I don't think anyone is exactly sure how IPL treats dry eyes, not even Dr. Toyos, but I have been reading a bit about it and I thought I would put all the possibilities together in one place:
1) Hot compress - IPL heats the oil, melts it, and then makes expression easy afterwards (not everyone I talked to agrees with this)
2) Kills bacteria in the eyelid margin
3) Kills demodex
4) Stimulates the meibomian glands to secrete oil (actually, I noticed this with both of my IPL treatments. The sebaceous glands on my face were really stimulated and were producing oil a few days after the IPL session. I assume the meibomian glands will also be stimulated)
5) Destroys thin blood vessels under the skin that carry inflammatory mediators to the eyelids and the glands thus reducing the inflammation in the glands (I don't know if everyone believes this either. This might only be true in Rosacea patients)
6) Dilates and opens the ducts and orifices thus making expression easier.
Does anyone have any idea which of these is the main mechanism? Or does anyone have any thoughts on which of these mechanisms is what worked for them? If we can figure this out, we may be able to figure out which patients will benefit and which will not.
NME
1) Hot compress - IPL heats the oil, melts it, and then makes expression easy afterwards (not everyone I talked to agrees with this)
2) Kills bacteria in the eyelid margin
3) Kills demodex
4) Stimulates the meibomian glands to secrete oil (actually, I noticed this with both of my IPL treatments. The sebaceous glands on my face were really stimulated and were producing oil a few days after the IPL session. I assume the meibomian glands will also be stimulated)
5) Destroys thin blood vessels under the skin that carry inflammatory mediators to the eyelids and the glands thus reducing the inflammation in the glands (I don't know if everyone believes this either. This might only be true in Rosacea patients)
6) Dilates and opens the ducts and orifices thus making expression easier.
Does anyone have any idea which of these is the main mechanism? Or does anyone have any thoughts on which of these mechanisms is what worked for them? If we can figure this out, we may be able to figure out which patients will benefit and which will not.
NME
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