Age related changes seen in human cornea in formalin fixed sections and on biomicroscopy in living subjects: A comparison

Abstract

The purpose of our experimental research was to assess the effects of aging on the main corneal structures in healthy corneas. Small, human cornea samples were collected from 20 Caucasian subjects during surgery for traumatic lesions to the eye. Ten subjects were adults (mean age 28 years) and 10 were elderly (mean age 76 years). Morphological analysis was carried out using light microscopy and electron microscopy. Another 40 patients (20 young: mean age <30 years; 20 elderly: mean age >70 years) were studied in vivo by confocal microscopy. The resulting images were analyzed qualitatively, quantitatively, and statistically. The basic light microscope revealed a decrease in endothelial cell density with age accompanied by an increase in endothelial cell size. Transmission electron microscopy revealed a corneal thinning and a decrease in the number of corneal stromal cells. A marked decrease in stromal nerve fibers was observed in the older subjects compared to the younger ones. Variable pressure scanning electron microscopy (VP-SEM) was used to make surface morphological observations and to determine the chemical composition of in vivo hydrated human corneas. Our results showed the effects of aging on normal corneal morphology highlighting the structural diversity of the corneal layers and revealing an age-related reduction in nerve fibers, thus explaining the decreased corneal sensitivity that may be observed in the elderly. Clin. Anat. 33:245-256, 2020.

Functional morphology of the cornea of the Little PenguinEudyptula minor(Aves)

“…Our results in E. minor indicate that in both the superficial epithelium and the endothelium there is a significant reduction in cell density with age. For the epithelium, our findings are consistent with those of Taurone et al (2020), who found a gradual loss of epithelial cells in humans with an increase in cell size. Similarly, Lemp et al (1990) and Gambato et al (2015) found that the mean diameter of superficial cells of the human cornea increases with age, resulting in a decrease in cell density.…”

Incidence, Risk, and Visual Outcomes after Repositioning of Acute Non-Traumatic Flap Dislocations Following Femtosecond-Assisted LASIK

“…Increased risk of flap dislocation in older patients may be due to age-related changes in the cornea. Senescent changes of the cornea include a reduction in keratocyte and endothelial cell densities [ 18 , 19 , 20 ], corneal stiffening [ 21 , 22 ], epithelial barrier dysfunction [ 23 , 24 , 25 , 26 ], and a greater incidence of dry eye [ 27 , 28 , 29 , 30 ]. We postulate that these and other age-related changes may lead to slower corneal healing and decreased flap adhesion, resulting in a greater incidence of flap dislocation.…”

“…Keratocytes play a crucial role in corneal wound healing by secreting growth factors and producing collagen [ 32 , 33 , 34 , 35 ]. The reduction in keratocyte density seen with aging likely contributes to slower flap healing in older patients [ 18 , 19 , 20 ]. Theories for the mechanism of early flap adhesion include osmotic pressure due to endothelial pump activity [ 36 , 37 ], electrostatic interactions in the stroma [ 38 ], and epithelial bridging at the edge of the flap [ 37 ].…”

“…Multiple studies have found brimonidine to reduce flap adherence and increase the risk of dislocation and cite its effects on endothelial pump activity as a possible cause [ 39 , 40 , 41 ]. Endothelial cell density and endothelial pump activity both decrease with age and could be related to an increased incidence of flap dislocation in older patients if osmotic pressure is indeed the mechanism for early flap adhesion [ 18 , 19 , 20 , 42 ]. However, no conclusive evidence for any of the possible mechanisms of flap adhesion was found in our review of current literature.…”

Oxidative stress and visual system: a review

“…The appearance of inflammatory processes affecting the eye and the exposure to various types of radiations or chemical agents can be directly responsible for the high increase in hydrogen peroxide in the eye, with a consequent increase in ROS responsible for oxidative action. The oxidative action exerted by free radicals at ocular level manifests as structural and functional alterations in the corneal epithelium associated with apoptotic processes in which keratocytes and stromal fibroblasts play a central role (Ung et al, 2017[ 59 ]; Taurone et al, 2020[ 54 ]). In the light of such scientific evidence, the aim of this review was to evaluate the antioxidant effects of ALA and SOD in the visual system, and the possible induction capacity of tissue regeneration following neurodegenerative damage caused by the accumulation of free radicals.…”