Repair and healing of established gastric mucosal injury.
Superficial injury of the gastric mucosa, such as occurs after ethanol or aspirin ingestion, is usually resurfaced in 1 or 2 h. This is accomplished by rapid migration of surface mucous cells to cover the defect, followed by a later increase in cellular proliferation to restore the pits to their original length. This rapid restitution has been documented with electron microscopy, and is also reflected in the speedy return to baseline of the transmucosal potential difference and ionic barrier function after superficial injury. Deeper mucosal injury--which occurs focally after injury by aspirin, other NSAIDs, and restraint stress--is evident as macroscopically visible erosions. These heal more slowly, and are resurfaced after several hours with apparently undifferentiated cells. These are probably derived from surviving surface mucous cells that rapidly dedifferentiate. Cell proliferation peaks after about 12 h, but too late to contribute to the resurfacing process. Specialized cells reappear 1 or 2 days later, and glandular remodeling is needed in the deeper lesions. Ulcers heal by processes analogous to the deeper erosions, but the time needed is much longer (weeks). Additional tasks are the re-formation of the muscularis mucosae, and the creation of pits and glands from the initially single sheet of migrating cells.
Yeomans
N D
ND
University of Melbourne Department of Medicine, Western Hospital, Australia.
Skeljo
M V
MV
D000818:Animals; D001241:Aspirin / Q000633:toxicity*; D002465:Cell Movement; D000431:Ethanol / Q000633:toxicity*; D005753:Gastric Mucosa / Q000473:pathology / Q000503:physiopathology*; D010437:Peptic Ulcer / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D014945:Wound Healing
D000431:Ethanol; D001241:Aspirin