The Experts below are selected from a list of 38157 Experts worldwide ranked by ideXlab platform
Anat Galor - One of the best experts on this subject based on the ideXlab platform.
-
Ocular Surface Pain: A Narrative Review
Ophthalmology and Therapy, 2020Co-Authors: Divy Mehra, Noah K. Cohen, Anat GalorAbstract:Ocular Surface pain is a frequent cause of visits to an eye care provider and has a substantial impact on healthcare cost, yet a complete understanding of its causative factors and tools for diagnostic workup are notably missing in many eye clinics. The cornea has the densest sensory innervation in the human body and has the potential to be a powerful producer of pain. Pain can manifest as a result of a noxious stimulus or disruption in the Ocular Surface anatomy (nociceptive pain), or it can result from abnormalities in the Ocular Surface neurosensory apparatus itself (neuropathic pain). Novel advances in neurobiology have sought to differentiate the two entities, particularly to identify when chronic dry eye symptomatology is driven by neuropathic Ocular pain. In this review, we seek to provide an overview of the prevalence, physiologic factors, and management of Ocular Surface pain complaints.
-
Ocular Surface Pain: A Narrative Review
Ophthalmology and Therapy, 2020Co-Authors: Divy Mehra, Noah K. Cohen, Anat GalorAbstract:Ocular Surface pain is a frequent cause of visits to an eye care provider and has a substantial impact on healthcare cost, yet a complete understanding of its causative factors and tools for diagnostic workup are notably missing in many eye clinics. The cornea has the densest sensory innervation in the human body and has the potential to be a powerful producer of pain. Pain can manifest as a result of a noxious stimulus or disruption in the Ocular Surface anatomy (nociceptive pain), or it can result from abnormalities in the Ocular Surface neurosensory apparatus itself (neuropathic pain). Novel advances in neurobiology have sought to differentiate the two entities, particularly to identify when chronic dry eye symptomatology is driven by neuropathic Ocular pain. In this review, we seek to provide an overview of the prevalence, physiologic factors, and management of Ocular Surface pain complaints.
-
The Microbiome and Ocular Surface Disease
Current Ophthalmology Reports, 2019Co-Authors: Arjun Watane, Kara M. Cavuoto, Santanu Banerjee, Anat GalorAbstract:Purpose of Review The human body lives in a symbiotic relationship with the bacteria, viruses, fungi, and protozoa that make up the microbiome. In this review, we discuss the compositions of the gut and Ocular Surface microbiomes in relationship to health and disease. Recent Findings The gut microbiome is dominated by Firmicutes, whereas the Ocular Surface is dominated by Proteobacteria. The compositions of the microbiome are similar between individuals at the phyla level, but differ at the genus level. Alterations in the microbiome have been associated with disease. For example, Ocular diseases such as uveitis, dry eye, and keratitis have been associated with gut dysbiosis. In addition, Ocular Surface dysbiosis has been reported in diseases including dry eye, blepharitis, keratitis, and diabetic retinopathy. Summary Compositions of the gut and Ocular Surface microbiomes have been found to differ in disease states compared with controls. Further understanding of dysbiosis specific to a disease is needed to target these Surfaces for therapeutic strategies.
-
The Microbiome and Ocular Surface Disease
Current Ophthalmology Reports, 2019Co-Authors: Arjun Watane, Kara M. Cavuoto, Santanu Banerjee, Anat GalorAbstract:The human body lives in a symbiotic relationship with the bacteria, viruses, fungi, and protozoa that make up the microbiome. In this review, we discuss the compositions of the gut and Ocular Surface microbiomes in relationship to health and disease. The gut microbiome is dominated by Firmicutes, whereas the Ocular Surface is dominated by Proteobacteria. The compositions of the microbiome are similar between individuals at the phyla level, but differ at the genus level. Alterations in the microbiome have been associated with disease. For example, Ocular diseases such as uveitis, dry eye, and keratitis have been associated with gut dysbiosis. In addition, Ocular Surface dysbiosis has been reported in diseases including dry eye, blepharitis, keratitis, and diabetic retinopathy. Compositions of the gut and Ocular Surface microbiomes have been found to differ in disease states compared with controls. Further understanding of dysbiosis specific to a disease is needed to target these Surfaces for therapeutic strategies.
