Electron microscopic study on the pathogenesis of recurrent aphthous ulceration as compared to Behçet's syndrome.

In the prickle-cell layer of the oral epithelium of recurrent aphthous ulceration (RAU) the reticuloid cells with homogeneous, electron-lucent nuclei were attached to the degenerated prickle cells and ingested the cytoplasm of the prickle cells. The reticuloid cells came in contact with small lymphocytes, to which the immunologic information was transferred, inducing them to undergo blast transformation. Lymphoid cells, corresponding to T-cells, may produce a cytotoxic factor, since the prickle cells ultimately undergo degeneration. These changes are consistent with those of delayed hypersensitivity reactions. The cytoplasm of prickle cells apparently acts as an autoantigen. In Behçet's syndrome the macrophages were encountered in the epithelium. Other consequences were quite similar to those of RAU. The nucleus of the macrophage is more electron dense and has condensed chromatin along with the nuclear membrane. This can be a difference between Behçet's syndrome and RAU only at the initial stage of the diseases.