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At least 55 records · Page 3Linked to original sources
PubMed2001

Elevated expression of transglutaminase 1 and keratinization-related proteins in conjunctiva in severe ocular surface disease.

PURPOSE: In severe ocular surface diseases, pathologic keratinization of the ordinarily nonkeratinized corneal and conjunctival mucosal epithelia results in severe visual loss. The expression in conjunctivalized corneas of various proteins known to play important roles in the physiological keratinization process in human epidermis was examined to better understand the mechanism of keratinization. METHODS: Conjunctiva covering the cornea was examined in 12 eyes with ocular surface disease in the chronic cicatricial phase. These comprised four Stevens-Johnson syndrome, four ocular cicatricial pemphigoid, and four chemical injuries. Normal conjunctivas from four age-matched individuals served as controls. Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to investigate transglutaminase 1 gene expression and immunohistochemistry to study the expression of transglutaminase 1 protein along with other keratinization-related proteins (involucrin, loricrin, filaggrin, and cytokeratins 1 and 10) and cytokeratin pairs 4/13 and 3/12. RESULTS: Semiquantitative RT-PCR showed that transglutaminase 1 mRNA expression was upregulated in keratinized conjunctiva compared with normal. Also, in this tissue, immunohistochemistry demonstrated elevated levels of transglutaminase 1, involucrin, filaggrin, and the cytokeratin pair 1/10. Levels of loricrin and cytokeratin pairs 4/13 and 3/12, however, remained the same. CONCLUSIONS: Various keratinization-related proteins, transglutaminase 1 included, are most likely involved in the pathogenesis of cicatrizing ocular surface diseases.

Adult↗
PubMed1997

Retrospective study of ocular surface squamous neoplasia.

BACKGROUND: Ocular surface squamous neoplasia (OSSN) encompasses the conditions of simple dysplasia to carcinoma in situ to invasive squamous cell carcinoma. It has a high rate of recurrence after treatment and the potential to metastasize. The present retrospective study was aimed at further defining the characteristics and clinical course of OSSN. METHODS: With ethical approval, the records of all major pathology laboratories in Queensland were surveyed. Two hundred and eighty-eight cases were identified: 155 dysplasia, 71 carcinomas in situ and 62 invasive squamous cell carcinoma. The records were analysed and an attempt was made to contact and re-examine the patients. RESULTS: Ocular surface squamous neoplasia occurs mainly in males (78.5%) with a mean age of 60.1 years (range 20-88 years). They present as irritation (40.1%) and are located usually at the limbus (87.8%). The majority of OSSN are treated by simple excision (87.5%), after which there is a high rate of recurrence (23.3%). The main predictors for recurrence include histological grade of the lesion, corneal location and larger size (> 2 mm). CONCLUSIONS: Management of OSSN requires adequate excision and careful follow up to monitor any recurrence. As with other ultraviolet light-related conditions, preventative measures must remain the key to disease control.

Adult↗
PubMed2003

COX-2 lack of function in hypoxia-induced ocular surface inflammation.

Injury to the ocular surface increases corneal epithelial production of cyclooxygenase (COX)-derived eicosanoids but this increase correlates poorly to the inflammatory sequelae. Moreover, corticosteroids are effective in treatment of this inflammation but NSAIDs are not. The discovery of COX-2 that is differentially affected by common NSAIDs reopened the question of the role of prostaglandins in ocular surface inflammation. We examined the presence and inducibility of COX-2 in the corneal epithelium following hypoxia-induced injury in vivo and in vitro. COX-2, but not COX-1, protein levels markedly increased following hypoxia. Use of the selective COX-2 inhibitor, NS-398, indicated that COX activity in hypoxic corneas or cells is essentially that of COX-2; in control cells, both COX-1 and COX-2 contributed equally to the production of PGE2. COX-2 protein overexpression induced by hypoxia was not associated with a parallel increase in PGE2 accumulation but the enzyme regained full catalytic activity when cells were re-exposed to normoxia in the presence of heme and arachidonic acid. Decreases in the levels of oxygen and heme, essential substrates/cofactors for COX catalytic activity, contributed to a diminished prostanoid production during hypoxia. These results suggest that in hypoxic injury, molecules other than COX-derived prostanoids play a major pro-inflammatory role. Furthermore, this study provides an explanation for the ineffectiveness of classical NSAIDs in the treatment of hypoxia-related ocular surface inflammation.

