The role of reactive oxygen intermediates in the pathogenesis of chronic apical periodontitis

Abstract

The level of malondialdehyde, a stable end product of lipid peroxidation induced by reactive oxygen intermediates and the activity of two potent antioxidant enzymes, superoxide dismutase and glutathione peroxidase, was investigated in tissue homogenates of 22 surgical periapical granuloma specimens. Malondialdehyde levels were significantly higher and glutathione peroxidase activity was significantly lower in periapical granuloma samples than in healthy gingival tissue homogenates, which were used as controls. The activity of superoxide dismutase was similar in periapical granuloma and in control samples. Our results indicate an altered balance between the production and the elimination of toxic oxygen metabolites in chronic apical periodontitis. We hypothesize that reactive oxygen intermediates, which are being produced by activated phagocytic cells abundantly present in periapical granulomas, can contribute to periapical tissue injury and bone loss in this disease.

Expression of Superoxide Dismutase Isoforms in Inflamed Gingiva

“…Similar SOD activities were found in periapical granuloma and healthy gingiva 8,17) . A remarkably higher SOD activity was shown in irreversible pulpitis, suggesting that SOD activity increases with the progression of inflammation 23) .…”

“…No alterations in antioxidant levels within GCF samples in response to elevated O2-production have been demonstrated in adult periodontitis 4,7) and chronic apical periodontitis 4,8) . Therefore, such imbalances in oxidant/antioxidant con-centrations, coupled with sources of iron and copper which exacerbate the production of the highly reactive․OH species, could potentiate severe periodontal tissue damage.…”

Oxidative Injury and Inflammatory Periodontal Diseases : the Challenge of Anti-Oxidants to Free Radicals and Reactive Oxygen Species

“…The interrelationships among poor sanitation (including poor oral hygiene), economic poverty, malnutrition, impaired immune function, infections, and many diseases with an inflammatory component, with particular attention to PE, have been recently discussed (Enwonwu, 1994(Enwonwu, , 1995 Silenko et al, 1991Silenko et al, , 1992Silenko et al, , 1994aVoskresenskii, 1991;Bobyrev, 1994a,b). Such an association may similarly be evident in the pathogenesis of human chronic apical PE (Marton et al, 1993). Only one study (Levitskii et al, 1987) indicated an unexplained, and never confirmed, concomitant increment in peroxidation parameters and some anti-oxidant mechanisms (i.e., GSH-red (Moore et al, 1994;Chapple, 1997).…”

Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapy

“…17 Similar SOD activities have been found in periapical granuloma and healthy gingiva. 23 Other studies 19 have found that gingival SOD activity is significantly higher in chronic periodontitis (CP), which suggested that SOD activity increases with the progression of inflammation.…”