vision in 58- and 67-year-old individuals without reactivating the disease. The keratectomy specimens showed an uneven epithelium and a spectrum of basement membrane abnormalities, including breaks, fragmentation, multiplication and entrapment within the subepithelial scar, reflecting recurrent erosions. The stromal cells consisted of varying proportions of bland and activated fibroblasts and myofibroblasts, reflecting different ages of scars. The family with the largest number of known affected generations originated from Southern Sweden. The phenotype in the Finnish ERED families is consistent with earlier reports of the c.3156C > T variant, although the severity has varied between reports. The phenotype may be modulated by other genes. This study suggests a likely founder effect of the variant in both Finnish and Swedish populations due to their shared population histories. If vision is compromised, PTK can be considered especially in older patients.

Efficacy of topical insulin for recurrent epithelial corneal erosions.

Topical insulin can promote and accelerate corneal regeneration, even in eyes with serious comorbidities, and offers several benefits over other treatment options. The aim of this study is to evaluate the effect of topical insulin in treatment of recurrent epithelial corneal erosion. Patients with recurrent epithelial erosions were included in a prospective non-randomized hospital-based study, divided into two groups, one of them received persistent epithelial defects (PEDs) conventional treatment and the other received the same treatment with insulin eye drops 4 times/day. All patients were examined carefully by slit lamp. Patients during the 1st, 2nd, 3rd, and 4th weeks as well as after 2months. Demographics, etiology, therapy, comorbidities, and the healing time of PED were performed. Area shows significant improvement after 2weeks (p = 0.006), 2months (p = 0.046), and 3months (p = 0.002) in group II (cornetears gel and topical insulin) as compared to group I (cornetears gel). The recurrence was statistically significant decreased with cornetears gel and topical insulin (group II) by 0.0%, as compared to cornetears gel (group I) by 3 patients (21.4%). Topical insulin can promote corneal reepithelization in recurrent epithelial erosion and decreases recurrence in these cases. Other advantages include excellent tolerance, availability, and cost-effectiveness.

Severe sterile inflammatory keratitis associated with recurrent epithelial erosion after small incision lenticule extraction

A 32-year-old man had undergone small incision lenticule extraction (SMILE) that was complicated by intraoperative epithelial detachment in the right eye. Corneal epithelial erosion reoccurred at two and four months after surgery. At the third time of epithelial erosion, slit-lamp examination revealed dense white infiltrates throughout the corneal cap-stromal interface. The patient was initially managed with high-dose topical antibiotics. After the negative culture and Gram staining results from the interface washout, diffuse lamellar keratitis was confirmed and topical steroids were administered. The inflammation resolved, and corneal transparency was achieved after treatment. Timely diagnosis and appropriate treatment are highly critical for prognosis.

Keratitis fugax hereditaria ‐ useful to consider when you have a child with non‐specific corneal findings and symptoms

AbstractPurpose: To report clinical findings in children diagnosed with the autosomal dominant periodic corneal autoinflammation, keratitis fugax hereditaria (KFH, MIM 148200), and to highlight its geographical distribution.Methods: Patients were clinically examined in the Helsinki University Hospital between February 4, 2006, and December 31, 2021, and genetically verified to be carriers of the c.61G > C (rs200154873) variant in NLRP3 by Sanger sequencing. Variant allele frequencies were determined from Genome Aggregation Database (gnomAD) version 2.1.1.Results: The data consist of 10 children from 8 families; 6 boys and 4 girls. Age of onset varied from 3 to 14 (median, 8) years. Patients had typical KFH symptoms: eye pain, photophobia, conjunctival injection, and foreign body sensation. Five patients had corneal oval opacities, and 3 had a mild anterior chamber reaction. Seven were correctly diagnosed at the first visit based on family history. The remaining three children were diagnosed 1, 3, and 8 years after the first visit. Initial diagnoses were anterior uveitis, corneal erosion, and herpetic keratitis. Additionally, epithelial recurrent erosion dystrophy (ERED) or subepithelial mucinous corneal dystrophy (SMCD) had been suspected. Geographically, KFH concentrates to the bilingual Swedish‐speaking coastal areas of Finland. Allele frequencies are 0.014% in Finland, and 0.011% in Sweden, based on gnomAD.Conclusions: Scandinavian ophthalmologists should be aware of the possibility of KFH in case of suspected anterior uveitis, herpetic keratitis, or recurrent corneal erosion in children. Symptoms of paediatric KFH patients are equal to those in adults, but the typical corneal opacity still might recover between the attacks.

