No abstract

Objective To investigate the effects of scleral collagen cross-linking (SXL) using riboflavin and ultraviolet A (UVA) light on the scleral thickness of different regions and expression of matrix metalloproteinase 2 (MMP-2) and membrane-type MMP-1 (MT1-MMP) in guinea pigs with lens-induced myopia. Methods Forty-eight 4-week-old guinea pigs were assigned to three groups (n = 16 per group): SXL group, lens-induced myopia (LIM) group, and control group. The sclera of the right eye of the guinea pig in the SXL group was surgically exposed, riboflavin was dropped on the treatment area for 10 minutes before the 30-minute UVA irradiation. The same surgical procedure was performed in the LIM group without UVA irradiation. The -10.00 D lenses were then placed on the right eyes of guinea pigs in the SXL and LIM groups for six weeks. The control group received no treatment. The left eyes were untreated in all groups. The ocular axial length (AXL) and refraction were measured at 4 weeks and 10 weeks of age. 10-week-old guinea pigs were sacrificed, and the right eyes were enucleated and evenly divided for preparation of hematoxylin and eosin (HE) stained sections, quantitative real-time polymerase chain reaction (qPCR) and western blotting. The scleral thickness of different regions was measured on HE stained sections. The temporal half of the sclera was harvested to measure the expression of MMP-2 and MT1-MMP by qPCR and western blotting. Results The AXL was significantly shorter, and the degree of myopic refraction was significantly lower in the SXL group than those in the LIM group at 10 weeks of age. The scleral thickness of the cross-linked area was significantly greater in the SXL group than that of the corresponding area in the LIM group, while the scleral thickness of the untreated nasal side was not significantly different between the SXL group and the LIM group. The expression of MMP-2 and MT1-MMP of the cross-linked sclera was significantly downregulated compared with that of the corresponding area in the LIM group. Conclusion Riboflavin/UVA SXL could slow myopia progression and thicken the cross-linked sclera in guinea pigs, which might be related to the downregulation of MMP-2 and MT1-MMP expression during the scleral remodeling process.

Introduction To investigate the feasibility and safety of scleral ultraviolet A (UVA) cross-linking (scleral CXL) on pathologically blindness. Methods This was a prospective, observational clinical study. Five patients with monocular blindness due to pathological myopic maculopathy were enrolled. Eyes with best corrected visual acuity (BCVA) under 0.05 were defined as experimental eyes. The fellow eyes were defined as control eyes. Patients first underwent posterior scleral reinforcement (PSR) surgery in the control eye. Thereafter, scleral CXL surgery was performed in the experimental eye on the same day. Visual acuity, BCVA, slit lamp biomicroscopic examination, intraocular pressure measurement, corneal specula microscopies, axis length measurement, funduscopy with pupil dilation, color fundus photography, full-field flash electroretinography, optical coherence tomography, and color Doppler flow imaging were performed at baseline, 1 week, 1 month, 3 months, 6 months, and 12 months after surgery. Results No signs of inflammation were observed after operation and throughout the follow-up period. Retinoschisis was improved, while choroidal neovascularization fibrosis and retinal and choroidal atrophy were unchanged after scleral CXL. There were no statistically significant differences in the ophthalmic artery, central retinal artery, and posterior ciliary artery parameters of color Doppler flow imaging or in retinal thickness, within experimental and control eyes, at baseline, 1 week, 1 month, 3 months, or 12 months ( P > 0.05). Conclusions This pilot study verified the feasibility and safety of scleral CXL on human blindness. The UVA-CXL on the sclera of human eyes seems to have the same effect as PSR in preventing progressive pathological myopia in the future. Trial Registration Chinese Clinical Trial Registry (ChiCTR2100042422).