Animals↗
PubMed1996

Vinblastine toxicity to the ocular surface.

Local ocular exposure to antineoplastic drugs occurs either during regular use of some of these drugs in ophthalmology or accidentally during the general use of these drugs. Many ocular side effects have been described after such intentional or accidental exposures. We describe a case of accidental ocular trauma by vinblastine. As in one of the only two previously published cases of ocular trauma by vinblastine, our patient showed acute keratopathy with a drop in visual acuity followed by the development of dry eyes and a subepithelial corneal scar. In addition, in an attempt to further evaluate the clinical course and the benefits of steroid treatment, nine rabbits were studied after ocular instillation of vinblastine. After the trauma, local steroid treatment was given in one eye of each rabbit; the second eye served as a control. The animal studies showed acute conjunctivitis and keratopathy with increasing severity in the first days and improvement thereafter. That course was similar to the one manifested in our patient. Local steroid treatment in the rabbit eye had no effect as compared with the control group. A possible mechanism for the induction of dry eyes is discussed.

Accidents, Occupational↗
PubMed2005

Neurogenic inflammation: a first line of defense for the ocular surface.

Neurogenic inflammation and innate immunity may work together to protect mucosal surfaces, including the ocular surface. When the eye is exposed to pathogens, chemical irritants, or mechanical disruption, neurogenic inflammation is produced through release of neuromodulators, such as substance P and calcitonin gene-related peptide. This leads to the breakdown of the blood-tissue barrier, edema, and release of polymorphonuclear leukocytes into the tears, thus allowing intervention of systemic immunity. Neurogenic mechanisms may have a significant role in the onset and chronicity of ocular surface inflammation in conditions such as dry eye.

Journal Article↗
PubMed2000

Short-term effect of latanoprost and timolol eye drops on tear fluid and the ocular surface in patients with primary open-angle glaucoma and ocular hypertension.

PURPOSE: To investigate and compare the short term effects of topical latanoprost and timolol on the tear fluid and ocular surface condition in patients with bilateral primary open angle glaucoma or ocular hypertension. METHODS: Thirty-seven patients were included in this randomized, double-masked, parallel group study. Patients received either latanoprost 0.005% (n= 18) or timolol 0.5% (n= 19) instilled once daily in the morning for a treatment period of 27 days. Routine ophthalmic examinations, including intraocular pressure measurement, as well as tests to evaluate tear fluid and the ocular surface were performed. RESULTS: After one drop of medication, tear secretion was significantly reduced by timolol, but not by latanoprost. At the end of the study the break-up time (BUT) was significantly decreased in the timolol group but not in the latanoprost group. The BUT still remained in the normal range in both groups, although it is important to note that timolol was administered at half the clinical dose. Both latanoprost and timolol tended to increase Rose-Bengal staining of the cornea and conjunctiva after one month of treatment but no statistically significant difference was found between the groups. Corneal sensitivity was within the normal range for all patients during the study. CONCLUSION: Regarding ocular surface effects, no clinically important differences between latanoprost and timolol were observed as all the effects remained in the normal range.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Ocular surface management of photorefractive keratectomy and laser in situ keratomileusis.

