A Biomechanical Hypothesis for Myopia Progression Involving Superior Oblique Muscle Traction and Orbital Fat Redistribution

The global epidemic of myopia is accelerating, and conventional hypotheses based on genetic growth and uniform tissue remodeling cannot fully account for clinical findings such as adult-onset myopia, unilateral progression, and optic disc tilt. We propose a novel biomechanical hypothesis: sustained downward gaze causes traction via the superior oblique muscle, leading to trochlear translation of the eyeball and asymmetric redistribution of orbital fat. This mechanical displacement creates localized stress at the posterior pole, stimulating scleral remodeling and axial elongation through the TGF-β and MMP signaling pathways. Supporting evidence includes MRI-based eye movement analysis, biomechanical modeling, anatomical findings of orbital structures, clinical OCT observations of optic disc tilt progression, and finite element analysis of extraocular muscle influence on the posterior pole. This hypothesis predicts that future longitudinal MRI and OCT studies will reveal correlations between orbital fat displacement and changes in axial length and optic disc morphology. If validated, this model could redefine myopia as a reversible biomechanical condition and support the development of new preventive, diagnostic, and therapeutic strategies.