[Animal Modeling] - Traumatic Cataract Animal Model

  1. Fagerholm et al. used 18 SD rats weighing approximately 250g to create a cataract model by threading a 0.4mm diameter suture needle through the rat cornea and 0.5mm near the anterior pole of the lens. The results showed that within 0-1 hours after injury, when the lens was punctured and removed, substances in the crystalline body immediately overflowed. In the first 1-2 minutes after injury, the subcapsular opacity expanded outward from the puncture site by about 5mm. Within the first hour after injury, the transparent lens becomes more cloudy. In the first 5 minutes after injury, there was no change in the size of the lens opacity under the anterior capsule. Epithelial cells were absent in the 0.5mm area around the injury, and residual epithelial cells showed nuclear pyknosis, swelling of mitochondria in the cytoplasm, and a large amount of ribosomes. Within the first hour, 10 out of 18 lenses experienced mild posterior subcapsular opacity. Microscopic radiography of the lens 5 minutes and 1 hour after injury showed protrusion of lens fibers at the edge of the lens capsule and significant swelling of the protruding lens fibers. There was a decrease in dry matter under the capsule around the wound, and 4 out of 6 damaged lenses showed posterior pole lens fiber swelling accompanied by a decrease in dry matter. Subcapsular opacity is more common 24 hours after injury (10/12), with protrusions of lens fibers dissolving. Radiographs of the fibers show prominent swelling of the lens fibers, a decrease in dry matter concentration in the wound area, and a reduction of more than 50% in dry matter at the posterior pole of 2/3 of the damaged lens. One week after the injury, proliferative epithelial cells seal the wound, and there is a rare overflow of substances in the crystalline body, with the damaged area becoming turbid. Microscopic radiation photos show epithelial regeneration beneath the material protruding from the injury area, with a decrease in dry matter concentration deep into the cortex. One month after the injury, the wound appeared as a white patch, with all subcapsular opacities reaching the entire anterior capsule except for one crystalline lens. Among the three damaged lenses, 2 had a significant decrease in dry matter under the entire capsule. One year after injury, one-third of the lenses were completely turbid, and two lenses showed areas of reduced dry matter.

  2. Hirayama et al. selected 80 (160 eyes) 4-week-old ddY mice and used a 0.6mm diameter puncture needle to puncture the anterior surface of the injured lens to create an animal model of traumatic cataract. The results showed that in 160 eyes, 121 eyes had anterior turbidity, 26 eyes had posterior turbidity, and no turbidity was observed in the rest. On the first day after injury, mature cataracts had formed in 121 eyes with anterior opacity. The sagittal section shows that the posterior cortex is mostly transparent, and the epithelial cells that damage the lens regress to the outer side of the lens. Under electron microscopy, there are two layers of cells at the edge of epithelial cells, with an inner layer composed of small cells. The cytoplasm of epithelial cells is filled with a large amount of myofibrin. At 14 days after injury, the edges of epithelial cells swelled and stratified. Under electron microscopy, proliferating cells contain mature rough endoplasmic reticulum, but mitochondria are rare. At high magnification, a large number of cell filaments can be seen. There is a large amount of myofibrin around the layered cells, but less in the central part. One month after the injury, the sagittal section still shows mature cataracts, with stratified epithelial cells completely covering the damaged area. Histologically, single-layer epithelial cells become multiple layers, consisting of 7-8 layers. Under electron microscopy, the proliferating cells are composed of black and bright cells. The surface and depth of proliferative epithelial cells in histology