Abstract
Purpose: To compare the efficacy of 0.1%, 0.18%, and 0.3% hyaluronic acid (HA) artificial tear in the treatment of experimental dry eye (EDE).Methods: EDE was established in female C57BL/6 mice through an air draft and subcutaneous scopolamine injection. The mice were divided into 5 groups according to topical treatment regimens (n = 5 each): EDE control, balanced salt solution (BSS), preservative-free 0.1% HA, 0.18% HA, and 0.3% HA. The tear film break-up time (TBUT) and corneal fluorescein staining scores were measured 5, 10, 14, 21, and 28 days after treatment. The corneal smoothness scores were measured. In addition, periodic acid–Schiff (PAS) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed.Results: The values for TBUT and corneal fluorescein staining showed greater improvements in all the HA groups (P < 0.05) than in the EDE and BSS groups after 10 days of treatment. Mice treated with 0.3% HA showed a more significant improvement in all clinical parameters than did those in the EDE control, BSS, 0.1% HA, and 0.18% HA groups (all P < 0.05) after 28 days of treatment. The goblet cell counts were higher in the 0.3% and 0.18% HA groups than in the 0.1% HA group. The number of TUNEL-positive cells was the lowest in the 0.3% HA group.Conclusions: In EDE, 0.3% HA artificial tears are more effective than the 0.1% and 0.18% HA in improving tear film instability and ocular surface staining and irregularity, in increasing the number of conjunctival goblet cells, and in decreasing corneal epithelial apoptosis.
Highlights
Dry eye disease (DED) is a multifactorial disease of the tears and ocular surface that is characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms.[1]
Twenty-one days after treatment, a significantly higher improvement in tear film break-up time (TBUT) was noted in the 0.18% hyaluronic acid (HA) group than in the 0.1% HA group (P = 0.047), as well as in the 0.3% HA group than in the 0.1% and 0.18% HA groups
Twenty-one days after treatment, a significantly higher improvement in the corneal fluorescein score was observed in the 0.3% HA group than in the 0.1% and 0.18% HA groups
Summary
Dry eye disease (DED) is a multifactorial disease of the tears and ocular surface that is characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms.[1]. DED is characterized by aqueous deficiency of tear volume loss, early tear film breakup, and increased evaporative loss from the ocular surface.[3] The tear film is composed of many substances, including lipids, proteins, mucins, and electrolytes.[3] All of these contribute to the integrity of the ocular tear film. The central mechanism of DED is lacrimal deficiency and increased evaporative loss leading to hyperosmolar tissue damage.[4] Research in humans and animal models has shown that this, either directly or by inducing inflammation, causes a loss of both corneal epithelial and conjunctival goblet cells.[4] The consequent decrease in ocular surface wettability leads to more rapid tear film breakup and amplifies tear hyperosmolarity and completes the vicious circle of events that lead to ocular surface damage.[4] The current management options for DED include treatments for tear insufficiency and eyelid abnormalities, as well as anti-inflammatory medications, surgical approaches,
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