-
Updates in Ocular Surface Tumor Diagnostics.
International ophthalmology clinics, 2017Co-Authors: Afshan A. Nanji, Anat Galor, Carolina Mercado, Sander R. Dubovy, Carol L. KarpAbstract:Purpose To evaluate technologies and techniques available for the diagnosis of Ocular Surface tumors. Methods A review of the literature from 1947 to 2017, through the PubMed Database, was conducted in order to evaluate current diagnostic methods for Ocular Surface tumors. Results Ocular Surface squamous neoplasia, conjunctival melanoma, and conjunctival lymphoma are the three most common Ocular Surface malignancies. Technologies available to assist with diagnosis of these conditions, in addition to full thickness biopsy, include vital dyes, aspiration and impression cytology, in vivo confocal microscopy, ultrasound biomicroscopy, genetic testing, and anterior segment optical coherence tomography. Conclusions Histology remains the gold standard for diagnosis for all 3 of these malignancies. However, multiple diagnostic techniques are available to assist in making preliminary and early diagnoses, in differentiating between similar-appearing lesions, and in some cases, avoiding biopsy prior to initiating treatment. As imaging and technology continue to evolve, these adjunctive techniques will likely continue to play a greater role in clinical practice.
Shigeru Kinoshita - One of the best experts on this subject based on the ideXlab platform.
-
Meibomian Glands and Ocular Surface Inflammation
Ocular Surface, 2015Co-Authors: Tomo Suzuki, Satoshi Teramukai, Shigeru KinoshitaAbstract:Abstract The purpose of this review was to systematically analyze publications related to the role of meibomian gland disease in Ocular Surface inflammation, with special reference to meibomitis as an inflammatory form of meibomian gland dysfunction (MGD). Meibomian gland inflammation is often present with the Ocular Surface inflammation in conditions such as blepharokeratoconjunctivitis, Ocular rosacea, and phlyctenular keratitis, but its contribution is often overlooked, especially in younger subjects. This can result in misdiagnosis, mistreatment, and, sometimes, severe visual impairment. We identified a related disease entity, seen predominantly in young patients, of Ocular Surface inflammation associated with meibomitis, which we termed meibomitis-related keratoconjunctivitis . Its specific clinical features are similar to those observed in the above-mentioned diseases, and the inflammatory form of MGD was found to be closely involved in the Ocular Surface inflammation seen in those four diseases, based on our statistical evaluation. The diagnosis and management of meibomitis, an inflammatory form of MGD, is vital for the successful treatment of the induced Ocular Surface inflammation. We propose that the Ocular Surface and the adnexal meibomian glands should be considered as one unit, i.e., the "meibomian gland and Ocular Surface" (MOS), when encountered in the clinical setting.
-
Ocular Surface inflammation is regulated by innate immunity.
Progress in retinal and eye research, 2012Co-Authors: Mayumi Ueta, Shigeru KinoshitaAbstract:Abstract On the Ocular Surface, as in the intestines and airway, the Surface epithelium serves a critical function as the front-line defense of the mucosal innate immune system. Although the detection of microbes is arguably the most important task of the immune system, an exaggerated epithelial host defense reaction to endogenous bacteria may initiate and perpetuate inflammatory mucosal responses. In this review we first describe commensal bacteria found on the Ocular Surface, which is in contact with the Ocular Surface epithelium. We also discuss the innate immunity of the Ocular Surface epithelium and we present the allergic reaction regulated by Ocular Surface epithelial cells. We address Ocular Surface inflammation due to disordered innate immunity and we present our hypothesis that the onset of Stevens-Johnson syndrome (SJS) with severe Ocular Surface complications, a devastating Ocular Surface inflammatory disease, is strongly associated with abnormality of the innate immune system. In this review we raise the possibility that some Ocular Surface inflammatory diseases are pathogenetically related with a disordered innate immune response. Focusing on the innate immunity of the Ocular Surface might help to elucidate the pathogenesis of various Ocular Surface diseases.
-
Ocular Surface inflammation mediated by innate immunity.
