Periodontal disease affects oral cancer progression in a surrogate animal model for tobacco exposure.

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 biofilm­induced 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, 4­nitroquinoline 1­oxide (4­NQO) 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 10­positive 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.

Efficacy of Essential Oil Mouthwashes With and Without Alcohol on the Plaque Formation: A Randomized, Crossover, Double-Blinded, Clinical Trial.

BACKGROUND: Essential oil (EO) mouthwash has been considered as one of the effective chemical agents as an adjunct to mechanical plaque control, without adverse effects compared with chlorhexidine (pigmentation, changes of taste, and formation of supragingival calculus), which limits its continuous use. New EO alcohol-based has emerged with questions regarding contraindications for its daily use. OBJECTIVE: To compare the efficacy of EO mouthwashes with and without alcohol on the early supragingival and subgingival plaque formation using a plaque-free zone score system. METHODS: This study was a crossover, randomized, double-blind clinical trial. Eleven participants, totaling 396 sites of evaluation, remained 4 days with no mechanical oral hygiene control and only used EO mouthwash with (control) and without alcohol (test) during this period. The presence of the plaque-free zone was recorded every 24 hours. Friedman and Wilcoxon tests were used with a 5% significance level. RESULTS: The control group showed a more significant number of buccal surfaces free of plaque at 48, 72, and 96 hours compared with the test group. Both groups presented satisfactory efficacy up to 72 hours with a significant difference in favor of the control group. The presence of subgingival plaque on both the proximal and free surfaces was significantly higher in the test group. CONCLUSION: EO with alcohol presented better results in retarding the early supragingival and subgingival plaque formation compared with EO without alcohol.

Can propranolol act as a chemopreventive agent during oral carcinogenesis? An experimental animal study.

The multistep process of oral carcinogenesis provides a biological rationale for the use of chemoprevention in individuals at increased risk of developing oral cancer. We aimed to determine if low doses of propranolol can prevent the development of oral cancer using a tobacco-relevant and p53-associated animal model of cancer initiation. Twenty-six Wistar rats were randomly allocated into two groups, vehicle, and propranolol. All animals received 4-nitroquinoline N-oxide (4NQO) at 25 ppm diluted in the drinking water for 20 weeks. Animals from the propranolol group received propranolol (0.1 mg/kg) 5 days per week by gavage for 18 weeks. The clinical analysis was performed by measuring the area of the lesion and assessment of scores based on lesion appearance (papule; plaque; nodule or ulcerated). Histopathological analysis was performed to determine the presence of epithelial dysplasia or invasive squamous cell carcinoma (SCC). The average lesion area in 4NQO + vehicle and in 4NQO + propranolol groups were 0.20 and 0.28 mm2, respectively (P = 0.53). The percentage of cases clinically graded as papules, thick plaques, nodular areas, and ulcerated lesions was similar between groups (P = 0.94). Histopathological diagnosis also did not differ between groups (P = 0.65), with 54.5 and 70% of cases being diagnosed as SCC in 4NQO and in 4NQO + propranolol groups, respectively. In conclusion, daily doses propranolol at 0.1 mg/kg were not as effective as a chemopreventive therapy in an animal model of 4NQO-induced carcinogenesis.

Effects of Low Molecular Weight Heparin on Alveolar Bone Loss in Wistar Rats.

This study aimed to assess the effects of low molecular weight heparin (LMWH) on alveolar bone loss (ABL), blood count, and counting of megakaryocytes and adipocytes in male Wistar rats. Forty male 60-day Wistar rats were randomly divided into four groups: Control (C), Periodontal Disease (PD), Heparin (Hp) and Heparin + Periodontal Disease (Hp+PD). LMWH was applied for 60 days at doses of 1 ml/kg/day. Blood samples were collected at baseline, 30 and 60. On day-49, PD and Hp+PD groups were subjected to ligature-induced periodontitis around second upper right molar. The left side was assessed as spontaneous alveolar bone loss. Mean ABL in the side with ligature showed significantly different between C (0.35±0.07 mm) and Hp+DP (0.49±0.09 mm) groups (p<0.001), between PD (0.55±0.11 mm) and Hp (0.32±0.06 mm) groups (p<0.001) and between Hp and Hp+DP groups (p<0.001). No significant differences were found among groups for ABL in the side without ligature. Animal weight, food intake, and water consumption showed no statistically significant difference among groups. Megakaryocytes and adipocytes were counted using optical microscopy and no statistically significant differences were found. Within-groups, there were an increase and a decrease, respectively, in the counting of lymphocytes (p=0.005 for C and p=0.009 for Hp+PD groups only) and leukocytes (p=0.003 for C, p=0.001 for PD, p=0.002 for Hp, and p<0.001 for Hp+PD groups). There was no decrease in the number of platelets in the three collection periods. LMWH was not able to affect ABL, but it may change the blood counting, especially increasing lymphocytes.

