Influence of obesity on experimental periodontitis in rats: histopathological, histometric and immunohistochemical study.

OBJECTIVES: This study assessed the influence of obesity on the progression of ligature-induced periodontitis in rats. MATERIALS AND METHODS: Forty-eight adult Wistar rats were randomly divided into two groups: the HL group (n = 24) was fed high-fat animal food to induce obesity, and the NL group (n = 24) was fed normolipidic animal food. Obesity was induced within a period of 120 days, and the induction of experimental periodontitis (EP) was subsequently performed for 30 days. The animals were euthanized after 7, 15, and 30 days, and the jaws were removed for histopathological, histometric, and immunohistochemical analyses. Tartrate-resistant acid phosphatase (TRAP), receptor activator of nuclear factor kappa beta ligand (RANKL), and osteoprotegerin (OPG) were analyzed via immunolabeling. RESULTS: Histological findings indicated that the inflammation was more extensive and lasted longer in the HL/EP; however, advanced destruction also occurred in the NL/EP. Greater bone loss was verified in the HL/EP group (2.28 ± 0.35) in the period of 7 days than in the NL/EP group (1.2 ± 0.29). High immunolabeling was identified in the HL/EP group in the initial periods for RANKL and TRAP, whereas the NL/EP group presented with moderate immunolabeling for both factors. The HL/EP and NL/EP groups showed low immunolabeling for OPG. CONCLUSIONS: Obesity induced by a high-fat diet influenced alveolar bone metabolism when associated with experimental periodontitis and caused a more severe local inflammatory response and alveolar bone loss. CLINICAL RELEVANCE: Obesity is related to greater alveolar bone loss and an accentuated local inflammatory response, which may be reflected in the clinical severity of periodontitis and dental loss.

Computer-assisted analysis of cell proliferation markers in oral lesions.

Abnormalities in any component of the cell cycle regulatory machine may result in oral cancer, and markers of cell proliferation have been used to determine the prognosis of tumor progression. The aim of this study was to determine whether silver-stained nucleolar organizer region (AgNOR) and Ki-67 measurements could improve the assessment of growth rates in oral lesions. Eighty-three oral biopsies were studied, 20 of which were classified as fibrous inflammatory hyperplasia (FIH), 40 as leukoplakia (LKP) and 23 as oral squamous cell carcinoma (OSCC). Within the LKP group, 22 out of 29 biopsies were diagnosed as non-dysplastic leukoplakia (LK) and 18 as dysplastic leukoplakia (DLK), presenting discrete, moderate and severe dysplasia. Ki-67 immunolabeling of the lesions increased steadily in the following order: FIH, DLK, LK and OSCC, indicating that Ki-67 is a good marker for predicting the proliferative fraction among benign, premalignant and malignant oral lesions. The median values of AgNOR parameters indicate that the morphometric index gives better results regarding the proliferative rate than the numerical one. A series of linear regressions between AgNOR parameters and Ki-67 showed positive associations. We conclude that a combination of Ki-67 and morphometric AgNOR analyses could be used as an aid in the determination of the proliferative status of oral epithelial cells in oral cancer.

Análise da superfície de esmalte de dentes decíduos submetidos a diferentes tempos de desmineralização / Deciduous enamel surface analysis after different periods of demineralization

É objetivo deste trabalho avaliar as alterações superficiais apresentadas pelo esmalte de dentes decíduos após diferentes períodos de desmineralização em ácido láctico (pH=4,5). Utilizou-se 25 dentes decíduos divididos nos seguintes grupos: I-Controle; II-Desmineralização por 12 horas; III-Desmineralização por 24 horas; IV-Desmineralização por 48 horas; V-Desmineralização por 72 horas. Logo após, as amostras foram analisadas macroscópica e microcospicamente. Observou-se que houve alterações estruturais superficiais no esmalte, o qual exibiu macroscopicamente perda de brilho e microscopicamente grande perda de mineral, sendo estas mais evidentes a partir de 48 horas de desmineralização. Os autores concluíram que as alterações subclínicas, devem ser de conhecimento do profissional para que ele possa educar e conscientizar seus pacientes quanto ao desenvolvimento de medidas preventivas efetivas, para evitar o desenvolvimento de futuras lesões de cárie

Presença do papilomavirus humano em lesöes malignas de mucosa oral / Presence of human papillomavirus in malignant oral lesions

O objetivo deste estudo foi investigar a prevalência do papilomavírus humano 6/11 e 16/18 em pacientes, com lesöes orais clínicamente diagnosticadas como leucoplasias, atendidas na Faculdade de Odontologia de Araraquara, UNESP, Brasil. Após a inclusäo em parafina, os cortes corados com H&E, foram selecionadas 30 biópsias e separadas em 3 grupos: lesöes sem displasia (n=10), lesöes com diferentes graus de displasia (n=10) e carcinoma espinocelular invasivo(n=10). As lesöes que apresentaram displasia epitelial foram classificadas de acordo com os critérios histopatológicos propostos por Van Der Waal. As lesöes foram investigadas para a presença de HPV por hibridizaçäo in situ com sondas biotiniladas de amplo espectro, 6/11 e 16/18. HPV 16/18 foi detectado em 20 por cento (n=2) das biópsias com displasia severa. A presença de HPV 16/18 em lesöes malignas sugere sua importância como fator de risco na carcinogênese oral

[Presence of human papillomavirus in malignant oral lesions]. / Presença do papilomavirus humano em lesões malignas de mucosa oral.

The purpose of this study was to investigate the prevalence of human papillomavirus 6/11 and 16/18 in patients, with oral lesions clinically diagnosed as leucoplakia, attending the School of Dentistry, University of São Paulo State/UNESP, Brazil. After paraffin embedded process, in the sections staining with H&E, 30 biopsies were screened and separated on 3 groups: 10 oral lesions without dysplasia, 10 with dysplasia, and 10 with invasive squamous cell carcinoma. The lesions with dysplasia were classified in agreement with Van Der Wall's histopathological standard method. Oral lesions were investigated for the presence of human papillomavirus (HPV) by in situ hybridization with wide-spectrum, 6/11 and 16/18 biotinylated probes. HPV 16/18 was found in 20% (n = 2) of the leucoplakia with severe-degree dysplasia. The presence of HPV 16/18 in malignant lesions suggests its importance as a risk factor for oral carcinogenesis.