None declared. Source of funding: FAPESP (grants 2006/00435-3 and 2006/06842-0). The study was approved by the Ethics committee of Araraquara Dental School, and all subjects volunteered to participate and signed find more an informed consent form. This study was supported by FAPESP (grants 2006/00435-3 and 2006/06842-0). The authors wish to acknowledge Mr. Jörg
Erxleben for preparing the coatings used in this study and Prof. Peter Hammer for his assistance with the XPS analysis. “
“Periodontitis is a “complex disease” and does not have a single aetiology.1 However, it is commonly described as a chronic disorder characterised by the breakdown of tooth-supporting tissues and the impaired host inflammatory immune response due to an ecological imbalance between the PF-562271 chemical structure normal microbial biofilm on teeth and the host tissues.2 Aspects of the inflammatory and immune processes, both humoral and cellular, which develop in response to the microbial insult from dental plaque, could be important in inflammatory periodontal disease.3 An increased oxidative and nitrosative stress, which is generally
associated with clinical conditions, such as cardiovascular disease, respiratory infection, diabetes, metabolic syndrome, and periodontitis, can play a crucial role in the exacerbation of periodontitis.2 and 4 In oral tissues, reactive oxygen species (ROS) are Thymidylate synthase generated as a result of both endogenous and exogenous oxidising agents. Oxidative species, such as superoxide, hydrogen peroxide, and hydroxyl radicals are common by-products of normal aerobic metabolism. These ROS are also generated by the immune system in inflamed or damaged tissues, such as in periodontitis.5 Although ROS are
necessary for defence of the host, they also expose the host tissue to oxidative damage. Several studies implicate polymorphonuclear leukocytes (PMNs) as the primary mediators of a host response against pathogenic microbes during inflammatory periodontal diseases. Studies demonstrate that PMNs produce a range of antimicrobial factors, which include ROS, during phagocytosis of periodontopathic bacteria in inflammatory periodontal diseases6 that can cause damage to gingival tissue, the periodontal ligament, and alveolar bone through several mechanisms.7 These mechanisms include a disruption of the extracellular matrix,8 induction of lipid peroxidation and proinflammatory cytokines that cause DNA damage and oxidation of enzymes, such as antiproteases,9 and increased apoptosis in the deepest area of the sulcular pocket.10 ROS are also produced by osteoclasts, which are responsible for bone destruction, and they may play a role in the remodelling of alveolar bone in health and disease. Some studies demonstrated that ROS are capable of degrading alveolar bone proteoglycans in vitro.