PURPOSE: To examine the effects of keratorefractive surgery and ocular surface management on goblet cell density, dry eye symptom incidence, and spherical equivalent refraction. METHODS: We performed a retrospective analysis of four myopia groups: Untreated controls (n = 53); PRK (n = 51); LASIK without ocular surface management (n = 56); LASIK with ocular surface management (n = 140). Ocular surface management involved the routine use of non-preserved artificial tears and other lubricants before, during, and after surgery. Lid hygiene procedures, topical anti-inflammatory agents, and punctal plugs were used on indication. Assessments were conducted before and up to 12 months after surgery (right eyes only in patients with both eyes operated, and in the left or right eye in patients with one eye operated). RESULTS: Surgery caused a significant reduction in goblet cell density, with the greatest reduction in the LASIK without ocular surface management group. No significant differences were detected in dry eye symptoms or spherical equivalent refraction between PRK and LASIK without ocular surface management. Ocular surface management significantly minimized LASIK-induced decreases in goblet cell density and was associated with significantly less myopic outcomes at months 1 to 3 and 6 to 9 after LASIK. After surgery (1 to 3 mo), dry eye symptoms were significantly lower in the LASIK with ocular surface management group. In all groups, significant inverse correlations existed between goblet cell density and dry eye symptoms. CONCLUSIONS: Ocular surface management minimized the negative impact of LASIK on goblet cell density and reduced dry eye symptoms. Without ocular surface management, goblet cell density and dry eye symptoms after LASIK were similar to or worse than after PRK.

Adult↗
PubMed2005

Current concepts and challenges in ocular surface reconstruction using cultivated mucosal epithelial transplantation.

Ocular surface disorders wherein corneal stem cells are deficient result in total conjunctivalization leading to severe visual dysfunction and blindness. Treatment of these diseases requires reconstruction of the ocular surface using epithelial transplantation to provide a smooth refractive corneal surface and biologic and physical barriers against a variety of destructive factors. Recently, regenerative medicine focusing on tissue-engineered techniques has been developed and established as a new clinical field. In particular, cultivated mucosal epithelial transplantation using well-differentiated, stratified epithelial sheets on amniotic membrane allows a rapid re-epithelial cover over the entire corneal surface, resulting in early reduction of inflammation and cicatrization. This surgical approach dramatically improves the prognosis of severe ocular surface diseases, especially severely inflamed corneal stem cell deficiency. This new approach not only provides early epithelialization but also allows reconstruction of the corneal surface using autologous cultivated epithelium including the cornea and oral mucosa from a small number of cell sources after amplification. Tissue-engineered strategies using autologous corneal or oral mucosal epithelial sheet transplantation avoid the risk of rejection and complications associated with immunosuppressive treatments. In addition to new cellular transplantation, combined automated lamellar therapeutic keratoplasty provides better refractive stromal interference and contributes to performance and safety of cataract surgery in severe corneal opacity cases. Although long-term prognosis and cell biologic behavior of tissue-engineered epithelium after transplantation should be carefully monitored, these recent surgical treatments have opened a new field for ocular surface reconstruction.

Corneal Transplantation↗
PubMed1983

Conjunctival autograft transplantation for unilateral ocular surface diseases.

Rehabilitation of the diseased ocular surface by autologous conjunctival transplantation as first described by Thoft has expanded the possibilities for eventual visual restoration of patients with severe ocular surface disease. This paper will introduce a new surgical technique for diseased ocular surface preparation and for the acquisition, transfer, and placement of a 360 degrees ring of autologous conjunctiva in patients with unilateral surface pathology. Patients representing different unilateral surface diseases with up to 2 years follow-up are presented and discussed.

Adult↗
PubMed1993

Quantitative evaluation of the effectiveness of taurine in protecting the ocular surface against oxidant.

