A series of routinely processed, paraffin‐embedded biopsies from 73 surgically treated oral precancerous lesions (OPL) (22 cases), and oral squamous cell carcinomas (SCC) (51 cases), was first screened using an in situ DNA hybridization technique with a human papillomavirus (HPV) DNA probe cocktail containing the 35S‐labelled DNA of HPV types 6, 11, 13, 16, 18 and 30. The specific HPV types in lesions shown to contain HPV DNA in this procedure were further analysed by using in situ hybridization and the 6 HPV DNA probes separately. A total of 12/73 (16.4%) of the lesions proved to contain HPV DNA; 6/51 (11.8%) carcinomas and 6/21 (28.6%) dysplasias. The most frequent sites of HPV DNA‐positive lesions were palate (4/7; 57%), followed by the floor of the mouth (2/8; 25%), the tongue and gingiva (11.8%). HPV 13 or HPV 30 were not found in any of the lesions studied. HPV 11 DNA was demonstrated in 2 mild dysplasia lesions, but not in carcinomas. One additional mild dysplasia proved to contain HPV 6 DNA. HPV 16 DNA was present in 5 biopsies; 3 carcinomas and 2 dysplasias. In one of the HPV 16‐positive carcinomas, HPV 18 DNA was simultaneously present. HPV 18 alone was found in 3 additional carcinomas and in one moderate dysplasia lesion. The results confirm the recently reported evidence on HPV involvement in OPL and oral cancer. The implications of these findings are discussed in terms of the possible HPV etiology of oral SCC. The use of the in situ DNA hybridization as a powerful tool (enabling the localization of specific HPV DNA sequences and the proper classification of the lesion at the same site) in the study of routinely processed oral biopsies is strongly advocated.

Oral hairy leukoplakia (HL) has been regarded as an early sign of HIV infection, and its clinical importance related to the poor outcome of the patients has been emphasized. Initially, HL was observed exclusively among male homosexuals, but subsequently demonstrated in all risk groups of HIV infection. The patient described in this article suggests that oral HL is not specific for HIV infection per se, but may be associated with immunosuppression also due to other causes. We describe an HIV-seronegative, heterosexual man suffering from an acute myeloblastic leukemia, who developed clinically and histologically typical HL while on cytostatics. Biopsy showed areas with characteristic ballooning cells, and hyphae of yeasts were demonstrated with PAS-stain. Using the in situ hybridization technique, Epstein-Barr virus (EBV) DNA with high copy numbers was disclosed in the superficial and intermediate cells, whereas human papillomavirus (HPV) DNA (types 6, 11, 16, 18) was not present.

Secondary amyloidosis is usually diagnosed by demonstrating amyloid deposits on histological sections by Congo red staining. An alternative method is a fine needle aspiration biopsy (FNAB) from subcutaneous fat which, in this study, was carried out on 301 patients. In order to test the efficiency of FNAB we analysed 146 patients from whom in addition to FNAB one or two histological samples including 125 oral and 65 rectal biopsies were available. FNAB proved very reliable for demonstrating secondary amyloidosis as estimated by the index of sensitivity (0.82). The corresponding figures for rectal and oral biopsy were 0.97 and 0.64 respectively. Although the rectal biopsy proved to be the best method, we strongly recommend FNAB from the subcutaneous fat as the preferred method for screening and diagnosing secondary amyloidosis.

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