I could not find any reference or even a hint concerning this question in literature available. However, it might do matter for a vast arrey of the gallbladder disease, from the chronic calculouse cholecystitis till the acute one and cancer of the organ
Virchows Arch B Cell Pathol Incl Mol Pathol. 1980;35(1):1-10.
Morphological and functional recovery of the canine gallbladder mucosa following two hours' ischemia.
Winistörfer B, Mirkovitch V, Robinson JW, Ozzello L
Dear Andrey, this old paper at least states the existance of the phenomenon. The presence of metaplasia and dysplasia near neoplastic gallbladder tissue is an indirect confirmation of the concept. However, you are right when consider that the problem is strongly underestimated.
Thank you very much!
The reference you gave is very valuable for me. Both the source and regulatory mechanisms of the gallbladder mucosal lining regeneration are not quite clear, especially in terms of a possible pathogenesis of the most common entities as the acute cholecystitis, etc. From 'the surgical point of view', so to say, why the acute cholecystitis leading to the organ gangrene will develop in one patient and will never in another one?
This very complications' development might being connected with some disorders of the gallbladder regeneration. If so, there may be a link exist between this and decision making who of the patients must be referred to elective surgery so that to prevent the acute destructive cholecystitis development, and who this is not necessary for.
In textbook (2009) "Surgical Pathology of the GI Tract, Liver, Biliary Tract, and Pancreas" edited by Robert D Odze & John R Goldblum, page 871, in discussion of gallbladder epithelial hyperplasia states: "Finally in some cases with gallbladder injury, regenerating mucosa may form prominent mucosal folds with a complex architecture. This phenomenon has been referred to as spongioid hyperplasia." Apparently this is a relatvely infrequent finding. Agree we seem to know very little of the role of gallbladder mucosal epithelial regeneration in the etiology of progression and natural history of acute cholecystitis.
Dr.Bowman,
Thank you so much for the reference on "Surgical Pathology...". I must confess I have not read it yet.
As for the role of the GB mucosal epithelial regeneration in the acute calculous cholecystitis ignition and natural history, we seem to know nothing at all. It may be an independent factor contributing to the former and latter, though.
The best what I found on this matter (just several hours ago) was an article by J.Lamote & G.Willems. DNA Synthesis, Cell Proliferation Index in Normal and Abnormal Gallbladder Epithelium. MICROSCOPY RESEARCH AND TECHNIQUE 38:609–615 (1997) [PMID: 9330349].
The gallbladder is quite different from the gastrointestinal mucosa in terms of regeneration both by its source (not from pits, glandular neck epithelium, or cripta); pattern (there is no permanent renewal, but on demand only, or so it is said); and by its rate (very slow). Taking altogether, all these is strange enough, because the normal gallbladder bile is the very aggressive medium (bile acids/salts, phosholipids, including app.10% of the lysolecithine in it, etc.).
The distention, other mechanical, chemical, and hormonal stimuli were found to be stimulators of the GB epithelial regeneration. However, all these factors were studied under the chronic, but not acute, conditions, from positions of:
1) gallbladder lithogenesis;
2) gallbladder carcinogenesis,
what is important and interesting without any doubt.
On the other hand, the former is very common, but not life-threatening entity by itself; the latter is the most dangerous, but very rare entity.
The acute cholecystitis are both life-threatening and relatively common disease. Risque factors for the acute calculous cholecystitis to develop are rather vague still. They are too wide and non-specific (diabetes mellitus, elder patients' group, and so).
As for the acute acalculous cholecystitis development, this entity is as 10-fold as lesser, and up to 10-fold as more dangerous than its 'stone brother'. It is evidently related to ischemia, local or general. However, it may or may not develop in patients with shock. One may hypothesize that the regeneration capability and condition play a role for this or that way to occur. Or, at any rate, it would be worth to check this up.
Here is another, most recent article on this matter, from Italy, L'Universita della Sapienza, if I remember correctly (prof.D.Alvaro, et al):
PMID: 24530598
However, there is a little controversy about the progenitor cell location between the earlier and this paper: either diffusely, or in cryptes only?
Unfortunately, I have no access to a fulltext version of the article, so that I do know details.
Prof.Ierardi,
Thank you very much! I hope I shall enjoy that. By the way, Prof.Alvaro sent me his article on the biliary epithelium once upon a time, in the 90th, in paper. Perhaps, he'll recall that event :))
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