Quantitative evaluation of the effectiveness of taurine against ocular surface damage caused by hypochlorous acid (HOCl) was investigated using albino rabbits. The activity of lactate dehydrogenase (LDH) released from ocular tissues into meniscus tears at eye irritation was used as an index of ocular surface damage. Instead of collecting meniscus tears directly with a glass micropipette, a new sampling method, where 150 microliters of saline was instilled into the cul-de-sac of rabbit eyes and collected all of the diluted tears within 10 s, was developed. The LDH activity after serial instillations of HOCl increased dose-dependently with increasing HOCl concentration. After serial instillation of taurine, HOCl was instilled in the same way. Pre-application of taurine effectively suppressed (p < 0.01, n = 11) the HOCl-induced LDH release as compared to saline, suggesting that the residual taurine in ocular surface tissues was still effective in protecting the tissues against HOCl by scavenging HOCl. LDH activity at 30 in after post-application of taurine was significantly lower (p < 0.01, n = 10) than that in the case of saline. This result indicates that taurine is effective in protecting the ocular surface after it has been attacked by HOCl. LDH activity in meniscus tears became a good index of quantitatively estimating ocular surface damage due to HOCl by devising the new sampling method. By using this method, we were able to prove objectively and quantitatively that taurine is effective in protecting the ocular surface against HOCl. It was suggested that taurine is clinically useful in the treatment of ocular surface damage caused by oxidants, such as HOCl.

Animals↗
PubMed2002

Changes in conjunctival clusterin expression in severe ocular surface disease.

PURPOSE: Clusterin is a unique gene transcript in the human ocular surface epithelia and is synthesized by and localized in mucosal epithelia in general. It is not present, however, in keratinized epithelia, such as epidermis. In severe ocular surface disease, pathologic keratinization (squamous metaplasia) of the ordinarily nonkeratinized corneal and conjunctival mucosal epithelia results in severe visual loss. In the current study, the expression of clusterin was examined in conjunctivalized corneas with severe ocular surface disease. METHODS: We examined conjunctiva covering cornea in eight eyes with ocular surface disease (Stevens-Johnson syndrome and ocular cicatricial pemphigoid) in which pathologic keratinization was present. Normal conjunctiva from four age-matched individuals served as the control. Semiquantitative RT-PCR was used to investigate expression of the clusterin gene. Immunohistochemistry was used to study the distribution of clusterin protein. RESULTS: The level of clusterin mRNA was significantly lower than normal in the diseased ocular surfaces. Clusterin protein was also markedly decreased in keratinized conjunctiva compared with that in normal eyes. CONCLUSIONS: Clusterin expression is markedly reduced in the pathologic, keratinized ocular surface epithelium, suggesting its importance in maintaining the ocular surface epithelium as a nonkeratinizing epithelium.

Adult↗
PubMed1997

Important concepts for treating ocular surface and tear disorders.

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.

Animals↗
PubMed1998

Antimetabolites in ocular surface neoplasia.

Malignant neoplasms of the ocular surface are uncommon but consist of squamous and melanocytic tumors. Surgical excision has been the mainstay of treatment and is perhaps the "gold standard." However, in those circumstances in which surgical intervention is not feasible, adjunctive treatments have been advocated. Recent attention has been given to the use of mitomycin C and 5-fluorouracil for the treatment of ocular surface squamous neoplasia. This article reviews the major publications relating to the use of antimetabolites in ocular surface neoplasia and highlights the most recent contributions to the ophthalmic literature.

Antimetabolites, Antineoplastic↗
PubMed1998

The pathology of dry eye: the interaction between the ocular surface and lacrimal glands.

BACKGROUND: Most dry-eye symptoms result from an abnormal, nonlubricative ocular surface that increases shear forces under the eyelids and diminishes the ability of the ocular surface to respond to environmental challenges. This ocular-surface dysfunction may result from immunocompromise due to systemic autoimmune disease or may occur locally from a decrease in systemic androgen support to the lacrimal gland as seen in aging, most frequently in the menopausal female. HYPOTHESIS: Components of the ocular surface (cornea, conjunctiva, accessory lacrimal glands, and meibomian glands), the main lacrimal gland, and interconnecting innervation act as a functional unit. When one portion is compromised, normal lacrimal support of the ocular surface is impaired. Resulting immune-based inflammation can lead to lacrimal gland and neural dysfunction. This progression yields the OS symptoms associated with dry eye. THERAPY: Restoration of lacrimal function involves resolution of lymphocytic activation and inflammation. This has been demonstrated in the MRL/lpr mouse using systemic androgens or cyclosporine and in the dry-eye dog using topical cyclosporine. The efficacy of cyclosporine may be due to its immunomodulatory and antiinflammatory (phosphatase inhibitory capability) functions on the ocular surface, resulting in a normalization of nerve traffic. CONCLUSION: Although the etiologies of dry eye are varied, common to all ocular-surface disease is an underlying cytokine/receptor-mediated inflammatory process. By treating this process, it may be possible to normalize the ocular surface/lacrimal neural reflex and facilitate ocular surface healing.

