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Background: Damage caused by periodontitis not only affects periodontal tissues, but also increases the severity of various illnesses such as rheumatoid arthritis, diabetes, and liver diseases. The aim of this study is to investigate the association between induced periodontitis and damage caused through its systemic effects on the liver. Methods: Twenty rats were divided into two groups: control and periodontitis. The following parameters were evaluated: gingival bleeding index (GBI), probing depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histopathologic examination of gingival and liver tissues; immunohistochemistry to cells positive for neural/glial antigen 2 (NG2) expressed in hepatic pericytes, glutathione (GSH), and malondialdehyde (MDA) concentrations in liver; and serum levels of alanine aminotransferase and aspartate aminotransferase. Results: GBI, PD, MPO, ABL, and histopathologic examinations demonstrated the development of periodontitis. There was a significant increase in microvesicular steatosis accompanied by a marked reduction in NG2+ pericytes in the periodontitis group compared with the control group. The periodontitis group had significantly lower GSH and higher MDA concentration in the liver compared with the control group. Conclusions: The present study results link the systemic effects of induced periodontitis with changes in hepatic tissues such as microvesicular steatosis, likely caused by an increase in oxidative stress and lipid peroxidation. The findings from the present study implicate an association between a decrease of pericytes and liver disease caused by ligature-induced periodontitis in rats

The aim of this study was to evaluate the radioprotector effect of sodium selenite on the ultrastructure of submandibular glands in rats. Fifty-seven male albino Wistar rats were randomized to 4 groups: control, irradiated, sodium selenite and irradiated/sodium selenite. The animals in the sodium selenite and irradiated/sodium selenite groups received intraperitoneal injections of sodium selenite (0.5 mg/kg body weight) 24 h before irradiation. The animals belonging to the irradiated and irradiated/sodium selenite groups were submitted to 15 Gy of gamma radiation in the head and neck region. The submandibular glands were removed at 4, 8, 12, 24, 48 and 72 h after irradiation. The ionizing radiation induced damage to the secretory cells, especially the serous cells, right from the first period. Vacuolization, lysis of cytoplasmic inclusions and nuclear alterations occurred. The sodium selenite group also presented cellular alterations in the study periods, but with less damage compared to that caused by radiation. There was greater similarity between the irradiated/sodium selenite group and the control group than with the other groups treated in all study periods. Despite the alterations observed in the sodium selenite group, sodium selenite presented a radioprotective action on the secretory cells of submandibular glands.

Neste estudo avaliou-se histometricamente a ação local da calcitonina de salmão em defeitos ósseos provocados cirurgicamente em fêmur de ratos. As avaliações foram feitas aos 7, 14 e 21 dias após o ato cirúrgico. Não se observou diferenças estatísticas aos 7 dias, entretanto no período de 14 dias houve diferenças com maior formação óssea no grupo tratado. No período de 21 dias, em ambos os grupos, não foi possível diferenciar o tecido ósseo neoformado e o adjacente. Os resultados demonstraram, que o efeito da calcitonina foi observado somente no início do processo de reparo dos defeitos ósseos criados cirurgicamente.The purpose of the present study was to histometrically evaluate the effects of salmon calcitonin on the bone healing of surgically created bone defects in rats. The animals were sacrificed 7, 14 and 21 days after the surgical procedure. After the 7- and 21-day periods, differences between the experimental and control groups were not observed (P > 0.01). After the 14-day period, a larger amount of new bone was observed in the experimental group (P < 0.01). Thus, within the limits of the present study, it can be concluded that although salmon calcitonin positively participated in the initial phase of bone healing, it did not result in a larger amount of new bone at the end of the experimental period.