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Oral pulse granuloma is one of the terms used to describe oral inflammatory lesions characterized microscopically by the presence of giant cells and hyaline rings. The various names proposed for these lesions reflect the lack of agreement regarding their pathogenesis. One theory advanced claims that the process represents a foreign‐body granulomatous reaction to implanted vegetable particles, more specifically those of pulses/legumes. In this study an animal model was developed where homogenized cooked legumes were implanted into the orofacial region of rats. Animals were killed at varying intervals ranging from one day to six months and the tissues associated with the implanted material were removed and processed for light microscopy. The experimentally produced lesions had many features similar to those found in humans, the similarities becoming more pronounced with time. The results indicate that the cellulose moiety of food particles of plant origin accidentally implanted into human tissues may cause the granulomatous reaction known as oral pulse granuloma.

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The presence and distribution of Epstein-Barr Virus receptors (EBVR's) on a range of normal (n = 18), dysplastic (n = 10) and malignant (n = 20) oral mucosa were studied by immunocytochemical methods using the monoclonal antibodies (MAb's) HB5 and B2. EBVR's were demonstrated as membrane staining of the spinous layers of normal non- and parakeratinized epithelium, indicating that EBVR's are differentiation-linked. This distribution was retained in dysplastic epithelium. Tissue from oral squamous cell carcinomas (SCC's) showed variable reactivity of only a few cells scattered randomly within the samples. Furthermore, a sensitive in situ hybridization (ISH) technique was used to determine if Epstein-Barr virus (EBV) was present in normal (n = 15) and oral squamous cell carcinoma tissue (n = 20). No EBV DNA was demonstrated within either normal or malignant epithelium, suggesting that the virus does not persist in normal oral stratified squamous epithelium nor is there any evidence for a role in oral carcinogenesis.