Slide 1
Composite: A histologic section of normal jejunum is seen in the upper left hand panel. With the dissecting microscope these villi have the appearance of that seen in the lower left hand panel. A histologic section as well as a dissecting microscopic view of gluten enteropathy are shown in the upper right and lower right hand panels respectively.

Slide 2
Gluten enteropathy or celiac disease is believed to be due to a hypersensitivity response of the intestinal mucosa to gliadin, a component of gluten, which is the major protein in wheat, rye, barley and oats. The mechanism of the disease is unclear, but some immunological basis is thought to be likely. Hypersensitivity to gluten results in destruction of the villus epithelial cells. The increased rate of cell loss results in an adaptive mucosal response that is characterized by hyperplasia and increased replication of the crypt epithelium. The crypts thus become elongated. When the adaptive capacity of the crypt cell population has been exhausted through more cell division, more rapid migration, and an increase in crypt cell numbers, a point will be reached where the proliferative compartment is incapable of reproducing the normal villus pattern of the mucosa, and the villus contours become simplified or atrophic. Celiac disease is an example of crypt hyperplastic villus "atrophy." The crypts, however, are markedly elongated such that the total mucosal thickness is not markedly decreased. There is also an increase in crypt cell mitoses.

Slide 3
As mentioned above, the cause of celiac disease is a hypersensitivity response of the intestinal mucosa to gluten. The lamina propria particularly shows a marked increase in the number of plasma cells and lymphocytes and transepithelial migration of lymphocytes across the surface epithelium (arrow) is common. Upon withdrawal of gluten, recovery is gradual and the villus morphology will return to normal in several months.