There is an increasing body of evidence now available to implicate reactive oxygen species (ROS) in the pathogenesis of variety of inflammatory disorders to which periodontal disease is no exception. A thick literature is available that implicates a clearly defined and substantial role for free radicals or ROS in periodontal tissue destruction. Here we are trying give the highlights of current updates in the area.
ROS is a collective term, which includes oxygen-derived free radical, such as superoxide radical (O2-), hydroxyl radical (OH) and nitric oxide radical (NO) species, and non-radical derivatives of oxygen, such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). The presence of one or more unpaired electrons in the outer orbital of oxygen-derived free radicals makes such species, extremely reactive in nature. In addition to providing an important function in normal metabolic reactions, ROS when produced in concentrations greater than normally required result in host tissue damage instead.
Periodontal disease is a common chronic adult condition. Several periodontopathogenic bacteria have been implicated in the etiology of this disease, which causes destruction of the connective tissue and bone around the root area of the tooth. It has been observed that the invading bacteria trigger the release of cytokines such as interleukin-1 (IL-1) and TNF-a, leading to elevated numbers and activity of polymorphonucleocytes (PMN). As a result of stimulation by bacterial antigen, PMN produce the ROS superoxide as part of the host response to infection. Patients with periodontal disease display increased PMN number and activity. It has been suggested that this proliferation results in a high degree of ROS release, culminating in a heightened oxidative damage to gingival tissue, periodontal ligament and alveolar bone.
Regarding the mechanism of periodontal tissue destruction, detailed investigations into the degradation of the glycosaminoglycans and proteoglycans associated with mineralized and non-mineralized periodontal tissues have been reported. In vitro studies were also made to relate the in vivo release of ROS by PMN during initial bursts and the more cumulative periods of disease activity by exposing proteoglycans and glycosaminoglycans to a broad spectrum of ROS species having wide range of reactivity. The exposure of glycosaminoglycans commonly associated with periodontal tissues to ROS, derived from cell free sources in vitro, demonstrated that all glycosaminoglycans undergo chain depolymerisation and residue modification to varying degrees, particularly in the presence of highly reactive OH species. The non-sulphated glycosaminoglycan, hyluronan, was identified as being more susceptible to degradation by ROS than sulphated glycosaminoglycans. Similar conclusions have also been made following the exposure of proteoglycans from gingival tissue to ROS.
In considering studies relating to the biochemical analyses of proteoglycans metabolites in GCF as associated with advanced periodontitis, it is evident that the metabolites are likely to originate from alveolar bone and be released into the GCF following their partial degradation. Biochemical analysis of inflamed gingival tissue have also identified that the core proteins of gingival proteoglycans present in inflamed tissues undergo extensive degradation.
Recently, there has been a tremendous expansion in dental research concerned with mechanism of periodontal tissue destruction involving reactive oxygen species. It has shown that serum collected from rapidly progressive periodontitis patients has enhanced levels of superoxide in normal neutrophils when compared with normal control serum. In one other study, it has been demonstrated that Fusobacterium species, a perioidontopathogen can induce increased production of oxygen radicals, cytokines and elastase in leukocyte activated under in vitro conditions, which might be a possible pathogenic factor in periodontitis. Fusobacterium species has suggested stimulating oxygen radical dependent lipid peroxidation in neutrophils and a possible cause of the emergence of inflammation and periodontitis. In the recent past, the potential role of nitric oxide derived nitrating species has been investigated in a rat model of ligation-induced periodontitis. The data suggest that resident bacteria of the gingivomucosal tissue induce an increase in reactive nitrogen species, which is greatly enhanced by the plaque formation in periodontitis. In order to early diagnosis of the disease, crevicular IL-1 beta and TBARS levels were assessed after Phase-1 periodontal therapy in patients with chronic periodontitis and found that the levels of crevicular IL-beta and gingival tissue TBARS were closely associated with periodontal status and that this relationship could be utilized in treating and monitoring periodontal disease progression. Data are available on that intracellular production and extracellular release of oxygen radicals by PMNs leads the production of high level of superoxide, which may damage not only periodontopathic bacteria but also PMNs themselves, and may be correlated, with the destruction of periodontal tissue by PMNs and oxidative stress. An association of periodontal diseases with reduced salivary antioxidant status and increased oxidative damage within the oral cavity has also demonstrated in an independent study.
Whilst a myriad of possible mechanisms leading to the destruction of periodontal tissue exist, the influence of other damaging metabolic species such as ROS cannot be overlooked undoubtedly. This has led the researchers to look for the antioxidant therapy as a possible strategy for the treatment of periodontal disease. Treatment with drugs that block the production of free ROS or block its effects might be therapeutically valuable. Antioxidant properties of constituents such as vitamin E, co-enzyme Q and curcumin should be exploited in treating andor preventing such pathology. An improved understanding of the role antioxidants play in periodontitis, and the influence of nutrition on antioxidant status, may lead to a possible nutritional strategy for the treatment of periodontal disease.