After rats were orally administrated with bovine serum albumin (BSA) for 14, 30 and 90 days, we examined the localization of the absorbed intact BSA immunohistologically and the production of the antibody against the absorbed BSA in the intestine.
Light microscopical sections with hematoxylin-eosin (H-E) stain, as compared with normal intestine, revealed an increased number of disrupted goblet cells and extended macrophages in the lamina propria.
By the immunofluorescent method, intact BSA absorbed by the intestine was found in macrophages, intestinal columnar cells, the lateral extracellular spaces between the columnar cells, goblet cells and mucous materials in the lumen.
The cytoplasm of the plasma, macrophages and intestinal columnar cells showed the antibody against BSA.
These findings suggest that orally administrated BSA is absorbed in macromolecular form by the intestine and the antibody against BSA produced in the plasma cells is secreted in the lumen as secretory IgA (SIgA). And consequently, immunocomplexes are formed in the lumen, and there is an increased number of disrupted goblet cells and mucous release.

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The lymphoepithelial cysts (LEC) of the oral cavity are present as asymptomatic, elevated, movable, round, soft and yellow-to-white lesions measuring about 0.1 to 1.0 cm in size. They are most commonly seen on the floor of the oral cavity, and other sites include the postlateral portion of the tongue, the soft palate, the buccal mucosa and lip. It has been reported that the highest frequency occurs between the ages of 20 and 60 years with a mean of 30 years in previous studies [1-4].
The origin of the intraoral LEC is not known, but several theories (BHASKER [2, 5], BERNIER [6] and KNAPP [7, 8]) have been reported.
Histologically, the LEC is completely or partially surrounded by lymphoid tissues which contain plasma cells, lymphocytes and reactive macrophages.
The distributions of IgG, IgA, IgM and C₃ on paraffin embedded sections of intraoral LEC and tonsillar crypts have been reported on employing the peroxidase-antiperoxidase method (PAP). TOTO suggested that the lymphoid tissues of the LEC reveal the inflammatory process [9].
Lectins, derived from both plants and animals, have unique ability specific sugar molecules. HOWARD [10] reported PNA binding sites of macrophages in several tissues (lymph nodes and tonsils) as compared with immunohistochemical staining for lysozyme. Hsu and REE pointed out that PNA and Con A binding sites of macrophages were more sensitive after sections were pretreated with trypsin [11-13].
This report is concerned with the identification and the distribution of IgG, IgA, IgM, lysozyme and lectin binding sites in the LEC of the oral cavity and neck. And also, we examined the differences in the findings between the LEC of the oral cavity and neck.

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Carbon sheets made of fine meshwork identical with the surface layer of the FRS implant were prepared as specimens and bone explants were cultured on the specimen aimed at observing the in vitro response of the bone tissue to the carbon fine Rahmen surface structure. The findings are summarized below.
1. The cells passed through the fine Rahmen surface structure layer of carbon in a short period of time.
2. The carbon fiber served as a scaffold for attachment of the cells.
3. The bone-derived cells proliferated to form a tissue matrix within the spaces of the fine Rahmen surface structure of the carbon.
4. Collagen fibers became either attached to the carbon fibers or interwoven with the carbon fibers or both, thus giving an anchoring effect.
5. The fine Rahmen surface structure of the carbon was buried in and unified with the tissue grown from bone.

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