Effects of low molecular weight heparin on alveolar bone loss in wistar rats

Abstract This study aimed to assess the effects of low molecular weight heparin (LMWH) on alveolar bone loss (ABL), blood count, and counting of megakaryocytes and adipocytes in male Wistar rats. Forty male 60-day Wistar rats were randomly divided into four groups: Control (C), Periodontal Disease (PD), Heparin (Hp) and Heparin + Periodontal Disease (Hp+PD). LMWH was applied for 60 days at doses of 1 ml/kg/day. Blood samples were collected at baseline, 30 and 60. On day-49, PD and Hp+PD groups were subjected to ligature-induced periodontitis around second upper right molar. The left side was assessed as spontaneous alveolar bone loss. Mean ABL in the side with ligature showed significantly different between C (0.35±0.07 mm) and Hp+DP (0.49±0.09 mm) groups (p<0.001), between PD (0.55±0.11 mm) and Hp (0.32±0.06 mm) groups (p<0.001) and between Hp and Hp+DP groups (p<0.001). No significant differences were found among groups for ABL in the side without ligature. Animal weight, food intake, and water consumption showed no statistically significant difference among groups. Megakaryocytes and adipocytes were counted using optical microscopy and no statistically significant differences were found. Within-groups, there were an increase and a decrease, respectively, in the counting of lymphocytes (p=0.005 for C and p=0.009 for Hp+PD groups only) and leukocytes (p=0.003 for C, p=0.001 for PD, p=0.002 for Hp, and p<0.001 for Hp+PD groups). There was no decrease in the number of platelets in the three collection periods. LMWH was not able to affect ABL, but it may change the blood counting, especially increasing lymphocytes.

Resumo O presente estudo objetivou verificar o efeito da heparina de baixo peso molecular (HBPM) sob a perda óssea alveolar (POA), contagem de células sanguíneas, megacariócitos e adipócitos em ratos Wistar machos. Quarenta ratos Wistar de 60 dias foram randomicamente divididos em quatro grupo: Controle (C), Doença Periodontal (DP), Heparina (Hp) e Heparina + Doença Periodontal (Hp+DP). HBPM foi aplicada durante 60 dias em doses de 1 mL/kg/dia. Coletas sanguíneas foram realizadas nos dias 0, 30 e 60. No dia 49, os grupos DP e Hp+DP receberam indução de doença periodontal por ligadura ao redor do segundo molar superior direito. No lado esquerdo, verificou-se perda óssea alveolar espontânea. A média de POA no lado com ligadura mostrou-se estatisticamente diferente entre os grupos C (0,35±0,07 mm) e Hp+PD (0,49±0,09 mm) (p<0,001), entre os grupos DP (0,55±0,11 mm) e Hp (0,32±0,06 mm) (p<0,001) e entre os grupos Hp e Hp+DP (p<0,001). Nenhuma diferente significativa foi observada entre os grupos no lado sem ligadura. Peso dos animais, consumo de ração e ingestão de água não mostraram diferenças significativas entre os grupos. Megacariócitos e adipócitos foram contados por microscopia óptica e nenhuma diferença significativa foi encontrada. Dentro dos grupos, houve um aumento e uma diminuição, respectivamente, na contagem de linfócitos (p=0,005 no grupo C e p=0,009 no grupo Hp+DP somente) e leucócitos (p=0,003 no grupo C, p=0.001 no grupo DP e p=0,002 no grupo Hp e Hp+DP). Não houve diminuição no número de plaquetas nos três períodos de coleta. HBPM não foi capaz de modificar a POA, porém modificou a contagem de células sanguíneas, especialmente aumentando o número de linfócitos.

Effects of alcohol and/or tobacco exposure on spontaneous alveolar bone loss in rat.

