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For decades, the link between poor oral hygiene and the increased prevalence of oral cancer has been suggested. Most recently, emerging evidence has suggested that chronic inflammatory diseases from the oral cavity (e.g., periodontal disease), to some extent, play a role in the development of oral squamous cell carcinoma (OSCC). The present study aimed to explore the direct impact of biofilm‑induced periodontitis in the carcinogenesis process using a tobacco surrogate animal model for oral cancer. A total of 42 Wistar rats were distributed into four experimental groups: Control group, periodontitis (Perio) group, 4‑nitroquinoline 1‑oxide (4‑NQO) group and 4NQO/Perio group. Periodontitis was stimulated by placing a ligature subgingivally, while oral carcinogenesis was induced by systemic administration of 4NQO in the drinking water for 20 weeks. It was observed that the Perio, 4NQO and 4NQO/Perio groups presented with significantly higher alveolar bone loss compared with that in the control group. Furthermore, all groups receiving 4NQO developed lesions on the dorsal surface of the tongue; however, the 4NQO/Perio group presented larger lesions compared with the 4NQO group. There was also a modest overall increase in the number of epithelial dysplasia and OSCC lesions in the 4NQO/Perio group. Notably, abnormal focal activation of cellular differentiation (cytokeratin 10‑positive cells) that extended near the basal cell layer of the mucosa was observed in rats receiving 4NQO alone, but was absent in rats receiving 4NQO and presenting with periodontal disease. Altogether, the presence of periodontitis combined with 4NQO administration augmented tumor size in the current rat model and tampered with the protective mechanisms of the cellular differentiation of epithelial cells.

Background: Certain drugs such as glucocorticoids may interfere with the modulation of periodontal disease. In contrast, corticosteroid treatment has been associated with a protective effect with regard to periodontal breakdown, depending on the dose, pathway, and exposure time. Considering the potential relevance of nucleotidases in coordinating the cardiovascular system and inflammation processes, the aim of this study was to investigate the nucleotidase activities in the blood serum of rats with periodontal disease exposed chronically to inhaled corticosteroids., Methods: Adult male Wistar rats (n=26) were randomly assigned to one of the following four study groups: a control group that received no intervention; a periodontal disease group that received saline solution; a 'low dose' group that received 30 μg of budesonide daily; and a corresponding 'high dose' group that received 100 μg daily over a 15-day time course. The hydrolysis of ATP, ADP, and AMP were analysed in blood serum., Results: Periodontal disease diminished the hydrolysis of ATP and enhanced the hydrolysis of ADP. Repeated administration of either a low or high dose in the periodontal disease model of inhaled corticosteroids reversed the observed increase in ADP hydrolysis, and only the repeated administration of low doses of inhaled corticosteroids was able to reverse the decrease in the hydrolysis of ATP induced by periodontal disease., Conclusion: The variables investigated in this study may be involved in the pathophysiology of periodontal disease and may participate in the mechanisms that mediate the development of some of the side effects of inhaled corticosteroids., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

There are many studies that evaluate possible risk factors for periodontal diseases in animals. Most of them have focused only on the biological aspects of disease occurrence; therefore, it has been difficult to compare studies of the different methodological approaches. The aim of the present study was to compare different methods - linear and area - of the evaluation of morphometrical alveolar bone loss. Sixty hemimaxillae, defleshed and stained with 1% methylene blue to delineate the cementoenamel junction and alveolar bone crest, were obtained from a previous study that induced periodontal disease by means of ligatures in two groups of fifteen Wistar rats during 9 weeks. Ligatures were placed around the right upper second molars, and the contra-lateral teeth remained as intra-group controls. Digital photographs were taken from the specimens and submitted to a single, calibrated, blind examiner who performed the morphometrical evaluation of alveolar bone loss using both linear and area methods. Mean values of linear and area measurements were obtained from each side - buccal and palatal - of the specimens. The degree of association between the two methods was determined by Pearson's Correlation Coefficient. An almost perfect association (0.98) was determined between the linear and area evaluations. A mathematical formula was subsequently created to estimate the total area of alveolar bone loss, from linear mean measurements. Both methods were suitable for detecting bone level alterations. The results of the present study allow for the transformation of data and better compilation of results from different studies.

The rat model is widely used in periodontal research and the quality of histological sections is essential. The purpose of this study was to evaluate the histological characteristics of periodontal tissues in Wistar rat maxillae, with different times of fixation and decalcified by nitric acid or formic acid (Anna Morse Solution). Fifteen rats were used. Fixation was performed for 24, 48 and 72 hours. The maxillae were hemi-sectioned and each part was decalcified either in nitric acid for 7 days or in Anna Morse solution for 35 days. Two trained and blinded examiners performed the evaluation. Fourty eight hours of fixation and decalcification with Anna Morse solution showed more clear characteristics of the epithelium-connective tissue interface and of the periodontal structures. Mean measurements between the cementum-enamel junction and the bone crest varied in the different experimental times from 176.5 (+/- 60.45) to 210.94 (+/- 39.33) pixels on the buccal aspect, and from 199.69 (+/- 38.33) to 298.55 (+/-70.81) pixels on the palatal aspect, with no statistically significant differences (ANOVA, p > 0.05). In the same fixation period, decalcification with nitric acid or Anna Morse solution did not display any statistically significant differences. It may be concluded that for a qualitative histological analysis, fixation should preferably be for 48 hours and the demineralization should be made by Anna Morse solution. For a histomorphometric analysis, the decalcification solution does not interfere in the results.

The aim of this study was to evaluate, in rats, the role of the systemic use of dexamethasone in the pathogenesis of induced alveolar bone loss. In 26 female Wistar rats, ligatures were placed around the second upper molars, and the contralateral ones served as intra-group controls. Two groups were formed. The test group received 0.5 mg/kg of dexamethasone subcutaneously every third day during thirty days. The control group received the same amount of saline solution. After thirty days, the animals were sacrificed and their maxillae were removed. Sodium hypochlorite was used to prepare the specimens, and the cementum-enamel junction was stained with 1% methylene blue. Morphometric analysis of the alveolar bone loss was performed with standardized digital photographs, and the distance between the cementum-enamel junction and the alveolar bone crest was measured with the software ImageTool 3.0. Intra-examiner calibration revealed a Pearson correlation coefficient of 0.99. Statistical analysis was performed by paired or independent samplet tests, as appropriate (alpha = 0.05). Dexamethasone increased the mean alveolar bone loss in ligature-induced periodontitis in relation to the control group (0.77 and 0.61 buccally, and 0.65 and 0.56 palatally, respectively). No significant differences were observed intergroups in the teeth without ligatures. In the animal model used here, the use of dexamethasone increased the progression of ligature-induced alveolar bone loss.