Aphthous ulcers are the most common oral mucosal lesions in the general population. Several precipitating factors for aphthous ulcers are suggested to operate on subjects with genetic predisposition. Sometimes aphthous ulcers can be the sign of systemic diseases. Therefore, it is essential to establish a correct diagnosis to determine suitable therapy. There are several diseases potentially responsible for oral ulcers. Sometimes appearance of periodic oral ulcers coincides with periodic fever and other symptoms leading to the diagnosis of a rare childhood disease: PFAPA (periodic fever, aphthous stomatitis, pharyngitis and adenopathy) syndrome. PFAPA or Marshall's syndrome is characterized by abrupt onset of periodic episodes of high fever accompanied by aphthous stomatitis, pharyngitis and cervical adenitis, often associated with headache and / or abdominal or joint pain. Owing to the periodic onset of oral symptoms, often an oral physician or pediatric dentist may be the first healthcare worker to evaluate a child with clinical signs compatible with PFAPA syndrome. Children diagnosed with this condition require systematic oral follow-up to monitor for signs of ulceration.

Gingival metastases are infrequent and invariably associated with a widespread disease and a poor prognosis. Because of their unremarkable clinical appearance, they can be difficult to distinguish from more common gingival hyperplastic or reactive lesions, such as pyogenic granuloma, peripheral giant cell granuloma, and peripheral ossifying granuloma. We are reporting here an unusual case of a 36-year-old man with a mixed testicular germ cell tumor presenting as a metastatic pure choriocarcinoma involving the maxillary gingiva, extending from the first left premolar to the left second maxillary molar, mimicking a 'benign looking' gingival mass. Gingival metastases may be the first manifestation of a widespread metastatic disease and therefore particular attention must be paid to gingival lesions associated with atypical clinical symptoms and/or signs.

Tumor cells can escape complement-dependent cytotoxicity (CDC) by expressing complement restriction factors (CRFs), CD46, CD55 and CD59. CRF-expression in non-neoplastic mucosa of the head and neck was compared with biopsies of the head and neck squamous cell carcinoma (HNSCC) and cell lines derived from oral squamous cell carcinomas (OSCC). Normal mucosa and HNSCC tumor tissue (poor, moderate, or well differentiated) specimens were immunostained with anti-CRF monoclonal antibodies. Immunostaining of the OSCC cell lines (SCC12 and SCC71) was examined under laser scan fluorescence microscopy. CD46, CD55 and CD59 were highly expressed in HNSCC cells including T1/T2N0M0 stages. The CRF expression was much lower or absent in non-neoplastic squamous epithelia or in the submucosa of both normal and tumor tissues. Enhanced staining of tumor tissues at stages T1/T2 indicates that the CRFs are overexpressed by primary tumors before metastasis to either lymph nodes or organs (N0M0 stage) suggesting that CRFs are formed early during tumorigenesis.

Journal of Oral Pathology & MedicineVolume 35, Issue 8 p. 520-522 Reply to Letter to the Editor J. Becker, J. Becker Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this authorA. Böcking, A. Böcking Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this authorU.R. Hengge, U.R. Hengge Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this authorD. Maraki, D. Maraki Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this author J. Becker, J. Becker Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this authorA. Böcking, A. Böcking Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this authorU.R. Hengge, U.R. Hengge Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this authorD. Maraki, D. Maraki Universitätsklinikum DüsseldorfE-mail: [email protected]Search for more papers by this author First published: 07 August 2006 https://doi.org/10.1111/j.1600-0714.2006.00453_2.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Volume35, Issue8September 2006Pages 520-522 RelatedInformation

