Biocompatibility of orthodontic adhesives in rat subcutaneous tissue

ABSTRACT OBJECTIVE: The objective of the present study was to verify the hypothesis that no difference in biocompatibility exists between different orthodontic adhesives. MATERIAL AND METHODS: Thirty male Wistar rats were used in this study and divided into five groups (n=6): Group 1 (control, distilled water), Group 2 (Concise), Group 3 (Xeno III), Group 4 (Transbond XT), and Group 5 (Transbond plus Self-Etching Primer). Two cavities were performed in the subcutaneous dorsum of each animal to place a polyvinyl sponge soaked with 2 drops of the respective adhesive in each surgical loci. Two animals of each group were sacrificed after 7, 15, and 30 days, and their tissues were analyzed by using an optical microscope. RESULTS: At day 7, Groups 3 (Transbond XT) and 4 (Xeno III) showed intense mono- and polymorphonuclear inflammatory infiltrate with no differences between them, whereas Groups 1 (control) and 2 (Concise) showed moderate mononuclear inflammatory infiltrate. At day 15, severe inflammation was observed in Group 3 (Transbond XT) compared to other groups. At day 30, the same group showed a more expressive mononuclear inflammatory infiltrate compared to other groups. CONCLUSION: Among the orthodontic adhesive analyzed, it may be concluded that Transbond XT exhibited the worst biocompatibility. However, one cannot interpret the specificity of the data generated in vivo animal models as a human response

Immunohistochemical detection of Ki-67 is not associated with tumor-infiltrating macrophages and cyclooxygenase-2 in oral squamous cell carcinoma.

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-11-20T18:14:00Z No. of bitstreams: 1 Boas DSV Immunohistochemical....pdf: 439218 bytes, checksum: f569901cc76550ae95534d03260b9b8e (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2014-11-20T18:14:11Z (GMT) No. of bitstreams: 1 Boas DSV Immunohistochemical....pdf: 439218 bytes, checksum: f569901cc76550ae95534d03260b9b8e (MD5)Made available in DSpace on 2014-11-20T18:30:16Z (GMT). No. of bitstreams: 1 Boas DSV Immunohistochemical....pdf: 439218 bytes, checksum: f569901cc76550ae95534d03260b9b8e (MD5) Previous issue date: 2010Federal University of Bahia. Institute of Health Sciences. Department of Bio-morphology. Salvador, BA, Brasil / Federal University of Rio de Janeiro. Institute of Biomedical Sciences. Department of Histology and Embryology. Rio de Janeiro, RJ, BrasilFederal University of Rio de Janeiro. Institute of Biomedical Sciences. Department of Histology and Embryology. Rio de Janeiro, RJ, BrasilFederal University of Rio de Janeiro. Institute of Biomedical Sciences. Department of Histology and Embryology. Rio de Janeiro, RJ, BrasilFederal University of Rio de Janeiro. Institute of Biomedical Sciences. Department of Histology and Embryology. Rio de Janeiro, RJ, BrasilFundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilFederal University of Rio de Janeiro. School of Dentistry. Department of Pathology and Oral Diagnosis. Rio de Janeiro, RJ, BrasilFederal University of Bahia. School of Dentistry. Laboratory of Oral Surgical Pathology. Salvador, BA, BrasilBACKGROUND: An inflammatory component consisting of cells and chemical mediators may influence the proliferation and dissemination of the oral squamous cell carcinoma (OSCC). In the present study, we evaluated the possible relationship between Ki-67, tumor-associated macrophages (TAMs), and COX-2 in OSCCs. In addition, the immunodetection of these proteins was associated with different histological grades of malignancy, including invasive and in situ tumors. METHODS: Twenty-seven OSCC cases were examined by light microscopy using criteria adopted WHO, and immunohistochemistry for Ki-67, CD68, and COX-2 using EnVision System in invasive and in situ lesions. Immunohistochemical detection of these proteins was assessed and scored for COX-2, and results were compared with their histological grades of malignancy. RESULTS: A correlation between Ki-67, COX-2, and CD68 was not found. Histological grade of malignancy (HDM) was associated with the Ki-67 immunostaining (P = 0.00), but this was not observed regarding both CD68 (P = 0.51) and COX-2 (P = 0.89). Furthermore, there was a COX-2 overexpression in 62.96% of the sample, and a high density of TAMs in both OSCCs and in situ carcinomas. CONCLUSIONS: Imunolabeling for Ki-67 was directly correlated with less-differentiated tumors, suggesting that this marker may contribute to understand the biological behavior of OSCC, and help to distinguish risk groups of OSCC. Furthermore, the lack of correlation between Ki-67, COX-2, and CD68 indicates that the latter two markers may play a pivotal role in oral carcinogenesis. However, further studies are needed to clarify their contribution for cell proliferation and tumor differentiation