Eye & contact lens, 2010Co-Authors: Mayumi Ueta, Shigeru KinoshitaAbstract:This review addresses three subjects: the innate immunity of the Ocular Surface epithelium, innate immunity and Ocular Surface inflammation, and Stevens-Johnson syndrome (SJS) and abnormality of innate immunity. In innate immunity of the Ocular Surface epithelium, Ocular Surface epithelial cells respond selectively to microbial components and induce limited inflammation, whereas immune-competent cells such as macrophages can recognize various microbial components through Toll-like receptors (TLRs) and induce inflammation to exclude the microbes. The difference between macrophages and Ocular Surface epithelial cells may be caused by the dissimilarity in the degree of coexistence with commensal bacteria. The unique innate immune response of Ocular Surface epithelium might contribute to coexistence with commensal bacteria. In innate immunity and Ocular Surface inflammation, we speculate that an abnormality in the proper innate immunity of the Ocular Surface may result in Ocular Surface inflammation. Our investigation shows that TLR3 positively regulates the late-phase reaction of experimental allergic conjunctivitis, which causes reduced eosinophilic conjunctival inflammation in TLR3KO (knockout) mice and pronounced eosinophilic conjunctival inflammation in TLR3Tg mice. We also demonstrate that human Ocular Surface epithelial cells can be induced to express many transcripts, including antiviral innate immune response-related genes and allergy-related genes, through polyI:C stimulation. Furthermore, we show that IkappaBzeta KO mice exhibit severe, spontaneous Ocular Surface inflammation accompanied by the eventual loss of almost all goblet cells and spontaneous perioral inflammation. IkappaBzeta is induced by diverse pathogen-associated molecular patterns and regulates nuclear factor-kappaB activity, possibly to prevent excessive inflammation in the presence of bacterial components. The spontaneous Ocular Surface inflammation observed in IkappaBzeta KO mice suggested that dysfunction/abnormality of innate immunity can play a role in Ocular Surface inflammation. In SJS and abnormality of innate immunity, we considered the possibility that there may be an association between SJS and a disordered innate immune response. In gene expression analysis of CD14 cells, we found that IL4R gene expression was different in patients with SJS/toxic epidermal necrolysis (TEN) and controls on lipopolysaccharide stimulation, being downregulated in patients with SJS/TEN and slightly upregulated in the controls. The expression of IkappaBzeta- and interleukin (IL)-1alpha-specific mRNA in patients with SJS/TEN was lower than in normal controls after 1-hour culture. Although SJS/TEN can be induced by drugs, not all individuals treated with these drugs developed SJS/TEN. Because the incidence of SJS/TEN is very low, we suspected a genetic predisposition and performed single-nucleotide polymorphism (SNP) association analysis using candidate genes associated with innate immunity, apoptosis, or allergy. We found that TLR3 SNP rs.3775296 and IL4R SNP rs.1801275 (Gln551Arg) were strongly associated (P
-
Innate immunity of the Ocular Surface.
Brain Research Bulletin, 2009Co-Authors: Mayumi Ueta, Shigeru KinoshitaAbstract:The Ocular Surface epithelium serves a critical function as the defensive front line of the innate immune system. While the detection of microbes is arguably its most important task, an exaggerated host defense reaction to endogenous bacterial flora may initiate and perpetuate inflammatory mucosal responses. The ability of cells to recognize pathogen-associated molecular patterns (PAMPs) mainly depends on the expression of a family of Toll-like receptors (TLRs). A healthy Ocular Surface is not inflammatory, even though Ocular Surface epithelium is in constant contact with bacteria and bacterial products. In this study, we show that human Ocular Surface epithelial cells, both corneal and conjuctival epithelial cells, respond to viral double-stranded RNA mimic polyI:C to produce pro-inflammatory cytokines through TLR3, while they fail to respond functionally to lipopolysaccharide, a TLR4 ligand. Moreover, human Ocular Surface epithelium responds to flagellins from Ocular pathogenic, but not Ocular non-pathogenic bacteria, to produce pro-inflammatory cytokines through TLR5. Thus, Ocular Surface epithelial cells selectively respond to microbial components and induce limited inflammation; immune-competent cells can recognize microbial components through TLRs and induce the inflammation. The unique innate immune response of the Ocular Surface epithelium may contribute to its coexistence with commensal bacteria. Inflammatory bowel disease is thought to result from an abnormal response to the gut microbiota. Thus, we also considered the possibility of an association between Ocular Surface inflammation and a disordered innate immune response. IkappaBzeta is important for TLR signaling, in mice, its knock-out produced severe, spontaneous Ocular Surface inflammation, the eventual loss of goblet cells, and spontaneous perioral inflammation, suggesting that dysfunction/abnormality of innate immunity can lead to Ocular Surface inflammation.
