Abstract
At birth, the eye is moderately hypermetropic but achieves emmetropia by the age of 5?6 years in a large majority (Chakraborty et al., 2020; Gwiazda et al., 1993). The process of emmetropization is attributed to changes in several components of the eye structure, predominantly cornea, crystalline lens and axial length. Emmetropization is possible only when there is a fine balance between the optical power of the eye and its focal length. The former is determined by the combined dioptric power of the cornea and crystalline lens and the latter by the axial length of the eyeball. Increase in axial length has been shown to be the most important factor for reaching emmetropia. The main determinant of this increase is reported to be expansion of the vitreous chamber (Mutti et al., 2005; Larsen, 1971). Growth of the vitreous body during postnatal development is well established. However, what initiates vitreous chamber expansion and what brings about its precise arrest at the point of emmetropization are aspects that have not been explored and remain an enigma. It is hypothesized herein that vitreous chamber expansion and resultant early increase in axial length that precisely stops at the point of emmetropia, occurs secondary to postnatal structural and conformational changes within the vitreous collagen and internal limiting membrane (ILM) collagen and molecular interactions between these two structures.