Phototherapeutic keratectomy versus epithelial debridement combined with anterior stromal puncture or diamond burr for recurrent corneal erosions

ObjectiveTo compare outcomes of phototherapeutic keratectomy (PTK) versus epithelial debridement combined with anterior stromal puncture (ASP) or diamond burr for the treatment of recurrent corneal erosions (RCES) in a large tertiary centre. MethodsPatients with a diagnosis of RCES secondary to trauma or epithelial basement membrane dystrophy who underwent a surgical procedure between 2009 and 2019 were included in the study. The following data were collected: demographics, ocular history, prior medical treatment, ocular surgeries, intervention, complete epithelialization at postoperative week 1, recurrences, and complications. Recurrence was defined as either an objective finding of a corneal epithelial defect or symptoms suggestive of recurrent epithelial erosion on history. Recurrence rate and time to epithelialization were compared between groups. ResultsA total of 97 eyes (73 patients) were included in the study. Mean patient age was 51 ± 16.1 years, and mean follow-up was 474 days. RCES was secondary to epithelial basement membrane dystrophy in 80% (n = 78 of 97), trauma (15%, n = 15 of 97), or idiopathic (4%, n = 4 of 97). Epithelial debridement with ASP was performed in 34 eyes (35%), diamond burr in 33 eyes (33%), and PTK in 30 eyes (31%). Compared with epithelial debridement with ASP (recurrence 29.4%), the recurrence rate was significantly lower for both the diamond burr (9.1%, p = 0.031) and PTK groups (10%, p = 0.048). The diamond burr and PTK groups also had a significantly higher rate of complete epithelialization at 1 week (p < 0.05). ConclusionCompared with epithelial debridement with ASP, diamond burr and PTK have significantly lower rates of recurrence and time to epithelialization and may be considered first for surgical management of RCES.

Autologous Blood Products: When, Where, and How?

Autologous blood eye drops have become an interesting, well-known, and widely used therapeutic option for many ocular surface diseases since their introduction into the ophthalmologic field forty-six years ago. The foundation for their use in the treatment of pathologies such as severe keratoconjunctivitis sicca, persistent epithelial defects, ocular chemical burns, recurrent epithelial erosions, Stevens-Johnson syndrome, ocular graft versus host disease, and, lately, in many other ocular surface conditions, relies on the fact that they contain proteins, vitamins, cytokines, and growth factors that participate in the signaling pathways of corneal epithelial healing in similar amounts to those found in normal, healthy tear films

Use of Acellular Umbilical Cord-Derived Tissues in Corneal and Ocular Surface Diseases.

Blood derived products have become a valuable source of tissue for the treatment of ocular surface diseases that are refractory to conventional treatments. These can be obtained from autologous or allogeneic sources (patient’s own blood or from healthy adult donors/umbilical cord blood, respectively). Allogeneic cord blood demonstrates practical advantages over alternatives and these advantages will be discussed herein. Umbilical cord blood (UCB) can be divided, generally speaking, into two distinct products: first, mononuclear cells, which can be used in regenerative ophthalmology, and second, the plasma/serum (an acellular fraction), which may be used in the form of eyedrops administered directly to the damaged ocular surface. The rationale for using umbilical cord serum (UCS) to treat ocular surface diseases such as severe dry eye syndrome (DES), persistent epithelial defects (PED), recurrent epithelial erosions, ocular chemical burns, graft versus host disease (GVHD), among others, is the considerably high concentration of growth factors and cytokines, mimicking the natural healing properties of human tears. Allogeneic serum also offers the opportunity for therapeutic treatment to patients who, due to poor heath, cannot provide autologous serum. The mechanism of action involves the stimulation of endogenous cellular proliferation, differentiation and maturation, which is highly efficient in promoting and enhancing corneal epithelial healing where other therapies have previously failed.

Experience in managing glaucoma filtration surgery complications with oral doxycycline: A case series.

To report the clinical profile and effectiveness of oral doxycycline as a non-invasive treatment for glaucoma filtering surgery complications. Prospective case series. Doxycycline is widely used in treating corneal melts, ocular surface diseases, meibomian gland disease, recurrent epithelial cell erosion, rosacea, and keratitis sicca. This prospective case series highlights the successful treatment of five patients with leaking blebs and conjunctiva erosion from glaucoma filtration surgery with the use of oral doxycycline. There was no adverse event reported in our cases. This study suggests that oral doxycycline may be a feasible non-surgical treatment modality due to its ability to inhibit collagenolysis, restore the Meibomian gland function, thereby stopping breakdown and promote conjunctival tissue healing.

Nuclear translocation of β-catenin induced by E-cadherin endocytosis causes recurrent erosion of diabetic cornea.

