Thanks for your detailed reply!
Again, this will be a wall of text so please bear with me! I need to cover a few points.
Currently, I think there must be different triggers for EC but a common aetiology. I agree that patients seem to get EC for a variety of reasons but I think there is a common mechanism.
In my case, I had a very severe outbreak of exfoliative chelitis following have a lip filler (stupid of me, I know). The severe peeling literally started the day after the injection and continued to get more severe over a two week period (I was applying aquaphor the whole time). After I stopped the Aquaphor, I had classic EC crusting formation that others have in the gallery (crusting on middle of top lip and severely on upper part of lower lip, although it is very severe). I was diagnosed by dermatologist with desquamation of the lip due to filler hypersensitivity. I agree that the first part of the diagnosis is right (desquamation of the lip) but I question the hypersensitivity part of the diagnosis (although I admit it could be right). The reason I question it is because I have realised retrospectively that I probably had a mild version of EC for years that I kept under control with Aquaphor. I thought at the time I had dry/chapped lips due to the Accutane I took a long time ago (I started using the Aquaphor while taking the Accutane and never stopped afterwards). If I didn’t use Aquaphor for a certain length of time I had very mild sort of triangle of dead skin on my upper lip and very thin strip of dry, brownish discolouration (from dry skin flakes) on my inner lower lips sometimes on waking. If I used Aquaphor all the time, my lips looked normal and were similar to the condition you described your lips have been in after partially healing from EC: “Technically this means that I no longer have EC (the 'itis' in 'cheilitis' refers to an inflammatory condition), although they are still very much exfoliating.” If anyone reading this is in doubt whether I now have EC, I actually sent my pictures to a top specialist on EC to ask whether he thinks I have the condition and he said he agreed it was indeed EC. My severe peeling has been ongoing now for five months.
So, if there is a common mechanism to EC, I think in some sense the unusualness of my case can maybe shed light on it.
The possibility is a) hypersensitivity (basically allergy hypothesis)
This is plausible. However, I do not think this is correct because the peeling impacts the upper layers of skin and the filler was injected deep under the skin. What it more the filler was injected in to the outer border of my vermilion and the peeling starts on the wet/dry border of the inner lips and is most severe in that region (I notice this is consistently the case across the Peeling Lips Image Gallery
). The peeling also happens in a very patterned way (the same parts are effected consistently over time i.e the mid portion of the top lip and the upper border of the lower lip), all suggesting some kind of structural problem with the lips. The mucous membranes of my lips are also involved and no product was injected into them. I was also on very strong (oral) steroids which did nothing for my condition. I could say more about this but I will leave it at that for now.
The other possibility
b) the other common hypothesis for EC is ”chronic wound” (I do not think this hypothesis has any merit. I explained my thinking on this here //www.curezone.org/forums/fm.asp?i=2360366#i
). In my case, the lip filler may have caused trauma to the inside of the lips but it did not traumatise my outer lip skin (the vermilion). The injections actually went in through the cheek skin near the oral commissures. The peeling and crusting started in a totally different area to the injection site. I did not pick, lick, bite ect my skin and quite frankly would have been terrified to do so given the severity of the reaction.
c) The third possibility. The filler plumped out and stretched my lip skin, causing parts of my mucous membrane near the wet/dry border that were originally inside my mouth to be exposed to the air constantly and this has something to do with the EC. It is hard to explain this but if you look at images of people who have massively overfilled lips such as Jordan James Parke you will see what I mean about how filler can cause mucous membrane to be exposed http://i.dailymail.co.uk/i/pix/2014/12/18/2422BEE100000578-2878560-image-a-44_1418898085336.jpg
. Obviously, my lips are not as big as this. Clearly people like James Parke reveal that EC does not happen just from the prolonged exposure of the mucosa to air (since he does not have EC – however, his lip skin doesn’t look particularly healthy). However, what if you have dry mucosa from xerostomia?
There is a documented link between xerostomia and Exfoliative chelitis in published research.
