The healing response in corneas after RGX is very similar to that observed after DE alone, suggesting that, along with its short treatment time and limited effect on keratocytes, RGX displays good potential for clinical cornea stiffening.
These results indicate that corneal stiffness increases after CXL, and further increases as a function of time after both RGX and UVX. Also, while biomechanical properties determined after ex vivo CXL are indicative of corneal stiffening, they may not provide entirely accurate information about the responses to CXL in vivo.
Purpose: To determine the effects of intravitreal atropine on scleral growth in the form-deprived chick as an experimental model of myopia. Methods: Five groups of five chicks were studied from day 0-12 post-hatching. One group remained untreated (C), and four were form-deprived by monocular light diffusers to induce myopia. Two groups (RL and A) wore diffusers for 9 days, and the other two groups (D and D + A) wore diffusers throughout the study. Group D received no further treatment (myopia positive control). Groups A and D + A received intravitreal injections of atropine for days 9-12. Measurements of refractive error and axial length were performed on days 0, 9, and 12. Sclera changes were assessed in cartilaginous and fibrous layers by histological analysis. Results: All form-deprived eyes had a myopic refractive error on day 9. All atropine-treated groups were hyperopic on day 12. The effect of atropine was most evident in Group D + A in which diffusers were maintained throughout treatment and changes in refractive error were statistically significant. The observed changes in axial length were in line with the changes in refractive error. The scleral fibrous layer thickness increased, and the sceral cartilaginous layer underwent a slight thinning compared to Group D, the myopia positive control. Conclusions: If the signals that induce growth remain during atropine treatment, morphological changes in sclera are produced: the scleral fibrous layer thickened, and the sceral cartilaginous layer thinned. These changes resulted in refractive error recovery, and the ocular growth was stopped. The data suggested the atropine was acting throughout the scleral fibrous layer.
PURPOSE. To study corneal wound healing after two cross-linking techniques using either rose bengal and green light (RGX) or the conventional treatment using riboflavin and UVA radiation (UVX). METHODS. Corneas of New Zealand rabbits were monolaterally treated with UVX (21 eyes) or RGX (25 eyes). Treatments involved corneal de-epithelialization (8-mm diameter), soaking with photosensitizer (0.1% riboflavin in 20% dextran for 30 minutes for UVX; 0.1% rose bengal for 2 minutes for RGX), and light irradiation (370 nm, 3 mW/cm 2 , 30 minutes for UVX; 532 nm, 0.25 W/cm 2 , 7 minutes for RGX). Contralateral eyes were used as controls. Clinical follow-up included fluorescein staining, haze measurement, and pachymetry. Healing events analyzed after euthanasia at 2, 30, and 60 days included cell death (TUNEL assay), cell proliferation (BrdU [bromodeoxyuridine] immunofluorescence), and differentiation to myofibroblasts (a-SMA [alpha smooth muscle actin] immunohistochemistry). RESULTS. Re-epithelialization and pachymetries were similar after RGX and UVX. The haze from day 1 to 15 was greater after UVX. Cell death was deeper after UVX, being localized in the anterior and middle stroma, and was superficial (anterior third) after RGX. Cell proliferation appeared after 2 days and was localized in the middle and posterior stroma in the UVX group but was superficial in the RGX group. After 60 days the number of stromal cells had not returned to the control number in either group. CONCLUSIONS. The deeper and longer-lasting cell damage caused by UVX compared to RGX may underlie the slower cell repopulation after UVX and other differences in healing. Shallower damage and a shorter treatment time suggest that RGX may be appropriate for stiffening thin corneas.
Purpose To evaluate corneal wound healing in the hen animal model after additive surgery with an intracorneal ring segment (ICRS). Methods We implanted one ICRS in each eye of 76 hens. In control group 1 (n=22 hens), the stromal channel was prepared but no ICRS was inserted. In control group 2 (n=2 hens), no surgery was performed. Animals were randomly separated into groups and euthanized after clinical follow-up of 4 and 12 hours, 1, 2, 3, and 7 days, and 1, 2, 3, 4, and 6 months. Corneas were stained with hematoxylin-eosin. Apoptosis was measured by terminal uridine nick end-labeling assays. Cell proliferation and myofibroblast-like differentiation were assayed by BrdU and α-smooth muscle actin immunofluorescence microscopy. Stromal matrix changes were documented by electron microscopy.Results Epithelial and stromal cell apoptosis around the ICRS-implanted and control group 1 eyes peaked at 12 hours, but continued for 72 hours. In ICRSimplanted eyes, epithelial and stromal proliferation was present at 12 and 24 hours, respectively, and peaked at 7 days and 72 hours, respectively. Some proliferation in the ICRS-implanted group continued through the 6-month follow-up, and myofibroblast-like cells differentiated one to three months after ICRS implantation. The segments rotated within the stroma as the limbal inferior angle approached the epithelium. Conclusions Wound healing after ICRS implantation in hen corneas was similar to that of other corneal surgical wounds in stages. However, there were some specific features related to the small size of the epithelial wound and the device permanently implanted inside the cornea.
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