Animals↗
PubMed2001

Characteristics of the human ocular surface epithelium.

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, ssig-h3, cathepsin L2 (cathepsin V), uroplakin Ib, and Ca(2+)-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 ssig-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-ss (TGF-ss), 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.

Apoptosis↗
PubMed2001

The role of nitric oxide in ocular surface diseases.

The role of nitric oxide (NO) in ocular surface diseases remains unknown. We investigated the conditions leading to increase NO generation in tears and the main sources of ocular surface tissue. We evaluated the possibility of a dual action (cell survival or cell death) depending on the amount of NO. The concentration of nitrite plus nitrate, the stable end-product of NO, was measured in the tears of various ocular surface diseases. We also examined the main source of nitric oxide synthase (NOS) using immunohistochemical staining & Western blot analysis. When cultured human corneal fibroblasts were treated with NO producing donor with or without serum, the viability of cells was studied. We found that sources of NO in ocular surface tissue primarily included corneal epithelium, fibroblasts, endothelium and inflammatory cells. Three forms of NOS (eNOS, bNOS, & iNOS) were expressed in experimentally induced inflammation. Cell death by NO revealed TUNEL positive staining, however in the EM finding, this NO specific cell death was an atypical necrosis showing perinuclear large vacuolization and mitochondrial swelling. In the fibroblasts culture system, the NO donor (SNAP, S-nitroso-N-acetyl-D, L-penicillamine) prevented the death of corneal fibroblasts caused by serum deprivation in a dose dependent manner up to 500 m SNAP, although a higher dose decreased cell viability. This study suggested that NO might act as a double-edged sword in ocular surface disease depending on the degree of inflammatory condition related with NO concentration.

Animals↗
PubMedDate not supplied

Adnexal surgery for severe ocular surface disease.

Secondary causes of ocular surface disease are-to a large extent-due to disorders of the ocular adnexae. The main pathomechanisms involved include exposure, abrasion and malnutrition, resulting from a multitude of disorders such as ec- or entropion (e.g. in cicatrizing conjunctivitis), lid retraction and severe aqueous deficiency. In the presence of these problems, surgical attempts of ocular surface reconstruction frequently fail. Here we review established and evolving new techniques in the field of adnexal surgery to specifically address these problems.

Corneal Diseases↗
PubMed2004

Successful primary culture and autologous transplantation of corneal limbal epithelial cells from minimal biopsy for unilateral severe ocular surface disease.

BACKGROUND: Patients with severe unilateral ocular surface disease require reconstruction of the damaged ocular surface. We succeeded in culturing primary corneal limbal epithelial cells taken from minimal biopsy and, once grown, transplanting them on denuded amniotic membrane (AM). METHODS: Autologous corneal limbal epithelial cells from a 3 mm(2) biopsy of the uninjured eye were grown for 3 weeks on a denuded AM carrier. The resultant sheet was then transplanted onto the unilateral severely chemically injured eye. RESULTS: Minimal biopsy showed the autologous cultivated corneal epithelial cells to have 4-5 layers of sufficient stratification and to be well differentiated. At 19 months post-transplantation, the ocular surface epithelium was stable and there were no epithelial defects. CONCLUSION: We document that it is possible to produce sufficiently stratified, well differentiated, autologous cultivated corneal limbal epithelium on AM from a minimal biopsy of the donor eye and to transplant it onto the injured eye.

Adult↗