-
Characteristics of the human Ocular Surface epithelium.
Progress in retinal and eye research, 2001Co-Authors: Shigeru Kinoshita, Wakako Adachi, Chie Sotozono, Kohji Nishida, Norihiko Yokoi, Andrew J. Quantock, Kousaku OkuboAbstract:An appreciation of the biological characteristics of the human Ocular Surface epithelium affords us a great insight into the physiology of the human Ocular Surface in health and disease. Here, we review five important aspects of the human Ocular Surface epithelium. First, we recognize the discovery of corneal epithelial stem cells, and note how the palisades of Vogt have been suggested as a clinical marker of their presence. Second, we introduce the concept of the gene expression profile of the Ocular Surface epithelium as arrived at using a new strategy for the systematic analysis of active genes. We also provide a summary of several genes abundantly or uniquely expressed in the human corneal epithelium, namely clusterin, keratin 3, keratin 12, aldehyde dehydrogenase 3 (ALDH3), troponin-I fast-twitch isoform, sig-h3, cathepsin L2 (cathepsin V), uroplakin Ib, and Ca2+-activated chloride channel. Genes related to limbal and conjunctival epithelia are also described. Third, we touch upon the genetic abnormalities thought to be involved with epithelial dysfunction in Meesmann's dystrophy, gelatinous drop-like corneal dystrophy, and the sig-h3-mutated corneal dystrophies. Fourth, we provide an update regarding the current state of knowledge of the role of cytokines, growth factors and apoptosis in relation to Ocular Surface homeostasis and tissue reconstruction; the main factors being epidermal growth factor (EGF), keratinocyte growth factor (KGF), hepatocyte growth factor (HGF), transforming growth factor-s (TGF-s), and some inflammatory cytokines. Fifth, corneal epithelial barrier function and dysfunction as measured by fluorophotometry is remarked upon, with an explanation of the FL-500 fluorophotometer and its ability to detect corneal epithelial dysfunction at a subclinical level. The research described in this review has undoubtedly generated a complete understanding of corneal epithelial pathophysiology—an understanding that, directly or indirectly, has helped advance the development of new therapeutic modalities for Ocular Surface reconstruction.
Ilene K. Gipson - One of the best experts on this subject based on the ideXlab platform.
-
The Ocular Surface Phenotype of Muc5ac and Muc5b Null MiceNo Ocular Surface Phenotype in Mice
Investigative ophthalmology & visual science, 2014Co-Authors: Christina K. Marko, Ann S. Tisdale, Sandra Spurr-michaud, Christopher M. Evans, Ilene K. GipsonAbstract:PURPOSE Recent development of mice null for either Muc5ac or Muc5b mucin allows study of their specific roles at the mouse Ocular Surface. A recent report indicated that Muc5ac null mice show an Ocular Surface phenotype similar to that seen in dry eye syndrome. The purpose of our study was to determine the effect of lack of Muc5ac or Muc5b on the Ocular Surface, and to determine if environmental desiccating stress exacerbated a phenotype. METHODS Muc5ac null and Muc5b null mice, and their wild-type controls were examined for Ocular Surface defects by fluorescein staining. The number of goblet cells per area of conjunctival epithelium was counted, and levels of mucin gene expression and genes associated with epithelial stress, keratinization, and differentiation, known to be altered in dry eye syndrome, were assayed. To determine if the null mice would respond more to desiccating stress than their wild-type controls, they were challenged in a controlled environment chamber (CEC) and assessed for changes in fluorescein staining, tear volume, and inflammatory cells within the conjunctival and corneal epithelia. RESULTS Unlike the previous study, we found no Ocular Surface phenotype in the Muc5ac null mice, even after exposure to desiccating environmental stress. Similarly, no Ocular Surface phenotype was present in the Muc5b null mice, either before or after exposure to a dry environment in the CEC. CONCLUSIONS Our results indicate that deleting either the Muc5ac or Muc5b gene is insufficient to create an observable dry eye phenotype on the Ocular Surface of these mice.
