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A series of 144 surgically treated benign oral mucosal lesions were analysed using an in situ DNA hybridization technique with 35S-labeled human papillomavirus (HPV) DNA probes to demonstrate the DNA of HPV types 6, 11, 13, and 16, in routinely processed, paraffin-embedded biopsy specimens. These lesions and an additional 62 benign oral mucosal biopsy specimens (total, 206 specimens) were also assessed by the indirect immunoperoxidase (IP-PAP) technique to detect the expression of HPV structural proteins (viral antigens). A total of 54/206 (26.2%) lesions were observed to express HPV antigens, being found in 45/92 (48.9%) of the squamous cell papillomas/condylomas, in 1/54 fibrous hyperplasias, in 1/8 true fibromas, and in 7/8 (87.5%) of the focal epithelial hyperplasia (FEH) lesions. Of the HPV DNA-positive lesions, 15/45 (33.3%) expressed HPV antigens, the expression not being related to any particular HPV type. HPV DNA sequences were found in 45/144 (31.3%) of the lesions. HPV DNA was present with the highest frequency in FEH (83.3%), followed by the papilloma/condyloma group (33.8%), papillary hyperplasia (28.6%), fibrous hyperplasia (24.4%), and true fibromas (14.3%). The most frequent HPV type was HPV 11, representing 37.8% of the DNA-positive lesions. HPV 13 DNA, previously regarded as specific to FEH, was disclosed as a single HPV type in seven cases, and as a double infection by HPV 11 and 13 in an additional three cases, including all five morphologically distinct entities. Noteworthy is the discovery of the high-risk HPV type 16 DNA in 17.8% of the DNA-positive lesions, four papilloma/condyloma lesions, three fibrous hyperplasias, and one FEH.(ABSTRACT TRUNCATED AT 250 WORDS)

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– A centrally located maxillary myxoma with malignant histologic appearance and aggressive clinical course is reported in a 40‐yr‐old man. The gelatinous polypoid tumor mass was diagnosed as a myxoma in the first biopsy. The tumor recurred rapidly (within 3 wk) eroding the bony structures of the maxillary sinus and the hard palate and infiltrating the adjacent soft tissues. In repeated biopsy (as well as reassessment of the first biopsy) the tumor was found to be composed of plump stellate cells, some of which were pleomorphic with atypical and bizarre mitotic figures. The amorphic myxoid matrix contained acid mucopolysaccharides and was completely devoid of lipids. Electron microscopy demonstrated that the tumor cells were identical to fibroblasts, which is consistent with the appearance of myxoma cells. When radiotherapy was unsuccessful, we removed the left maxilla with orbital excenteration and reconstructed the jaw. Three years later the patient died accidentally. At autopsy, no recurrence of myxoma or distant metastases were found. Due to the malignant histologic appearance and the aggressive clinical course, this tumor can be called an odontogenic myxosarcoma and should be added to the WHO classification as a malignant variant of odontogenic myxoma.