Direct immunofluorescence (IF) investigations in oral aphthae were performed in 17 patients with recurrent aphthous ulcers (RAU) and in 9 patients with Behçet’s disease (BD). In addition, cutaneous hyperreactivity lesions from 2 BD patients were examined. The results were compared to direct IF findings in 28 patients with nonaphthous oral diseases. There was no difference between direct IF on oral aphthae in RAU compared to BD. Deposition of C3 in vessel walls of the subepithelial connective tissue was observed in 13 of 17 patients with RAU and in all patients with BD. IgM deposits in vessel walls were found in 5 RAU and 3 BD patients. Deposition of C1q or C4 was not present. By contrast, IgG and/or IgM, C1q, C3 and C4 were detected in dermal vessel walls of skin hyperreactivity lesions from 2 BD patients. This finding is considered to be a true immune complex vasculitis. Compared to nonaphthous oral lesions, oral aphthae of BD and RAU were characterized by C3 deposition in the subepithelial vessel walls.

Comparative in vivo examinations of skin (cutaneous pathergy test, skin window technique over 24 h according to Rebuck) were carried out in 12 patients with Behçet’s disease (BD) and in 13 healthy volunteers serving as controls. 10 out of 12 patients at active phases of BD showed a positive papular (-pustular) skin reactivity to needle prick or vene puncture. These 10 patients simultaneously revealed an increased chemotactic activity of polymorphonuclear leukocytes (PMNL) in vitro. In the controls all pathergy tests were negative and chemotaxis of PMNL was within normal range. The proportion of PMNL initially coming up to 100% in the skin window preparations, very rapidly decreased in patients with BD as compared to a distinctly slower drop in the controls. Conversely to the number of PMNL, the skin window cellular pattern was built up by monophagocytic cells replacing the PMNL. The phenomenon of ‘rapid depletion of PMNL’, from skin window can be considered an additional hint on the functional disturbance of the PMNL involved in the pathogenesis of BD.