BackgroundCondyloma acuminata caused by human papilloma viruses, (HPV) is a sexually transmitted disease (STD) appearing most frequently as soft, pink cauliflower like growths in moist areas, such as the genitalia, mouth and other places. The disease is highly contagious, can appear singly or in groups, small or large. In children, the isolation of a sexually transmitted organism may be the first indication that an abuse has occurred. Although the presence of a sexually transmissible agent from a child beyond the neonatal period is suggestive of sexual abuse, exceptions do exist.Case presentationThe authors report the clinical case of a five-year-old Caucasian male with lesions located in the dorsal surfaces of the posterior tongue and palate. Both lesions had a firm consistency, reddish appearance and presence of whitish areas and regions of ulceration. During the interview, the mother reported that the boy had been sexually abused.ConclusionSexually transmitted disease may occur during sexual abuse. Dentists as well as pediatricians have a role to play in identifying and treating these children. The diagnosis is essentially clinical (anamnesis and physical examination), but also the use of cytology eventually resorts to biopsy of the suspicious lesions for histological examination. The therapeutic option was the excision of the lesions.

Screening for expression of amelogenesis-related proteins represents a powerful molecular approach to characterize odontogenic tumors and investigate their pathogenesis. In this study, we have examined the presence and distribution of odontogenic ameloblast-associated protein (ODAM), amelotin (AMTN), ameloblastin (AMBN), and amelogenin (AMEL) by immunohistochemistry in samples of adenomatoid odontogenic tumor (AOT), calcifying epithelial odontogenic tumor (CEOT), developing odontoma, ameloblastoma, calcifying cystic odontogenic tumor (CCOT), ameloblastic fibroma (AF), myxoma, odontogenic fibroma (OF), and reduced enamel epithelia (REE). Positive results were obtained in those tumors with epithelial component, except for AF, OF, and ameloblastoma. ODAM was found around mineralized structures (dystrophic calcifications) and CEOT's amyloid, whereas AMTN stained the eosinophilic material of AOTs. The CCOT transitory cells to ghost cells were strongly positive with all proteins except AMEL, and the REE as well as odontomas showed immunoexpression for ODAM, AMTN, AMBN, and AMEL similar to those found in normal rat tooth germs. Based on these results, some histopathogenetic theories were formulated.

he adenomatoid odontogenic tumor (AOT) is a clinically benign lesion. Discussions about the AOT hamartomatous or neoplastic nature, and the probable odontogenic epithelial cell it originates from still exist. This research aimed to study and discuss the subject by the immunohistochemical detection of cytokeratins, laminin, collagen IV, PCNA and p53 in 8 tumor samples and 8 dental follicle samples containing reduced enamel epithelium. The results have shown that CK14 labelling indicated differentiation grades for secreting ameloblasts or ameloblasts in the post-secreting stage in the adenomatoid structure of AOT. Laminin, found on the luminal surface of adenomatoid structures, was compatible with the reduced enamel epithelium during the "protective stage of amelogenesis". PCNA specifically labelled the spindled areas and peripheral cords of the AOT, indicating that these areas are responsible for tumor growth. After considerations about pathogenesis, the authors suggested that the nature of AOT is hamartomatous with histogenesis from the reduced enamel epithelium. Uniterms: Odontogenic neoplasms; Adenomatoid odontogenic tumor; Immunohistochemistry. tumor odontogênico adenomatóide (TOA) é uma lesão clinicamente benigna, cujas discussões acerca de sua natureza hamartomatosa ou neoplásica, e provável célula epitelial odontogênica de origem ainda existem. Este projeto de pesquisa teve por objetivo estudar o assunto através da detecção imuno-histoquímica das citoqueratinas, laminina, colágeno IV, PCNA e p53, utilizando-se para isso 08 amostras do tumor e 08 amostras de folículo pericoronário contendo epitélio reduzido do órgão do esmalte (EROE). Os resultados mostraram que a marcação da CK14 sinalizou graus de diferenciação para ameloblastos secretores ou pós-secretores nas estruturas adenomatóides do TOA, e a laminina presente em sua superfície luminal foi compatível com o EROE durante o "estágio protetor" da amelogênese. O PCNA marcou especificamente áreas enoveladas e cordões periféricos do TOA, indicando serem estes os responsáveis pelo seu crescimento. Após considerações sobre patogênese, os autores propuseram natureza hamartomatosa e histogênese a partir do EROE para o TOA. Unitermos: Neoplasias odontogênicas; Tumor odontogênico adenomatóide; Imunoistoquímica.

Social isolation has affected a large number of people and may lead to impairment of physical and mental health. Although stress resulting from social isolation may increase cancer progression, its interference on tumorigenesis is poorly known. In this study, we used a preclinical model to evaluate the effects of social isolation stress on chemically induced oral carcinogenesis. Sixty-two 21-day-old male Wistar rats were divided into isolated and grouped groups. After 90 days of age, the rats from both groups underwent oral carcinogenesis with 4-nitroquinoline 1-oxide (4NQO) for 20 weeks. All rats were assessed for depressive-like behavior and euthanized for oral squamous cell carcinoma (OSCC) diagnosis and measurement of inflammatory mediators in the tumor microenvironment. Social isolation stress increased the OSCC occurrence by 20.4% when compared to control. Isolated rats also showed higher tumor volume and cachexia than the grouped rats. Social isolation did not induce changes in the depressive-like behavior after carcinogenic induction. Tumors from stressed rats had increased levels of the inflammatory mediators, TNF-alpha, IL1-beta and MCP-1. The concentrations of TNF-alpha and MCP-1 were significantly increased in the large tumors from isolated animals. Higher tumor levels of TNF-alpha, IL-6, IL1-beta and MCP-1 were positively correlated with OSCC growth. This study provides the first evidence that social isolation stress may facilitate OSCC occurrence and tumor progression, an event accompanied by increased local levels of inflammatory mediators.

Cyclosporin, phenytoin, and nifedipine led to phased and drug-related gene expression patterns, resulting in impaired collagen metabolism, despite the lack of prominent clinical signs.