Abstract:The choroid is a vascular tissue which plays a range of critical roles in the normal physiology of the eye, such as supplying the outer retina with oxygen and nutrients and the regulation of intraocular pressure. There is also substantial evidence, particularly from animal studies, that the choroid plays an important role in the regulation of eye growth and the development of common refractive errors like myopia. In recent years, advances in optical coherence tomography technology have improved our ability to … Show more
“…It is nowadays evident that myopia is strongly correlated with the axial length of the eye and not with its refractive power [18]. The growth of the eye globe is a complex event, which appears to be regulated by signals coming from the retina and the choroid, independent from the brain [19,20]. Some described chemical mediators of this signaling mechanisms are dopamine [21], TGFβ [22], and melatonin [23].…”
Background: The etiology and the mechanism behind atropine treatment of progressive myopia are still poorly understood. Our study addressed the role of scleral and choroidal fibroblasts in myopia development and atropine function. Methods: Fibroblasts treated in vitro with atropine or 7-methylxanthine were tested for ECM production by Western blotting. Corneal epithelial cells were treated with atropine in the presence or absence of colostrum or fucosyl-lactose, and cell survival was evaluated by the MTT metabolic test. Results: Atropine and 7-methyl-xanthine stimulated collagen I and fibronectin production in scleral fibroblasts, while they inhibited their production in choroidal fibroblasts. Four days of treatment with atropine of corneal epithelial cells significantly decreased cell viability, which could be prevented by the presence of colostrum or fucosyl-lactose. Conclusions: Our results show that atropine may function in different ways in different eye districts, strengthening the scleral ECM and increasing permeability in the choroid. The finding that colostrum or fucosyl-lactose attenuate the corneal epithelial toxicity after long-term atropine treatment suggests the possibility that both compounds can efficiently blunt its toxicity in children subjected to chronic atropine treatment.
“…It is nowadays evident that myopia is strongly correlated with the axial length of the eye and not with its refractive power [18]. The growth of the eye globe is a complex event, which appears to be regulated by signals coming from the retina and the choroid, independent from the brain [19,20]. Some described chemical mediators of this signaling mechanisms are dopamine [21], TGFβ [22], and melatonin [23].…”
Background: The etiology and the mechanism behind atropine treatment of progressive myopia are still poorly understood. Our study addressed the role of scleral and choroidal fibroblasts in myopia development and atropine function. Methods: Fibroblasts treated in vitro with atropine or 7-methylxanthine were tested for ECM production by Western blotting. Corneal epithelial cells were treated with atropine in the presence or absence of colostrum or fucosyl-lactose, and cell survival was evaluated by the MTT metabolic test. Results: Atropine and 7-methyl-xanthine stimulated collagen I and fibronectin production in scleral fibroblasts, while they inhibited their production in choroidal fibroblasts. Four days of treatment with atropine of corneal epithelial cells significantly decreased cell viability, which could be prevented by the presence of colostrum or fucosyl-lactose. Conclusions: Our results show that atropine may function in different ways in different eye districts, strengthening the scleral ECM and increasing permeability in the choroid. The finding that colostrum or fucosyl-lactose attenuate the corneal epithelial toxicity after long-term atropine treatment suggests the possibility that both compounds can efficiently blunt its toxicity in children subjected to chronic atropine treatment.
“…These results suggest that exposure of the retina to a regionally distinct, rather than a spatially uniform, pattern of myopic defocus may provide additional cues to the eye that result in an increased response of the choroid to myopic defocus. An increase in choroidal thickness is thought to contribute to the long‐term slowing of ocular growth . Therefore, the greater thickening of the macular choroid in response to a regionally distinct, rather than spatially uniform imposed myopic defocus, may also provide a potential mechanism explaining the greater efficacy of bifocal and multifocal spectacle lenses, multifocal soft contact lenses and orthokeratology compared to the symmetrical defocus of bilateral myopic under‐correction in slowing the progression of myopia.…”
Section: Discussionmentioning
confidence: 99%
“…Research with animal models suggests that eye growth is influenced by retinal image defocus, with the choroid playing a significant role in mediating the effects of defocus on ocular growth and the development of refractive errors . Studies in a range of species show that a thinning or thickening of the choroid in response to hyperopic or myopic defocus results in a rapid movement of the retina towards the defocused image plane, followed by alterations in scleral growth that eventuates in the development of experimental myopia or hyperopia, respectively .…”
Purpose
To examine the regional changes in human choroidal thickness following short‐term exposure to hemifield myopic defocus using optical coherence tomography (OCT).