Recurrent epithelial erosion and refractory corneal ulcer are the clinical features of diabetic keratopathy (DK), which eventually lead to corneal scar and visual disturbance. In this study, we sought to determine the abnormalities of cell junction in diabetic corneal epithelial cells and the effect of high glucose on the β-catenin/E-cadherin complex. Corneal histology showed that corneal epithelial cells of high glucose mice were loosely arranged, and the immunohistochemistry showed that the expression of E-cadherin decreased, the levels of β-catenin increased in nuclear. High glucose-induced degradation and endocytosis of E-cadherin of corneal epithelial cells reduce the formation of β-catenin/E-cadherin complex and promote the nuclear translocation of β-catenin. Moreover, high glucose also activated the transcription and expression of matrix metallopeptidase and snail, which interfered with the adhesion of corneal epithelial cells to the basement membrane. These findings reveal that DK is associated with the dissociation of cell junctions. The maintenance of the stability of the β-catenin/E-cadherin complex may be a potential therapeutic target of refractory corneal ulcers in patients with diabetes.

Corneal Endothelial Cell Toxicity Determines Long-Term Outcome After Ocular Exposure to Sulfur Mustard Vapor.

Ocular exposure to sulfur mustard (SM) vapor causes acute loss of corneal endothelial cells (CECs). Persistent corneal endothelial pathologies are observed in eyes that do not recover from SM exposure, suggesting that endothelial toxicity contributes to mustard gas keratopathy (MGK). Here, we evaluated the contributions of endothelial loss to acute and chronic corneal injuries in SM-exposed eyes. Rabbit eyes were exposed in vivo to equivalent doses of SM using 9-, 11-, or 14-mm vapor caps. The effects of exposure area on corneal injury progression were longitudinally evaluated over 12 weeks using clinical evaluations. The effects of exposure area on CEC morphology, endothelial and epithelial ultrastructure, and endothelial barrier function were determined from 1 day to 12 weeks. SM exposure caused loss of CECs and failure of endothelial barrier integrity at 1 day, independent of exposure cap size. By 3 weeks, eyes exposed with the 14-mm vapor cap exhibited increased corneal permeability, repopulation of the endothelium by cells with fibroblastic morphology, and abnormal deposition of extracellular matrix. Eyes exposed with 9- or 11-mm vapor caps exhibited transient symptoms of injury that fully resolved, with the rate of recovery correlated with cap size. The nonlinear correlation between endothelial lesion size and probability of developing MGK suggests that the CEC loss is a determinative factor for emergence of MGK. These studies illustrate the importance of endothelial repair in preventing MGK. Furthermore, they exclude chemical modification of basement membrane as a mechanistic cause of recurrent epithelial erosions in MGK eyes.

Corneal recurrent erosions dystrophy in citizens and migrants in Finland

AbstractThe epithelial recurrent erosion dystrophy (ERED) is a rare autosomal dominant corneal disease. Recently, mutations in collagen type XVII, alpha 1 (COL17A1) gene were identified as the cause of ERED. We have identified four Finnish families and one Armenian family with recurrent erosions and a dominant inheritance pattern. Affected patients reported recurrent corneal erosions beginning at the age of 4–12 years. The frequency of erosions decreased in adult age. Corneal scarring and anterior stromal opacities with varying degree were observed. The visual acuity of some patients slowly deteriorated. Next‐generation exome sequencing was performed in seven affected individuals from the five families focusing on the large COL17A1 gene. Sequencing analysis revealed that all seven patients carried a known synonymous splice‐altering variant c.3156C&gt;T. Furthermore, five more family members were studied with Sanger sequencing. All twelve patients carried the same c.3156C&gt;T variant. The variant was not present in gnomAD database including of 12,562 Finns. A genealogical analysis revealed that in one Finnish family the variant originated from Sweden. The variant c.3156C&gt;T in COL17A1 is reported previously in English, American, Thai, New Zealand, and Tasmanian families with ERED. Our finding of the same variant in yet two other populations strengthens the evidence that this variant is the most frequent cause of ERED. The c.3156C&gt;T codon seems to be a hot spot for recurrent mutations.

Corneal dystrophies as a cause of recurrent erosions

AbstractEspecially in anteriorly located corneal dystrophies, recurrent erosions can be observed and are associated with many different histopathological and genetic etiologies: with microcysts in Meesmann corneal dystrophy (MECD) from KRT3 and KRT12 mutations, with aberrant epithelial basement membrane in epithelial basement membrane dystrophy (EBMD), with gradual scarring from COL17A1 mutation in epithelial recurrent erosions dystrophy (ERED), with distinct deposits in the five epithelial‐stromal TGFBI‐related corneal dystrophies, and with deposits and epithelial thinning in macular corneal dystrophy (MCD) from CHST6 mutations. Rarely does a secondary form occur in the Fuchs endothelial corneal dystrophy (FECD) due to an erosive rupture of an epithelial bleb.