Abstract
Purpose: :
To establish a mouse model of neurotrophic keratopathy and examine the corneal epithelial wound healing in this model.
Methods: :
Seven to 10 week-old male C57BL/6 mice (n=32) underwent trigeminal stereotactic electrolysis (TSE) to destroy the ophthalmic branch of right trigeminal nerve. Coagulation of the nerve was performed with a cauterization bipolar needle of 18 or 20 gauge (G) (power: 100%, 3 min). The blinking reflex of the model mice was tested with air jet method. Clinical follow-up using biomicroscopy of cornea was performed. Wound healing of central epithelial defect in cornea was evaluated in 20 G bipolar treated mice (N=6) at 3 to 30 hrs after epithelial ablation. Cauterization of the trigeminal nerve was confirmed by using histology with Hematoxilin-Eosin (HE) and Kluver-Barrera's (KB) stains.
Results: :
The corneal blink reflex was abolished both 18G and 20G bipolar treated mice. The 18G bipolar-treated mice developed a progressive corneal tissue destruction, while the 20 G bipolar-treated mice did not exhibit a discernible histological difference in the cornea. Trigeminal denervation mice of 20G bipolar group, however, showed an impairment of closure of a corneal epithelial defect at 24 hrs post-wounding. Bipolar cauterization of the trigeminal nerve was histologically confirmed.
Conclusions: :
A surgical approach, TSE, successfully induced neurotrophic keratopathy in mice. Trigeminal denervation not only breaks homeostasis but also impairs wound healing in a mouse cornea.
Keywords: pathobiology • wound healing • cornea: basic science