The aim of the present study was to evaluate the effect of alcohol and/or tobacco exposure on spontaneous alveolar bone loss in Wistar rats. Twenty-four, male, 60 day-old, Wistar rats were assigned to 4 groups: Group 1 received 10 mL/kg of glucose solution (5%). Group 2 received 2 g/kg alcohol (20%). Group 3 was exposed to tobacco smoke (6 cigarettes/60 min). Group 4 received both interventions of groups 2 and 3. Alcohol was given by gastric gavage and cigarette exposure was performed using a forced ventilation chamber. After 30 days, animals were sacrificed and the upper maxillae removed and defleshed. Morphometric analysis of alveolar bone loss (ABL) around the second molar was performed in standardized digital photographs. Statistical analysis was conducted using paired t-test, one-way ANOVA and occurrence of spontaneous periodontal disease (ABL ≥ 0.39 mm) was analyzed by Fisher's exact test. Significant differences in body weight were observed between all groups. Group 2 presented higher body weight as compared to the 3 other groups at 4 weeks (p≤0.05). Mean ABL values were 0.31 mm (±0.08), 0.29 mm (±0.07), 0.33 mm (±0.10), and 0.33 mm (±0.08) for groups 1, 2, 3, and 4, respectively. No significant differences were found among groups. In the analysis of occurrence of periodontal breakdown, alcohol exposure decreased the occurrence of ABL and cigarette exposure increased ABL. The combination of alcohol and cigarette exposure did not differ from the control group. Alcohol consumption decreased the occurrence of periodontal breakdown, while tobacco increased this rate.

Effects of Alcohol and/or Tobacco Exposure on Spontaneous Alveolar Bone Loss in Rat

The aim of the present study was to evaluate the effect of alcohol and/or tobacco exposure on spontaneous alveolar bone loss in Wistar rats. Twenty-four, male, 60 day-old, Wistar rats were assigned to 4 groups: Group 1 received 10 mL/kg of glucose solution (5%). Group 2 received 2 g/kg alcohol (20%). Group 3 was exposed to tobacco smoke (6 cigarettes/60 min). Group 4 received both interventions of groups 2 and 3. Alcohol was given by gastric gavage and cigarette exposure was performed using a forced ventilation chamber. After 30 days, animals were sacrificed and the upper maxillae removed and defleshed. Morphometric analysis of alveolar bone loss (ABL) around the second molar was performed in standardized digital photographs. Statistical analysis was conducted using paired t-test, one-way ANOVA and occurrence of spontaneous periodontal disease (ABL ≥ 0.39 mm) was analyzed by Fisher's exact test. Significant differences in body weight were observed between all groups. Group 2 presented higher body weight as compared to the 3 other groups at 4 weeks (p≤0.05). Mean ABL values were 0.31 mm (±0.08), 0.29 mm (±0.07), 0.33 mm (±0.10), and 0.33 mm (±0.08) for groups 1, 2, 3, and 4, respectively. No significant differences were found among groups. In the analysis of occurrence of periodontal breakdown, alcohol exposure decreased the occurrence of ABL and cigarette exposure increased ABL. The combination of alcohol and cigarette exposure did not differ from the control group. Alcohol consumption decreased the occurrence of periodontal breakdown, while tobacco increased this rate.

O objetivo do presente estudo foi avaliar o efeito da exposição do álcool e/ou tabaco sobre a perda óssea alveolar (POA) espontânea em ratos Wistar. Vinte e quatro ratos, machos, com 60 dias de vida foram divididos em 4 grupos: Grupo 1 recebeu 10 mL/kg de solução de glicose (5%). Grupo 2 recebeu 2 g/kg de álcool (20%). Grupo 3 foi exposto a fumaça do tabaco (6 cigarros/60 min). Grupo 4 recebeu a mesma intervenção dos grupos 2 e 3. A solução de álcool foi dada por meio de gavagem e a exposição ao tabaco foi realizada por meio de câmara de ventilação forçada. Após 30 dias de experimento, os animais foram sacrificados e as maxilas removidas. Análise morfométrica da POA ao redor do segundo molar superior foi realizada de modo padronizada. A análise estatística dos dados foi realizada por meio de teste t pareado e ANOVA. Ocorrência de doença periodontal espontânea (POA ≥ 0,39 mm) foi realizada pelo teste exato de Fisher. Diferenças significativas no peso corporal médio foram observadas em todos os grupos. Grupo 2 apresentou maior peso corporal médio quando comparado aos outros 3 grupos ao fim do experimento (p≤0,05). A média de POA foi 0,31 mm (±0,08); 0,29 mm (±0,07); 0,33 mm (±0,10) e 0,33 mm (±0,08) para os grupos 1, 2, 3 e 4, respectivamente. Não houve diferenças significativas entre os grupos. Na análise de ocorrência de destruição periodontal, a exposição de álcool diminuiu sua ocorrência, enquanto que exposição ao tabaco aumentou a POA espontânea. A combinação de álcool e tabaco não diferiu do grupo controle.