Occlusion of retinal capillaries caused by glial cell proliferation in chronic ocular inflammation.

The inner blood-retinal barrier is a gliovascular unit in which glial cells surround capillary endothelial cells and regulate retinal capillaries by paracrine interactions. During chronic ocular inflammation, microvascular complications can give rise to vascular proliferative lesions, which compromise visual acuity. This pathologic remodelling caused by proliferating Müller cells determines occlusion of retinal capillaries. The aim of the present study was to identify qualitative and quantitative alterations in the retinal capillaries in patients with post-traumatic chronic ocular inflammation or post-thrombotic vascular glaucoma. Moreover, we investigated the potential role of vascular endothelial growth factor (VEGF) and pro-inflammatory cytokines in retinal inflammation. Our electron microscopy findings demonstrated that during chronic ocular inflammation, thickening of the basement membrane, loss of pericytes and endothelial cells and proliferation of Müller cells occur with irreversible occlusion of retinal capillaries. Angiogenesis takes place as part of a regenerative reaction that results in fibrosis. We believe that VEGF and pro-inflammatory cytokines may be potential therapeutic targets in the treatment of this disease although further studies are required to confirm these findings.

Immunohistochemical profile of VEGF, TGF-ß and PGE2 in human pterygium and normal conjunctiva: experimental study and review of the literature.

Human pterygium is made up of chronic proliferative fibro-vascular tissue growing on the ocular surface. This disease exhibits both degenerative and hyperplastic properties. Some fibroangiogenic factors have recently been shown to play a potential role in fibrovascular diseases via the angiogenesis process. The aim of this study is to evaluate VEGF, TGF-ß and PGE2 expression in the epithelial, endothelial and stromal cells of human pterygium and normal conjunctiva in order to determine whether these factors participate in the development of pterygium. Ten specimens from patients with pterygium and two normal conjunctivas (cadavers) were analyzed by immunohistochemistry using specific antibodies against these growth factors. The technique used was ABC/HRP (Avidin complexed with biotinylated peroxidase). Immunoreactivity of VEGF was significantly increased in the epithelium, vascular endothelium and stromal cells in primary pterygium as compared with normal conjunctiva. A moderate expression of TGF-ß in the pterygium was observed in the epithelial and stromal layers. On the contrary, immunolabeling of this growth factor in the human normal conjunctiva was weak. PGE2 was strongly expressed in the epithelium of patients with pterygium, as in control conjunctival tissues, and the immunolabeling was moderate in the stroma from the same patients. Our results suggest that these growth factors may contribute to the progression of primary pterygium by increasing angiogenesis, thus leading to the formation of new blood vessels from the pre-existing vasculature. We conclude that VEGF, TGF-ß and PGE2 may be potential therapeutic targets in the treatment of this disease although proof of this evidence requires further studies.

Keratoconus: the possible involvement of inflammatory cytokines in its pathogenesis. An experimental study and review of the literature.

OBJECTIVE: Keratoconus (KC) is generally described as a non-inflammatory disease, characterized by thinning in the central region of the cornea with consequent tissue degradation producing impaired visual acuity. MATERIALS AND METHODS: In our experimental study, we analyzed the presence and implications of several inflammatory cytokines in the corneal tissues of patients suffering from keratoconus by immunohistochemical analysis. RESULTS: The analysis showed increased levels of inflammatory factors in the pathological tissues compared to controls, confirming that KC cannot be considered an entirely non-inflammatory pathology and that its etiopathogenesis includes several chronic inflammatory events. CONCLUSIONS: In the light of these results, the classification of KC as an inflammatory pathology or as a pathology related to inflammation might be useful in directing future research aimed at developing effective anti-inflammatory therapies to pharmacologically target the inflammatory mediators which contribute to the development and progression of the disease.

The role of inflammation in diabetic retinopathy: a review.

OBJECTIVE: Diabetic retinopathy and diabetes represent serious health conditions, being considered among the main causes of blindness. In recent years, anti-VEGF therapies have been of great help in the treatment of retinal pathology and, until now, they represent the primary choice therapy for diabetic retinopathy. Nevertheless, many patients do not experience significant benefits of vision after an anti-VEGF monotherapy. For this reason, several researchers recently focused their attention on the mechanisms that play a central role in the development and progression of diabetic retinopathy. RESULTS: Available scientific evidence confirms that diabetic retinopathy requires other molecules capable of modifying the mechanisms that, together with angiogenesis, contribute to the development of the condition, such as vascular and neuroinflammation. CONCLUSIONS: This review summarizes the current knowledge of the pathological changes that occur in diabetic retinopathy and that might contribute to identify possible new strategies for the treatment of this condition.

[Waardenburg Syndrome: a review of literature and case reports]. / Revisione critica della letteratura sulla Sindrome di Waardenburg e presentazione di due casi clinici.

Waadernburg syndrome (WS) is an autosomal dominant disease clinically and genetically heterogeneous. It is characterized by non-progressive sensorineuronal hearing loss of variable degree and anomalous pigmentation (of the eyes, skin and stria vascularis of cochlear duct) caused by melanocytes absence. The syndrome is caused by mutations in genes that regulate the melanocytes differentiation from the neural crest during embriogenetic development. This study will review the literature on WS and explain more in detail the ocular findings in WS, while reporting new findings on two newly diagnosed cases.

Idiopathic juxtafoveal retinal telangiectasis and retinal macroaneurysm treated with indocyanine green dye-enhanced photocoagulation.

This case report presents the use of indocyanine green dye-enhanced photocoagulation (ICG-DEP) for the treatment of idiopathic juxtafoveal retinal telangiectasis and a retinal macroaneurysm. A 35-year-old male with 20/20 vision had been followed for 5 years for a retinal macroaneurysm with retinal telangiectasis outside the macular area. He then presented with a recently decreased vision in his right. He had macular edema with a new area of idiopathic juxtafoveal retinal telangiectasis. After 4 focal argon laser treatments, angiographic closure of the lesions was not obtained and the retinal edema remained. After 3 sessions of ICG-DEP, the lesions were closed and the edema absorbed. The 810 nm infrared laser with ICG-DEP should be considered for the treatment of idiopathic juxtafoveal retinal telangiectasis and retinal macroaneurysms. In this case the procedure appears to be safe and well tolerated. It may allow for more direct energy absorption than that of the argon laser to these types of retinal lesions with better tissue closure.