A study recently published in Eye evaluated the efficacy of Botulinum toxin A (BTX-A) in the treatment of dry eye disease (DED).
Give me some background.
Studies have reported that BTX-A can have varying impacts on dry eye symptoms depending on the location of the injection:
- Periocular BTX-A injection could worsen dry eye by reducing tear production of the lacrimal and meibomian glands as well as increase tear evaporation due to potential eyelid malposition and abnormal blinks
- BTX–A injection in the medial eyelids could treat DED symptoms like tear retention and osmolarity by impairing lacrimal drainage (similar to a punctal plug)
Let’s dig deeper.
The study authors outlined that by suppressing the release of acetylcholine from parasympathetic nerve endings, BTX-A modulates the autonomic regulation of tear production—helping to restore balance in tear secretion.
Consequently: When BTX-A is injected into specific ocular and periocular sites, it can enhance tear film stability—a critical factor in alleviating symptoms of DED, including dryness and irritation.
In addition: BTX-A’s ability to relax the orbicularis oculi muscle, which controls blink rate and eyelid closure, further stabilizes the tear film by reducing excessive blinking and preventing tear evaporation.
Now, back to the study.
Investigators conducted a systematic search of studies on DED and BTX-A published through December 2024 across multiple databases, including:
- PubMed
- Cochrane Library
- Scopus
- Web of Science
- Embase
In total: 14 studies (n = 634 patients) were included in the analysis.
The inclusion criteria encompassed randomized controlled trials (RCTs) and non-RCTs examining BTX-A’s effects on DED with the following primary outcomes:
- Tear breakup time (TBUT)
- Schirmer test scores
- Tear meniscus height (TMH)
- Ocular Surface Disease Index (OSDI)
Findings?
In 10 of the studies (n = 513 participants), BTX-A significantly improved multiple DED parameters as follows:
- TBUT increased by 1.79 seconds (95% confidence interval [CI]: 1.48 to 2.10, p < 0.00001)
- Schirmer increased test scores by 3.72 mm (95% CI: 3.50 to 3.95, p < 0.00001)
- OSDI scores decreased by -7.51 points (95% CI: -10.76 to -4.26, p < 0.00001)
In addition: While not statistically significant, TMH also increased by 0.10 mm (95% CI: 0.08 to 0.11, p < 0.00001).
Expert opinion?
In addition to the mechanisms listed above, the anti-inflammatory properties of BTX-A also play a critical role in its efficacy for DED.
- Why: It modulates inflammatory processes that exacerbate tear film instability and ocular surface damage.
- How: By decreasing the release of inflammatory mediators, such as substance P and calcitonin gene-related peptide from sensory nerve terminals, BTX-A reduces neurogenic inflammation
Meaning: Tear film stability improves and ocular surface irritation is alleviated, providing symptom relief, particularly in severe or refractory cases of DED.
Take home.
These findings suggest that BTX-A effectively enhances clinical outcomes in DED with the following post-treatment improvements:
- An increase in TBUT
- An improvement in Schirmer test scores
- A decrease in OSDI scores
- An increase in TMH
As such: BTX-A injections enhanced tear stability, production, and symptom relief—supporting its use in clinical practice as a promising treatment for DED.
Next steps?
The study authors recommended that future studies prioritize:
- Identifying patients with severe or refractory DED
- Optimizing dosing intervals
- Tailoring injection sites to individual patient needs
Moreover: Incorporating additional markers, such as inflammatory cytokines, may further elucidate BTX-A’s mechanisms and broaden its clinical utility—paving the way for more personalized and effective DED management.