-
Distribution of mucins at the Ocular Surface
Experimental eye research, 2004Co-Authors: Ilene K. GipsonAbstract:Mucins are vital for maintenance of a healthy, wet Ocular Surface. Once only thought to be secreted by goblet cells, mucins are now also known to be of the membrane-associated type. Stratified Ocular Surface epithelia express at their apical-tear fluid Surface a repertoire of membrane-associated mucins including MUC1, MUC4, MUC16. These mucins are concentrated on the tips of the microplicae, forming a dense glycocalyx at the epithelial tear film interface. A major mucin of the secretory class is the goblet-cell-derived gel-forming mucin MUC5AC. A small soluble mucin, MUC7, is expressed by the lacrimal gland acini. Our hypothesis of the role/distribution of the secreted and membrane-associated mucins at the Ocular Surface is that the secreted mucins are soluble in the tear fluid, and are moved about and shunted to the nasolacrimal duct and by the eyelids during blinking. Thus, in the tears, the secreted mucins act as clean-up/debris removing multimeric networks that at the same time, through their hydrophilic nature, hold fluids in place and harbor defense molecules secreted by the lacrimal gland. Membrane-associated mucins, on the other hand, form a dense barrier in the glycocalyx at the epithelial tear film interface. This barrier prevents pathogen penetrance and is a lubricating Surface that allows lid epithelia to glide over the corneal epithelia without adherence. The secreted mucins move easily over the glycocalyx mucins because both have anionic character that creates repulsive forces between them. Little is known regarding regulation of expression and glycosylation of mucins by Ocular Surface epithelia. Since Ocular Surface drying diseases alter both goblet cell and mucin production, and production and glycosylation of membrane-associated mucins, studies of mucin gene regulation and glycosylation may yield treatment modalities for these diseases.
Stephen C Pflugfelder - One of the best experts on this subject based on the ideXlab platform.
-
Autoimmunity at the Ocular Surface: pathogenesis and regulation
Mucosal Immunology, 2010Co-Authors: M E Stern, C S Schaumburg, R Dana, M Calonge, J Y Niederkorn, Stephen C PflugfelderAbstract:A healthy Ocular Surface environment is essential to preserve visual function, and as such the eye has evolved a complex network of mechanisms to maintain homeostasis. Fundamental to the health of the Ocular Surface is the immune system, designed to respond rapidly to environmental and microbial insults, whereas maintaining tolerance to self-antigens and commensal microbes. To this end, activation of the innate and adaptive immune response is tightly regulated to limit bystander tissue damage. However, aberrant activation of the immune system can result in autoimmunity to self-antigens localized to the Ocular Surface and associated tissues. Environmental, microbial and endogenous stress, antigen localization, and genetic factors provide the triggers underlying the immunological events that shape the outcome of the diverse spectrum of autoimmune-based Ocular Surface disorders.
-
Autoimmunity at the Ocular Surface: pathogenesis and regulation
Mucosal Immunology, 2010Co-Authors: M E Stern, C S Schaumburg, R Dana, M Calonge, J Y Niederkorn, Stephen C PflugfelderAbstract:A healthy Ocular Surface environment is essential to preserve visual function, and as such the eye has evolved a complex network of mechanisms to maintain homeostasis. Fundamental to the health of the Ocular Surface is the immune system, designed to respond rapidly to environmental and microbial insults, whereas maintaining tolerance to self-antigens and commensal microbes. To this end, activation of the innate and adaptive immune response is tightly regulated to limit bystander tissue damage. However, aberrant activation of the immune system can result in autoimmunity to self-antigens localized to the Ocular Surface and associated tissues. Environmental, microbial and endogenous stress, antigen localization, and genetic factors provide the triggers underlying the immunological events that shape the outcome of the diverse spectrum of autoimmune-based Ocular Surface disorders.
