Purpose Degenerative myopia is a significant cause of vision loss; yet there is no accepted way of controlling its causative phenotypeFprogressive high axial myopia. Scleral reinforcement, introduced over 50 years ago, was discredited as a useful technique. This 5-year 'proof of concept' study examines buckling of the posterior pole for myopia control and follows the course of untreated fellow eyes. Method A total of 59 adult eyes, with myopic refractive corrections ranging from À9 to À22 D and axial lengths from 27.8 to 34.6 mm, were studied. A 1-cm-wide flexible buckle of donor sclera was positioned over the posterior pole and secured, under positive tension, to the anterior globe. The eyes were monitored for 5 years, as were unsupported fellow eyes. The axial lengths, visual acuities, and optical coherence tomography macular scans were collected and all complications were noted. Results Over 5 years, axial length control was achieved by scleral buckling, whereas axial extension progressed in the untreated group. No serious complication occurred and no eye lost visual acuity from the procedure. Temporary intra-ocular pressure elevation, small choroidal effusions, and variable periods of abduction limitation occurred after surgery. In one case of tractional myopic macular schisis, a full correction was achieved by buckling and visual acuity improved.

There has been generally little attention paid to the utilization of biomaterials as an anti-myopia treatment. The purpose of this study was to investigate whether polymeric hydrogels, either implanted or injected adjacent to the outer scleral surface, slow ocular elongation. White Leghorn (gallus gallus domesticus) chicks were used at 2 weeks of age. Chicks had either (1) strip of poly(2-hydroxyethyl methacrylate) (pHEMA) implanted monocularly against the outer sclera at the posterior pole, or (2) an in situ polymerizing gel [main ingredient: poly(vinyl-pyrrolidone) (PVP)] injected monocularly at the same location. Some of the eyes injected with the polymer were fitted with a diffuser or a −10D lens. In each experiment, ocular lengths were measured at regular intervals by high frequency Ascan ultrasonography, and chicks were sacrificed for histology at staged intervals. No in vivo signs of either orbital or ocular inflammation were observed. The pHEMA implant significantly increased scleral thickness by the third week, and the implant became encapsulated with fibrous tissue. The PVP-injected eyes left otherwise untreated, showed a significant increase in scleral thickness, due to increased chondrocyte proliferation and extracellular matrix deposition. However, there was no effect of the PVP injection on ocular elongation. In eyes wearing optical devices, there was no effect on either scleral thickness or ocular elongation. These results represent "proof of principle" that scleral growth can be manipulated without adverse inflammatory responses. However, since neither approach slowed ocular elongation, additional factors must influence scleral surface area expansion in the avian eye.

No abstract

No abstract