Structural and biochemical changes in the sclera of experimentally myopic eyes.

Introduction The refraction of the eye is determined by four ocular components: corneal power, anterior chamber depth, lens power and vitreous chamber depth. From birth to adulthood the axial diameter of the human eye increases by approximately 7 mm. This change would result in significant refractive error (> 15 D) if compensatory changes in the other ocular components did not occur. However, for the majority of individuals (approx. 65%) there is precise regulation of the development of the ocular components such that the image of distant objects is brought to a sharp focus on the photoreceptive layer of the retina. This process of coordinated development of the ocular components is known as emmetropization. In a significant minority of the population, however, there is a breakdown of this regulatory process such that hyperopia or more commonly myopia (shortsightedness) results. Myopia is a condition that affects approximately 25% of the population in both western European countries and the USA. [ 1, 21, with an even higher incidence reported in Asian populations. In addition to the economic impact involved owing to the cost of spectacles, progressive or pathological myopia is a major cause of world blindness [3] as a result of degenerative changes that take place as a sequelae to the excessive axial elongation of the eye. In recent years research on experimental models of pathological myopia has concentrated more on the biochemical changes that may be involved. Several studies have demonstrated changes in retinalneurotransmitter levels of myopic eyes [4, 51, and that altering neurotransmitter levels in the eye can reduce or eliminate the excessive axial elongation of the eye found in experimentally induced myopia [6-81. However, it is only very recently that work has begun in an attempt to elucidate the biochemical mechanisms responsible for the structural changes observed in the sclera of myopic eyes.