Salivary antioxidants and periodontal disease status

Abstract

Periodontal disease is a common chronic adult condition. The bacteriumPorphyromonas gingivalishas been implicated in the aetiology of this disease, which causes destruction of the connective tissue and bone around the root area of the tooth. It has been observed that invadingP. gingivalisbacteria trigger the release of cytokines such as interleukin 8 and tumour necrosis factor α, leading to elevated numbers and activity of polymorphonucleocytes (PMN). As a result of stimulation by bacterial antigens, PMN produce the reactive oxygen species (ROS) superoxide via the respiratory burst 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 heightened oxidative damage to gingival tissue, periodontal ligament and alveolar bone. Antioxidant constituents in plasma have been well-documented, being chiefly ascorbate, albumin and urate, and these are known to display sensitivity to dietary antioxidant intakes. The concentration of antioxidants in saliva does not appear to mirror those of plasma. The extent of dietary influence upon salivary antioxidant status is unclear. Urate is the predominant salivary antioxidant, with albumin and ascorbate providing minor contributions. Previous research has found reduced salivary antioxidant activity in patients suffering from periodontal disease. 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.

HtrA in Porphyromonas gingivalis can regulate growth and gingipain activity under stressful environmental conditions

“…In addition to having elevated temperatures, the periodontal pocket is an oxidative environment due to the presence of reactive oxygen species (Chapple, 1997;Katsuragi et al, 2003;Sculley & Langley-Evans, 2002). Consistent with reports of other organisms (Ibrahim et al, 2004;Mutunga et al, 2004;Wonderling et al, 2004), our data also suggest that the htrA-defective mutant is more susceptible to hydrogen peroxide than the wild-type.…”

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

“…ROS have recently been reviewed in the pathogenesis of periodontitis (Canakci et al 2005). It has been suggested that as a result of stimulation by bacterial antigens, PMNs produce and release a large quantity of ROS, culminating in heightened oxidative damage to gingival tissue, periodontal ligament, and alveolar bone (Sculley and Langley-Evans 2002). ROS are active in the depolymerization of extracellular matrix components, lipid peroxidation, oxidation of enzymes such as anti-proteases, induction of pro-inflammatory cytokines, and DNA damage (Canakci et al 2005;Ozmeric 2005).…”

Level of salivary uric acid in gingivitis and periodontitis patients

“…2 More severe destructive periodontitis is associated with gum recession, loss of gingival tissue and deterioration of the underlying alveolar bone. 1 Periodontitis is an oral inflammatory disorder that causes tissue damage and loss as a result of the complex interaction between pathogenic bacteria and the host's immune response. 3 Periodontal disease is initiated by bacterial pathogens, such as Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and Bacteriodes forsythus, of which P. gingivalis is the most dominant.…”

“…3 Periodontal disease is initiated by bacterial pathogens, such as Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and Bacteriodes forsythus, of which P. gingivalis is the most dominant. 1 Phagocytosis is a cellular process for destruction of antigen particles and bacteria. 4 Its system responses are divided into two pathways, oxidative and non-oxidative.…”