From a research article on xerostomia " Oral mucosal manifestations in primary and secondary Sjögren syndrome and dry mouth syndrome" .. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4793060/ ."The most frequent complaints as obtained from history were[...associated with decreased saliva] were dryness of the mouth in the morning and at night, frequent need to sip water, lip dryness, exfoliation, fissuring,[...] Half of the patients presented with dryness of the oral mucosa. It was dry, with no elasticity, easily adhering to fingers or a dental mirror. In only 2 (9.1%) female patients marked dryness was accompanied by bright red colour of the mucosa. [...] The second most frequent sign was angular cheilitis, cheilitis, including exfoliative cheilitis. The lips were fissured, exfoliative, bleeding easily. The patients reported the need to frequently moisten and lubricate the lips. In 5 female patients, non-specific ulceration or oral aphtae were observed. The majority of patients reported a tendency towards such lesions and complained of their chronic and long-lasting treatment. [...] Candida albicans infection accompanies angular cheilitis and exfoliative cheilitis very often observed in Sjögren syndrome patients [...] In simple cheilitis dominant manifestations are bad lips exfoliation and cracking, their proneness to bleeding, periodic swelling and burning (Figure 1). The lesions are mostly limited to lip vermillion, less often labial mucosa or the facial skin around the vermillion is affected. Protective ointments containing lanoline, vitamin A or clobetasol provide an effective treatment. In exfoliative cheilitis thick brown keratin plaques are formed, too. Skin redness over the lip vermillion and swelling are more often observed. In the treatment of exfoliative cheilitis, protective ointments containing lactic acid or ointments and preparations with tacrolimus or steroids are applied ."
Ok, given that patient histories of Sjorgen’s Syndrome prove that xerostomia produces Exfoliative Chelitis, it seems that more exposure of the mucosa to air in a patient already prone to xeostomia would lead to more severe chelitis.
Actually, somebody posted here on the forum a while back that they got EC following a rhinoplasty which altered the angle between their nose and upper lips. //www.curezone.org/forums/am.asp?i=2019566#i
and she attributes her condition to the fact that the surgery caused her to breathe through her mouth. So again this supports the hypothesis.
Also a google book I read on Exfoliative chelitis in HiV patients suggested the condition was associated with hyposalivation https://books.google.co.uk/books?id=U3WyAFrXVfIC&pg=PA354&dq=exfoliative+cheilitis+HIV&hl=en&sa=X&ved=0ahUKEwio-IzWlIDTAhXiJMAKHbDACKwQ6AEIODAF#v=onepage&q=exfoliative%20cheilitis%20HIV&f=false
Ok, so now we get to my point about the saliva gel. I have not been applying the gel to outer, dry part of my lip (the vermilion). I agree that saliva should not be getting on your dry vermilion skin. I have been applying the saliva gel to the labial mucosa (the inner lips). The labial mucosa are mucous membranes and thus require totally different conditions to your outer lips. It’s equivalent to the inside and outside of your eyelid (the inner eyelid surface is naturally wet, the outer eyelid is dry). The labial mucosa are naturally constantly covered with saliva and if they aren’t covered in enough saliva this is definitely a bad thing which leads to irritation of the tissues. I explained how I have been applying the saliva gel in this post: //www.curezone.org/forums/fm.asp?i=2360402#i
A saliva gel company (Bioxtra) actually told me (because I sent an email to them to ask if the gel would be safe to apply in this way) that it would actually be safe to get the gel on the vermilion and hospitals sometimes apply the gel over the whole lips in patients who are suffering from dry lips due to radiation therapy. However, I do not recommend applying it in this way (especially if using a brand other than Bioxtra). I think it is good to apply gloves in a bottle to the vermilion and the saliva gel to the labial mucosa only.
I do not think drinking water throughout the day is equivalent to applying the gel because I have tried that as well to no avail. I think the problem is specifically that the labial mucosa is too dry. I think that it is important for it to be moisturised at night too.
Ok, now we get to alternative causes of EC you proposed. You suggested in your case that subtle systemic inflammation and leaky gut caused your case.
I think systemic disorders certainly have everything to do with various health problems. I myself have other conditions as well (hashimoto’s thyroiditis, chronic fatigue syndrome) which I definitely think has something to do with EC.
However, EC is clearly a localised inflammatory disorder or the lips and/or mouth.
Thus I think the relationship between systemic inflammation and EC is probably akin to relationship between diabetes and glaucoma (it is definitely connected but still there is a form of localised inflammation that requires treatment).
Afterall, in my case the hashimoto’s thyroiditis might have caused the xerostomia, the prior Accutane use might have lead to tendency to dry skin, the Chronic-Fatigue-Syndrome
might have lead to compromised immuny, so the EC might actually involve a cascade of biochemical events.
However, I still think the cause of the localised inflammation is xerostomia (of course caused by systemic factors) so my theory is that trying to control the xerostomia might result in the best effects.
I think that xerostomia might not be the only cause. There might be another factor like dry skin from xerostomia leading to psoriasis-like lesions in susceptible individuals.
That’s my two cents anyhow!
I do think your blood vessel theory has merit as well, it's just not something I know a great deal about so not sure I have anything to contribute here.
Feel free to correct me if I am incorrect on anything. I think the lack of interest from doctors in the condition means us patients are going to have to do most of the investigative work.