Mechanism of myopic axial elongation related to Bruch´s membrane

The process of myopic axial elongation has not been fully uncovered yet. Here we propose a Bruch´s membrane (BM)-related hypothesis und present anatomical and clinical findings supporting it.

The hypothesis is that ocular axial elongation beyond the age of 3 years occurs by a retina-triggered annular segmental growth of BM in the posterior fundus midperiphery between approximately 10° to 80° anterior to the posterior pole, with a maximum growth at approximately 25° anterior to the posterior pole.

The location of the posterior midperiphery is supported by anatomical findings of an axial length-related thinning of retinal layers, sclera, and retinal pigment epithelium in the posterior midperiphery, the location of pathologic changes at the anterior and posterior border of the BM growth zone (patchy atrophies, parapapillary myopia beta zone and gamma zone, optic nerve head canal widening, cobble stones), and results of clinical trials on myopia prevention in adolescents by circular progressive contact lenses or glasses. The notion of BM as compared to sclera as the primary structure elongating the eye is supported by the axial length-related choroidal thinning most marked at the posterior pole, the axial length-related increase in BM volume, the axial length-related shift of BM-opening of the ONHC into the macular direction, the biomechanical properties of BM, and by primarily not involving the retina, RPE and choriocapillaris in the foveal region.

If BM is the primary effector structure for axial elongation, future research may address the retinal messenger molecule directing the RPE to locally produce BM.