-
Dry Eye and Ocular Surface Disorders - Dry eye and Ocular Surface disorders
2004Co-Authors: Stephen C Pflugfelder, Roger W. Beuerman, Michael E. SternAbstract:Dry Eye: The Problem. The Lacrimal Functional Unit. The Normal Tear Film and Ocular Surface. Dysfunction of the Lacrimal Functional Unit and its Impact on Tear Film Stability and Composition. The Conjunctiva and Tear Film Maintenance. Mechanisms of the Ocular Surface Immune Response. Impact of Systemic Immune Disease on the Lacrimal Functional Unit. Sex and Sex Steroid Influences on Dry Eye Syndrome
-
Tear Fluid Influence on the Ocular Surface
Advances in experimental medicine and biology, 1998Co-Authors: Stephen C PflugfelderAbstract:A healthy Ocular Surface is essential for maintaining a comfortable eye and clear vision. Despite many advances in the field of dry eye and Ocular Surface disease, the role of the tear fluid in maintaining a healthy Ocular Surface has not been defined. It is unknown whether tear fluid constituents influence the growth and differentiation of the Ocular Surface epithelium, and if they do, whether this is a primary or redundant function. Furthermore, it is not clear whether the concentration or activity of biologically active tear factors changes in dry eye conditions.
Kazuo Tsubota - One of the best experts on this subject based on the ideXlab platform.
-
Atopic Ocular Surface disease: implications on tear function and Ocular Surface mucins.
Cornea, 2005Co-Authors: Murat Dogru, Naoko Okada, Naoko Asano-kato, Mari Tanaka, Ayako Igarashi, Yoji Takano, Kazumi Fukagawa, Jun Shimazaki, Kazuo Tsubota, Hiroshi FujishimaAbstract:Purpose: To describe tear function, mucin alterations, and Ocular Surface disorder in patients with atopic diseases. Methods: Subjects underwent comeal sensitivity measurements, Schirmer test, tear film break-up time (BUT) assay, and fluorescein and rose Bengal staining of the Ocular Surface. Conjunctival impression cytology and brush cytology were also conducted. Impression cytology samples underwent PAS and immunohistochemical staining for MUC5AC. Brush cytology specimens underwent evaluation for inflammatory cell expression and RT-PCR for MUC5AC mRNA expression. Differences related to tear function and Ocular Surface examination parameters among patients with and without comeal ulceration and healthy control subjects were studied. Results: Mean corneal sensitivity and BUT values were significantly lower in atopic patients with comeal ulcers compared with patients without ulcers and controls (P < 0.001). Brush cytology specimens from patients with corneal ulcers revealed significantly higher expression of inflammatory cells compared with patients without ulcers and controls (P < 0.001). Impression cytology samples from eyes with comeal ulcers showed significant squamous metaplasia and reduction of goblet cell density compared with eyes without ulcers and control subjects. Specimens from eyes with comeal ulcers showed PAS (+) mucin pick up and did not stain positive for MUC5AC. MUC5AC mRNA expression was significantly lower in eyes with corneal ulcers compared with in eyes without ulcers and control subjects. Conclusions: Ocular Surface inflammation, tear film instability, and decreased conjunctival MUC5AC mRNA expression are important in the pathogenesis of noninfectious comeal shield ulcers in atopic Ocular Surface disease.
-
Atopic Ocular Surface disease: implications on tear function and Ocular Surface mucins.
Cornea, 2005Co-Authors: Murat Dogru, Naoko Okada, Naoko Asano-kato, Mari Tanaka, Ayako Igarashi, Yoji Takano, Kazumi Fukagawa, Jun Shimazaki, Kazuo Tsubota, Hiroshi FujishimaAbstract:To describe tear function, mucin alterations, and Ocular Surface disorder in patients with atopic diseases. Subjects underwent corneal sensitivity measurements, Schirmer test, tear film break-up time (BUT) assay, and fluorescein and rose Bengal staining of the Ocular Surface. Conjunctival impression cytology and brush cytology were also conducted. Impression cytology samples underwent PAS and immunohistochemical staining for MUC5AC. Brush cytology specimens underwent evaluation for inflammatory cell expression and RT-PCR for MUC5AC mRNA expression. Differences related to tear function and Ocular Surface examination parameters among patients with and without corneal ulceration and healthy control subjects were studied. Mean corneal sensitivity and BUT values were significantly lower in atopic patients with corneal ulcers compared with patients without ulcers and controls (P<0.001). Brush cytology specimens from patients with corneal ulcers revealed significantly higher expression of inflammatory cells compared with patients without ulcers and controls (P<0.001). Impression cytology samples from eyes with corneal ulcers showed significant squamous metaplasia and reduction of goblet cell density compared with eyes without ulcers and control subjects. Specimens from eyes with corneal ulcers showed PAS (+) mucin pick up and did not stain positive for MUC5AC. MUC5AC mRNA expression was significantly lower in eyes with corneal ulcers compared with in eyes without ulcers and control subjects. Ocular Surface inflammation, tear film instability, and decreased conjunctival MUC5AC mRNA expression are important in the pathogenesis of noninfectious corneal shield ulcers in atopic Ocular Surface disease.