Journal of Oral Pathology & MedicineVolume 35, Issue 8 p. 524-524 Reply to Letter to the Editor S. Nigam, S. Nigam Maulana Azad Medical (MAM) College, Bahadur Shah Zafar Marg, New Delhi 110002, IndiaE-mail: info@mamc.ac.inSearch for more papers by this authorK. K. Dhingra, K. K. Dhingra Maulana Azad Medical (MAM) College, Bahadur Shah Zafar Marg, New Delhi 110002, IndiaE-mail: info@mamc.ac.inSearch for more papers by this authorA. Gulati, A. Gulati Maulana Azad Medical (MAM) College, Bahadur Shah Zafar Marg, New Delhi 110002, IndiaE-mail: info@mamc.ac.inSearch for more papers by this author S. Nigam, S. Nigam Maulana Azad Medical (MAM) College, Bahadur Shah Zafar Marg, New Delhi 110002, IndiaE-mail: info@mamc.ac.inSearch for more papers by this authorK. K. Dhingra, K. K. Dhingra Maulana Azad Medical (MAM) College, Bahadur Shah Zafar Marg, New Delhi 110002, IndiaE-mail: info@mamc.ac.inSearch for more papers by this authorA. Gulati, A. Gulati Maulana Azad Medical (MAM) College, Bahadur Shah Zafar Marg, New Delhi 110002, IndiaE-mail: info@mamc.ac.inSearch for more papers by this author First published: 07 August 2006 https://doi.org/10.1111/j.1600-0714.2006.00452_2.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume35, Issue8September 2006Pages 524-524 RelatedInformation

Journal of Oral Pathology & MedicineVolume 35, Issue 7 p. 459-460 Author index to abstracts First published: 07 July 2006 https://doi.org/10.1111/j.1600-0714.2006.00476.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume35, Issue7August 2006Pages 459-460 RelatedInformation

This report describes the 'Skull from Bangkok', collected by Rudolf Virchow (Berlin, Germany) in the late 19th century. The skull is part of an extensive anthropological collection of skeletons and skulls from all over the world. The skull was probably brought to Berlin during the years 1882-1883. An inscription on the frontal bone gives the name of the skull: 'Skull from Bangkok'. The few remaining teeth of the maxilla show brown black stains because of betel quid chewing. In the collection, there is an extensive number of skulls from South- and Southeast Asia with similar betel stains. Virchow himself was aware of this habit and has described some of the skulls in detail often mentioning the black stains because of betel quid chewing. The Skull from Bangkok is a proof that betel quid chewing was prevalent in Siam of the late 19th century.

Molecular epidemiological studies have now provided evidence that an individual susceptibility to cancer is mediated by genetic and environmental factors. Genetic polymorphisms have been described for enzymes involved in the metabolism of tobacco carcinogens and cancer risk is determined by the degree of expression and/or activity of enzymes involved in carcinogen activation or deactivation. The objective of this study was to investigate the GSTM1 null polymorphism and the risk for oral leukoplakia in individuals with tobacco-smoking habit in a Brazilian population. A total of 52 tobacco-smoking patients with oral leukoplakia and 52 tobacco-smoking controls were recruited in a Brazilian population. The GSTM1 genotypes were studied by polymerase chain reaction-based methods. The frequency of the GSTM1 null genotype in the group with oral leukoplakia (57.7%) was statistically different from the controls (34.6%; OR: 2.57, 95% CI: 1.16-5.69, P < 0.05). The stratification of the samples according to the level of dysplasia showed increased prevalence of GSTM1 null genotype on lesions with moderate/severe histological dysplasia (68.2%) compared with the control group (31.9%). This difference was statistically significant (OR: 4.59, 95% CI: 1.29-16.33, P < 0.05). In conclusion, the GSTM1 null genotype may increase the risk for oral leukoplakia development.

Angiokeratoma is a rare, cutaneous vascular disorder that can occur in several clinically distinct conditions. It usually presents as multiple, red to blue or black, asymptomatic papules on the skin. Oral mucosal involvement is common in the systemic form, but very rare in the localized forms of angiokeratomas. We report the second case of a solitary papular angiokeratoma of the oral cavity.