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Updated: Jul 26, 2025
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
Published on: August 4, 2022
Transitory alkali exposure on meibomian gland orifices induces meibomian gland dysfunction
Jinghua Bu1, Yang Wu2, Kechun Li3
1Department of Ophthalmology, Xiang'an Hospital of Xiamen University, Eye Institute of Xiamen University, Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Fujian Engineering and Research Center of Eye Regenerative Medicine, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Purpose:
To determine pathological changes of meibomian glands (MGs) after transient exposure of the rat eyelid margin to alkali solution.
Methods:
Filter paper infiltrated with 1 N sodium hydroxide solution was applied to the eyelid margin of Sprague-Dawley rats for 30 s under general anesthesia, without touching the conjunctiva, after which the ocular surface and eyelid margin were examined by slit-lamp microscopy. In vivo confocal microscopy and stereomicroscopy were subsequently applied to observe MG morphology on day 5, day 10 and day 30 post alkali injury. Eyelid cross-sections were processed for H&E staining, Oil red O staining and immunofluorescent staining.
Results:
After alkali injury, there was marked plugging of MG orifices, telangiectasia and hypertrophy of the eyelid margin, while corneal epithelium was intact at post-injury days 5 and 10. However, 30 days after alkali injury, mild corneal epithelial damage was observed. Degeneration of MG acini was observed at days 5 and became aggravated at days 10 and 30, along with MG duct dilation and acini loss. Oil red O staining showed lipid accumulation in the dilated duct. Inflammatory cell infiltration and the presence of apoptotic cells was seen in the MG loci 5 days post injury, but diminished at days 10 and 30. Cytokeratin 10 expression was increased in dilated duct, while cytokeratin 14, PPAR-γ, Ki67 and LRIG1 expression were decreased in the acini of injured loci.
Conclusions:
Transitory alkali exposure of the rat eyelid margin obstructs the MG orifice and induces pathological changes of MG dysfunction.
Insights
Transient alkali exposure to rat eyelids causes meibomian gland (MG) obstruction and dysfunction. This study details the pathological changes in MGs following alkali injury, impacting gland structure and function.
Area of Science:
- Ophthalmology
- Pathology
- Toxicology
Background:
- Meibomian glands (MGs) are crucial for ocular surface health.
- Alkali injuries can significantly impact ocular structures, including the eyelids.
Purpose of the Study:
- To investigate the pathological changes in rat meibomian glands (MGs) after transient alkali exposure to the eyelid margin.
Main Methods:
- Rats' eyelid margins were exposed to 1N sodium hydroxide solution for 30 seconds.
- Ocular surface and eyelid margin examined using slit-lamp, confocal, and stereomicroscopy.
- Histological analyses included H&E, Oil red O, and immunofluorescent staining.
Main Results:
- Alkali injury led to MG orifice plugging, eyelid margin changes, and MG acini degeneration.
- Lipid accumulation in dilated ducts and altered expression of cytokeratins and key proteins (PPAR-γ, Ki67, LRIG1) were observed.
- Inflammation and apoptosis in MG loci were noted initially, diminishing over time.
Conclusions:
- Transient alkali exposure obstructs meibomian gland orifices.
- This obstruction induces significant pathological changes, leading to meibomian gland dysfunction.
