Abstract
Purpose :
A novel meibomian gland dysfunction (MGD) model should help us understand pathophysiology in MGD, and evaluate Azithromycin ophthalmic solution (Azithromycin). In this study the MGD was induced in HR-1 hairless mice to by feeding a special diet limiting lipids (HR-AD).
Methods :
Male HR-1 hairless mice were bred with HR-AD diet for 16 weeks. Development of MGD was assessed by histopathology at the intervals of 4 weeks. Lid margin of the mice were observed by slit lamp examination. After the cessation of HR-AD diet, the mice were bred by normal diet to regain normal condition. We evaluated the effect of topically applied Azithromycin on the plugged orifice using this model.
Results :
After 4 weeks of HR-AD diet, histopathology showed thick hyperkeratinization of the ductal epithelium in the meibomian gland. After 8 weeks, the ductal hyperkeratinization lead to extreme loss of acini followed by atrophy of the gland. Slit lamp examination revealed markedly plugged orifice, telangiectasia around the orifices and toothpaste like meibum compared with those of the normal eyelid. The cessation of feeding HR-AD recovered of both MGD signs and the atrophy of acini. Azithromycin significantly decreased the number of plugged orifices and histopathologically recovered the atrophy.
Conclusions :
We developed novel model mimicking human MGD symptoms in HR-1 hairless mice feeding HR-AD diet. Azithromycin demonstrated therapeutic improvement of plugging and atrophy of acini in the model. This MGD model could be useful to evaluate the pathophysiological efficacy of drug candidates.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.