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Clinical and histopathological features were investigated in 43 cases of oral lobular capillary hemangiomas (LCH) with a special reference to characteristics of the vascular elements. The lesions affected females more than males by a ratio of 1:1.5. Average age of the patients was 52.7 years. The lesions involved the gingiva (n = 15), the tongue (n = 13), the labial mucosa (n = 10) and other sites. The lesions appeared usually as a pedunculated mass with ulceration; size of the lesions was up to 15 mm. Histologically, a lobular area and an ulcerative area were distinguished. The density of vessels was about 1045/mm2 and 160/mm2 in the lobular and ulcerative areas, respectively. The average diameter of the vascular lumen was 9.1 5.6 mm (range: 2.8-42.0 mm) and 18.8 20.9 mm (range: 5.6-139.7 mm) in the lobular and ulcerative areas, respectively. In the lobular area, most of the vessels had an inner layer of endothelial cells showing positive reaction for von Willebrand factor (vWF) and CD34, as well as an outer layer of mesenchymal cells showing positive reaction for alpha-smooth muscle actin (ASMA). However, in the ulcerative area, there was a variety of types of vessels consisting of various proportions of both endothelial and ASMA-positive perivascular mesenchymal cells. These results indicate that most of the vascular elements in the lobular area resemble more pericapillary microvascular segments than they do capillaries. Thus, the authors propose the term 'lobular pericapillary hemangioma' to represent this type of lesion.

The pathogenic ability of hepatitis B e antigen (HBeAg) to induce membranous glomerulonephritis was evaluated by the most specific method presently available. Monoclonal antibody was raised against HBeAg, and F(ab')2 fragments were obtained and labeled with fluorescence. By this reagent, 10 out of 16 patients with membranous glomerulonephritis with hepatitis B surface antigen in the serum revealed granular deposition of HBeAg along glomerular capillary walls. Among the cases with glomerular HBeAg deposits, nine had detectable HBeAg in the serum and one had antibody to HBeAg (anti-HBe). The specificity of HBeAg staining was ascertained by blocking and inhibition tests, and the fluoresceinated anti-HBe F(ab')2 reagent did not stain the glomerular immune deposits in the patients with membranous glomerulonephritis who did not carry hepatitis B virus (HBV). None of the studied patients showed deposition of hepatitis B surface or core antigens in the glomerulus. On the basis of these results, immune complexes involving HBeAg may induce membranous glomerulonephritis in persons who carry HBV.

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