-
Current concepts in Ocular Surface reconstruction
Seminars in ophthalmology, 2005Co-Authors: Murat Dogru, Kazuo TsubotaAbstract:Diseases that affect the limbal stem cells are multifactorial and present with different stages of severity. The most important features to be considered in evaluating these patients include the degree of limbal stem cell loss, the extent of conjunctival disease, and the presence and etiology of Ocular Surface inflammation. Other important factors are tear film and eyelid abnormalities, keratinization of the Ocular Surface, laterality of the disease process, health and age of the patient. Careful consideration of all of these factors help tremendously in tailoring the most suitable method of treatment for each patient. The management of severe Ocular Surface disease has benefited from numerous advances in recent years. At one time, available techniques for visual rehabilitation consisted of superficial keratectomy, use of artificial tears, tarsorraphy as well as lamellar and penetrating keratoplasty. A lamellar or penetrating keratoplasty procedure resulted in a stable Surface only for as long as the donor epithelium was present and once the epithelium sloughed off, the Ocular Surface failed due to conjunctivalization. The last few decades enjoyed the development and, especially, progress of new Ocular Surface reconstruction techniques such as amniotic membrane transplantation, limbal stem cell transplant procedures, transplantation of cultivated oral mucosal or limbal stem cell sheets. This review will briefly focus on the indications and methodology of each procedure and the currently available clinical data on the results of these procedures.
-
Ocular Surface management in corneal transplantation, a review.
Japanese Journal of Ophthalmology, 1999Co-Authors: Kazuo TsubotaAbstract:Abstract Purpose: To discuss the importance of Ocular Surface management in corneal transplantation, especially in limbal transplantation. Methods: Since the corneal epithelium is not completely recovered after corneal transplantation, meticulous attention should be paid to the Ocular Surface to prevent infection and rejection, which are the major causes of corneal transplantation failure. Preoperative evaluations of the Ocular Surface should be carried out, followed by appropriate surgical procedures, depending on the condition of each patient. Vigorous immunosuppressive measures should be taken after surgery. Results: In both case reports presented in this study, each patient underwent successful surgery and his condition was controlled by medication suited to his needs. Conclusions: For those patients with stem cell deficiency, limbal transplantation, possibly with the use of autologous serum drops, should be considered to reconstruct and maintain the Ocular Surface. Ocular Surface management is necessary for the success of corneal transplantation, especially for limbal transplantation.
-
Important concepts for treating Ocular Surface and tear disorders.
American journal of ophthalmology, 1997Co-Authors: Scheffer C. G. Tseng, Kazuo TsubotaAbstract:Purpose To outline important concepts for treating Ocular Surface and tear disorders. Method A review was conducted of recently published findings. Results Five concepts were delineated: Ocular Surface health is ensured by a close relationship between Ocular Surface epithelia and the preOcular tear film; a stable tear film is inherently maintained by external adnexae; the intact protective mechanism is controlled by effective neuroanatomic integration; corneal epithelial stem cells are located at the corneoscleral limbus; and Ocular Surface epithelial cell function is supported by stromal fibroblasts and matrix. Conclusions These concepts stress that Ocular Surface epithelia and the preOcular tear film function as a unit and, furthermore, that several corneal and external diseases can be categorized as Ocular Surface and tear disorders. These concepts also help one formulate unified diagnostic and therapeutic strategies for management of these diseases.
