In-vivo characterization of scleral rigidity in myopic eyes using fundus-pulsation optical coherence elastography.

The sclera plays an important role in the structural integrity of the eye. However, as myopia progresses, the elongation of the eyeball exerts stretching forces on the posterior sclera, which typically happens in conjunction with scleral remodeling that causes rigidity loss. These biomechanical alterations can cause localized eyeball deformation and vision impairment. Therefore, monitoring scleral rigidity is clinically important for the management and risk assessment of myopia. In this study, we propose fundus pulsation optical coherence elastography (FP-OCE) to characterize posterior scleral rigidity in living humans. This methodology is based on a choroidal pulsation model, where the scleral rigidity is inversely associated with the choroidal max strain obtained through phase-sensitive optical coherence tomography (PhS-OCT) measurement of choroidal deformation and thickness. Using FP-OCE, we conducted a pilot clinical study to explore the relationship between choroidal strain and myopia severity. The results revealed a significant increase in choroidal max strain in pathologic myopia, indicating a critical threshold beyond which scleral rigidity decreases significantly. Our findings offer a potential new method for monitoring myopia progression and evaluating therapies that alter scleral mechanical properties.

Intravitreal injection analysis at the Bascom Palmer Eye Institute: evaluation of clinical indications for the treatment and incidence rates of endophthalmitis.

OBJECTIVE: To report the incidence of endophthalmitis, in addition to its clinical and microbiological aspects, after intravitreal injection of vascular-targeting agents. METHODS: A retrospective review of a consecutive series of 10,142 intravitreal injections of vascular targeting agents (bevacizumab, ranibizumab, triamcinolone acetonide, and preservative-free triamcinolone acetonide) between June 1, 2007 and January 31, 2010, performed by a single service (TGM) at the Bascom Palmer Eye Institute. RESULTS: One case of clinically-suspected endophthalmitis was identified out of a total of 10,142 injections (0.009%), presenting within three days of injection of bevacizumab. The case was culture-positive for Staphylococcus epidermidis. Final visual acuity was 20/40 after pars plana vitrectomy surgery. CONCLUSIONS: In this series, the incidence of culture-positive endophthalmitis after intravitreal injection of vascular agents in an outpatient setting was very low. We believe that following a standardized injection protocol, adherence to sterile techniques and proper patient follow-up are determining factors for low incidence rates.

Matrix metalloproteinase-9 knockout confers resistance to corneal epithelial barrier disruption in experimental dry eye.

Altered corneal epithelial barrier function is the cause for ocular irritation and visual morbidity in dry eye disease. Increased matrix metalloproteinase (MMP)-9 activity has been observed in the tear fluid of dry eye patients. To determine the pathogenic role of MMP-9 in the corneal epithelial disease of dry eye, the effects of experimentally induced dry eye on corneal epithelial morphology and barrier function were compared in MMP-9 knockout mice and their wild-type littermates. Dry eye was created through cholinergic blockade and exposure to a desiccating environment. The tear fluid MMP-9 concentration increased in response to dryness in wild-type mice. Corneal epithelial permeability to three different-sized molecules increased in dry eye wild-type mice, but not in MMP-9 knockout mice. Topical administration of active MMP-9 to dry eye MMP-9 knockout mice significantly increased corneal epithelial permeability. Compared to MMP-9 knockout mice, wild-type mice showed greater desquamation of differentiated apical corneal epithelial cells that expressed the tight junction protein occludin in response to dryness. This was accompanied by an increase in lower sized (50 kd) occludin in the corneal epithelia of wild-type mice. These findings could be replicated in cultured human corneal epithelial cells that were treated with active MMP-9. These studies indicate that increased MMP-9 activity on the ocular surface in response to dryness disrupts corneal epithelial barrier function. This appears to be because of accelerated loss of tight junction bearing superficial corneal epithelial cells, perhaps by proteolytic cleavage of occludin.