38 Consistent with an earlier study, we observed an increase in the TBARS level in rats with EP,39 a finding that could be effectively suppressed with vitamin E treatment. SOD catalyses the dismutation of superoxide radicals to hydrogen peroxide and serves to protect cells against oxidative stress. SOD accumulation is caused by augmented ROS via the activation of redox-sensitive transactivating factors. In this study, besides the inhibition of lipid peroxidation, treatment with vitamin E caused a decrease in SOD activity, which

implies a reduced production Everolimus of ROS and consequently a reduced oxidative stress to periodontal tissues. In conclusion, our results suggest that vitamin E could improve the inflammatory process in the rat model of ligature-induced experimental periodontitis. However, vitamin E showed no protection against alveolar bone loss associated

with experimental periodontitis and, moreover, demonstrated an anxiogenic effect. Thus, the possibility check details of using this compound as adjunct therapy deserves further investigation. The authors would like to thank Renata Leitão, Mariana Vale from the Faculty of Medicine, and the Federal University of Ceará for the histopathological analysis. Funding: This study had the financial support of the Research Foundation of the State of Ceará (FUNCAP) and the Brazilian National Research Council (CNPq). Competing interests: The authors declare they have no conflict of interest. Ethical approval: This study was approved by Federal University of Ceará ethics committee (reference number 052/07). “
“Despite many crucial histological and structural differences between teeth and implants, their clinical similarities Farnesyltransferase lead researchers

to apply some general well accepted statements in periodontal field to implant dentistry. The inflammation restricted to soft tissues in early stages followed by bone loss and increased pocket depth could exemplify these similarities. In addition, peri-implant and periodontal diseases share some risk factors such as age, tobacco use and levels of oral hygiene.1, 2, 3 and 4 The fact that risk factors for periodontal disease could also increase the risk of development of peri-implant disease confirms that both disorders share some etiopathogenic aspects. Moimaz et al.5 reported smoking, a recognized risk factor for periodontitis, as the most important risk factor for the development of mucositis. For peri-implant disease similar findings were also observed by Karbach et al.6 in a sample of 100 patients with single implants. Interestingly, periodontitis history per se may also be considered a risk factor for peri-implant disease.4 Schou et al.,7 in a systematic review, showed a significantly increased incidence of peri-implantitis and peri-implant bone loss in subjects with periodontitis associated tooth loss. Similarly, Safii et al.