Intense pulsed light (IPL) therapy has shifted rapidly from a dermatologic curiosity to a genuine therapeutic option for dry eye disease (DED), particularly in patients with meibomian gland dysfunction (MGD). Yet questions have persisted: How many sessions are optimal? Are the benefits mechanistic or merely symptomatic? And can tear biomarkers help us understand the biological response?
A new randomized Scientific Reports study offers some of the clearest clinical evidence to date — demonstrating that IPL not only improves tear film stability and meibomian gland performance, but also modulates ocular surface inflammation, with a three-treatment regimen outperforming two sessions in key parameters.
Thirty patients with DED, diagnosed using TFOS DEWS II criteria, were randomized into two groups: Group A, receiving three IPL sessions at baseline, week 3, and week 6; and Group B, receiving only two sessions at baseline and week 3. Follow-up continued to 12 weeks. Importantly, baseline characteristics—including NITBUT, meibomian gland scores, and OSDI—were comparable between the two groups.
By week 6, both groups had demonstrated clinically meaningful improvements:
NITBUT increased from ~4.8 seconds to over 7 seconds.
Meibomian gland expressibility (MGEx) improved significantly.
Corneoconjunctival staining decreased in both groups.
OSDI scores improved by 25–30%.
These changes reinforce what many clinicians observe: IPL acts quickly, stabilizing the tear film and reducing symptoms within a few weeks.
Where the study becomes clinically instructive is at weeks 9 and 12, when differences between the regimens become apparent.
At 12 weeks, Group A outperformed Group B in several objective measures:
NITBUT: 8.13 vs 5.43 seconds.
Tear meniscus height: significantly higher in Group A.
Tear-film lipid layer quality (TFLL): superior in the three-session group.
MGEx and MGQ: both significantly better in Group A.
Notably, while symptoms (OSDI) improved in both groups, subjective scores did not differ significantly at 12 weeks, suggesting that patient-perceived benefit may plateau earlier, even as objective signs continue to respond.
One of the most intriguing aspects of the study is its inclusion of lymphotoxin-alpha (LT-α), an emerging tear biomarker linked to ocular surface inflammation. Baseline LT-α levels were low in all participants, consistent with previous findings that DED reduces LT-α concentrations.
By week 12, only the three-session regimen produced a significant rise in LT-α. This suggests IPL may help restore immune homeostasis, not merely mask symptoms.
In short, the study offers compelling evidence that IPL is more than just a cosmetic add-on — it is a biologically active therapy capable of reshaping tear film dynamics and ocular surface health. It may be time to reconsider IPL not as a supplemental option, but as a core strategy in managing evaporative DED.
