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To present a case series of patients with corneal scars who were successfully fitted with mini scleral contact lenses (mSCL).

Purpose: To investigate intraoperative anterior segment optical coherence tomography (AS-OCT) to compare pachymetry changes between two methods (group 1: speculum-on, group 2: speculum-off during riboflavin instillation stage) during corneal cross-linking /CXL) (9 mW/cm2for 10 min) in keratoconic patients. Methods: In this interventional case series, 11 eyes (11 patients) in group 1 and 14 eyes (14 patients) in group 2 were enrolled. Pachymetry measurements by spectral domain OCT was performed at baseline, after epithelial removal, after 30 min of imbibition with riboflavin, and after UV irradiation. Repeated measures analysis of variance was used to compare the trend of changes in different stages of the procedure within and between two groups. Results: The corneal thinnest pachymerty (CTP) at baseline, after epithelial removal, 30 min of riboflavin instillation, and irradiation was 469.8±26.5, 438.0±27.1, 354.3±28.4, 367.1±31.8 microns in group 1 and 463.2±25.1, 438.0±27.1, 421.6±54.0, 386.9±34.0 microns in group 2, respectively. Group 1 showed a significantly greater decrease in the corneal pachymetry (P<0.001) during riboflavin instillation, while in group 2 a greater decrease in CTP was observed during the UV irradiation phase (P=0.002). Conclusions: Using the intraoperative OCT, the speculum-off group had a more stable corneal pachymetry during riboflavin instillation time. Despite this, the effect was not lasting throughout the procedure; significant changes were noted in the corneal pachymetry at the end of operation in both groups; further highlighting the limitations imposed by corneal stromal shrinkage using isotonic dextran containing riboflavin solution for CXL.

Purpose Propagation of light through the optical pathway within the eye can lead to a deformation of the wave front that might affect objective but also subjective refraction depending on pupil size. The aim of this study was to investigate the change in wave front refraction that is calculated on the basis of second order Zernike polynomials when varying the pupil size from 6 mm to 3 mm. The change was correlated with the amount of fourth and sixth order spherical aberration and fourth and sixth order astigmatism.Methods Wave front aberrations were measured in 130 eyes by means of a Tscherning wave front sensor at a pupil size of 6 mm. Wave front aberrations in terms of Zernike coefficients up to sixth order were approximated for 6 mm and 3 mm pupil size. The wave front refraction was calculated based on the second order Zernike coefficients for both pupil diameters. Resulting differences in wave front refraction (sphere or cylinder) due to the change in pupil size were correlated with the initial higher order aberrations determined for the 6.0 mm pupil by means of a linear regression (Spearman rank correlation coefficient).Results The correlation between the change in sphere and cylinder on one hand and the spherical aberration and higher order astigmatism on the other hand was found to be highly significant (p<0.001), with a correlation coefficient of R = 0.96 for sphere and R = 0.85 for cylinder.Conclusions Calculating the wave front refraction on the basis of second order Zernike polynomials is plagued with the influence of the higher order aberration preexisting in the individual eye. This is one reason why this method does not represent precisely enough subjective refraction. Other methods that calculate the refraction based on wave front measurement independent from the pupil size should be established in the ophthalmic community.

Age-related macular degeneration (AMD) is a main causes of severe visual impairment in the elderly in industrialized countries. The pathogenesis of this complex diseases is largely unknown, even though clinical characteristics and histopathology are well described. Because several aging changes are identical to those observed in AMD, there appears to exist an unknown switch mechanism from normal ageing to disease. Recent anatomical studies using elegant innovative techniques reveal that there is a 30% rod loss in normal ageing, which is increased in early AMD. Those and other observations by Curcio and co-workers indicate that early rod loss is an important denominator of AMD (Curcio CA. Eye 2001; 15:376). As in retinitis pigmentosa (RP), rods appear to die by apoptosis. Thus it seems mandatory to study the regulation of rod cell death in animal models to unravel possible mechanisms of rod loss in AMD. Our laboratory investigates signal transduction pathways and gene regulation of rod death in our model of light-induced apoptosis. The transcription factor AP1 is essential, whereas other classical pro- and antiapoptotic genes appear to be less important in our model system. Caspase-1 gene expression is distinctly upregulated after light exposure and there are several factors which completely protect against light-induced cell death, such as the anesthetic halothane, dexamethasone and the absence of bleachable rhodopsin during light exposure. A fast rhodopsin regeneration rate increased damage susceptibility. Our data indicate that rhodopsin is essential for the initiation of light-induced rod loss. Following photon absorption, there may be the generation of photochemically active molecules wich then induce the apoptotic death cascade.

Structure-function analysis as well as studies with knock-out and transgenic mice have assigned distinct functions to c-Fos and Fra-1, two components of the transcription factor AP-1 (activator protein-1). To test whether Fra-1 could substitute for c-Fos, we generated knock-in mice that express Fra-1 in place of c-Fos. Fra-1 rescues c-Fos-dependent functions such as bone development and light-induced photoreceptor apoptosis. Importantly, rescue of bone cell differentiation, but not photoreceptor apoptosis, is gene-dosage dependent. Moreover, Fra-1 fails to substitute for c-Fos in inducing expression of target genes in fibroblasts. These results show that c-Fos and Fra-1 have maintained functional equivalence during vertebrate evolution.

AbstractSilent sinus syndrome is a rare disease of the maxillary sinus characterized by bony absorption processes leading to progressive sinus wall thinning with consecutive enophthalmos and hypoglobus. It represents a benign cause of acquired enophthalmos and is often accompanied by painless vertical diplopia, the latter treated surgically in all cases published to date. We report a 56-year-old patient with silent sinus syndrome in whom vertical diplopia was treated with prisms showing that conservative treatment alone may, in mild cases, be an effective alternative to reconstructive surgery.

Purpose:Corneal collagen crosslinking can arrest the progression of LASIK-induced keratectasia. We report a patient who developed bilateral iatrogenic keratectasia only during her first pregnancy at three years after initial LASIK. We performed bilateral corneal collagen crosslinking. In the following two consecutive years, keratectasia remained stable and even regressed. Upon her second pregnancy at two years after crosslinking, keratectasia exacerbated again.