Methods
The central 26˚ visual field of the left eye of 25 healthy young adults (mean age 26 ± 5 years) was exposed to 60 min of clear vision (control session), +3 D full‐field, +3 D superior retinal and +3 D inferior retinal myopic defocus, with the right eye occluded. Choroidal thickness across the central 5 mm (17°) macular region was examined before and after 60 min of defocus using a high‐resolution, foveal centred vertical OCT line scan, with optical defocus simultaneously imposed using a Badal optometer and cold mirror system mounted on a Spectralis OCT device.
Results
Averaged across the central 5 mm macular area, choroidal thickness decreased by −4 ± 7 μm during the control session (p = 0.01), most likely due to the unique stimulus conditions of this study. The mean macular choroidal thickness increased during full‐field (+2 ± 8 μm), inferior retinal (+3 ± 7 μm) and superior retinal myopic defocus (+5 ± 9 μm), representing a significant thickening of the choroid compared to the control session (all p < 0.05). The defocus induced changes in macular choroidal thickness differed between the superior and inferior hemiretinal regions (F2.26, 54.27 = 29.75, p < 0.001). When only the superior retina was exposed to myopic defocus, the choroid thickened in the superior region (+7 ± 8 μm, p < 0.001), but did not change significantly in the inferior region (+3 ± 9 μm, p = 0.12). When only the inferior retina was exposed to myopic defocus, the choroid thickened inferiorly (+4 ± 8 μm, p = 0.005), with no significant change observed in the superior region (+1 ± 8 μm, p = 0.46).
Conclusions
These findings provide evidence supporting a local regional choroidal response to myopic defocus in the human eye, with hemifield myopic defocus leading to significant thickening of the choroid localised to the retinal region exposed to defocus. The novel finding of a localised response of the human choroid to hemifield myopic defocus, particularly in the superior hemiretina, may have important implications in optimising the optical design of myopia control interventions.
“…Experimental settings in both animals [9][10][11][12] and humans [8] show a modulation of choroidal thickness in response to visual inputs which also leads to choroidal secretion of scleral growth regulators [13]. Consequently, the choroid is believed to play an active part in eye growth regulation [14,15]. Eyes that develop myopia both experience a thinning of the choroid and an elongation of the eyeball [16,17] and a study following 101 Australian children over an 18 month period found an association between choroidal thinning and increasing axial length growth [18].…”
Background: Myopic eyes are longer than nonmyopic eyes and have thinner choroids. The purpose of present study was to investigate whether a thinner subfoveal choroid at 11 years of age predicted axial eye elongation and myopia during adolescence. Methods: Longitudinal, population-based observational study. Axial length was measured using an interferometric device and choroidal thickness was measured by spectral-domain optical coherence tomography. Myopia was defined as non-cycloplegic subjective spherical equivalent refraction ≤ − 0.50 diopters. Results: Right eyes of 714 children (317 boys) were examined at age (median (IQR)) 11.5 (0.6) years and 16.6 (0.3) years during which axial length (median (IQR)) increased by 243 (202) μm in eyes without myopia (n = 630) at baseline compared with 454 (549) μm in eyes with myopia (n = 84) at baseline, p < 0.0001. A thicker baseline subfoveal choroid was associated with increased five-year axial elongation after adjustment for baseline axial length in nonmyopic eyes (β = 27 μm/100 μm, 95%CI 6 to 48, p = 0.011) but not in myopic eyes (p = 0.34). Subfoveal choroidal thickness at 11 years of age did not predict incident myopia at 16 years of age (p = 0.11). Longer baseline axial length was associated with greater five-year axial elongation in both myopic (β = 196 μm/mm, 95%CI 127 to 265, p < 0.0001) and nonmyopic eyes (β = 28 μm/mm, 95%CI 7 to 49, p = 0.0085) and the odds for incident myopia increased with 1.57 (95%CI 1.18 to 2.09, p = 0.0020) per mm longer axial length at baseline. Conclusion: A thin subfoveal choroid at age 11 years did not predict axial eye elongation and incident myopia from age 11 to 16 years. A longer eye at age 11 years was associated with greater subsequent axial eye elongation and with increased risk of incident myopia at age 16 years.
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