Immunohistochemical expression of p53, p16 and hTERT in oral squamous cell carcinoma and potentially malignant disorders

Oral carcinogenesis is a multi-step process. One possible step is the development of potentially malignant disorders known as leukoplakia and erytroplakia. The objective of this study was to use immunohistochemistry to analyze the patterns of expression of the cell-cycle regulatory proteins p53 and p16INK4a in potentially malignant disorders (PMD) of the oral mucosa (with varying degrees of dysplasia) and in oral squamous cell carcinomas (OSCC) to correlate them with the expression of telomerase (hTERT). Fifteen PMD and 30 OSCC tissue samples were analyzed. Additionally, 5 cases of oral epithelial hyperplasia (OEH) were added to analyze clinically altered mucosa presenting as histological hyperplasia without dysplasia. p53 positivity was observed in 93.3% of PMD, in 63.3% of OSCC and in 80% of OEH. Although there was no correlation between p53 expression and the grade of dysplasia, all cases with severe dysplasia presented p53 suprabasal immunoexpression. p16INK4a expression was observed in 26.7% of PMD, in 43.3% of OSCC and in 2 cases of OEH. The p16INK4a expression in OEH, PMD and OSCC was unable to differentiate non-dysplastic from dysplastic oral epithelium. hTERT positivity was observed in all samples of OEH and PMD and in 90% of OSCC. The high hTERT immunoexpression in all three lesions indicates that telomerase is present in clinically altered oral mucosa but does not differentiate hyperplastic from dysplastic oral epithelium. In PMD of the oral mucosa, the p53 immunoexpression changes according to the degree of dysplasia by mechanisms independent of p16INK4a and hTERT

Carcinoma de células escamosas oral - contribuição de vírus oncogênicos e alguns marcadores moleculares no desenvolvimento e prognóstico da lesão: uma revisão Oral squamous cell carcinoma - contribution of oncogenic virus and some molecular markers in the development and prognosis of the lesion: a review

O carcinoma de células escamosas oral é um evento de muitas etapas, cuja incidência cresce continuamente, particularmente em jovens, numa amplitude que não pode ser completamente explicada pelo aumento da exposição a fatores de risco, como o tabaco e o álcool. Recentes investigações moleculares sugerem que existem múltiplos eventos genéticos, e vírus oncogênicos que são capazes de alterar as funções normais de oncogenes e genes de supressão tumoral. O objetivo deste artigo foi revisar o conhecimento atual sobre o papel do papilomavírus humano (HPV), Epstein-Barr vírus (EBV), P53 e telomerase no desenvolvimento e prognóstico do carcinoma de células escamosas oral.<br>Oral squamous cell carcinoma is a multistep event that continues to increase in incidence, particularly in the young, and to an extent that cannot be fully explained by increased exposure to known risk factors, as tobacco or alcohol. Recent molecular investigations suggest that there are multiple genetic events, and oncogenic virus that are able to alter the normal functions of oncogenes and tumor suppressor genes. The aim of the present article was to review the current knowledge on the role of Human papillomavirus (HPV), Epstein-Barr virus (EBV), P53 and telomerase in the development and prognosis of the oral squamous cell carcinoma