Lipid peroxidation caused by oxygen radicals from Fusobacterium-stimulated neutrophils as a possible model for the emergence of periodontitis

• Published in: Oral diseases 2001, Vol.7 (1), p.41-46
• Main Authors: SHEIKHI, M, BOUHAFS, R. K. L, HAMMARSTRÖM, K-J, JARSTRAND, C
• Format: Article
• Language: English
• Subjects: Adult; Analysis of Variance; Antioxidants - pharmacology; Biological and medical sciences; Dentistry; Ent. Stomatology; Facial bones, jaws, teeth, parodontium: diseases, semeiology; Fat Emulsions, Intravenous - metabolism; Fusobacterium nucleatum - pathogenicity; Humans; Investigative techniques, diagnostic techniques (general aspects); Lipid Peroxidation - drug effects; Luminescent Measurements; Medical sciences; Neutrophil Activation; Neutrophils - drug effects; Neutrophils - metabolism; Non tumoral diseases; Otorhinolaryngology. Stomatology; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Periodontitis - immunology; Periodontitis - metabolism; Periodontitis - microbiology; Reactive Oxygen Species - metabolism; Vitamin E - pharmacology
• ISSN: 1354-523X; 1601-0825
• DOI: 10.1034/j.1601-0825.2001.0070109.x

The possible contribution of bacteria and polymorphonuclear neutrophils (PMN) to the disease process of periodontitis was evaluated. Fusobacterium nucleatum has been associated with chronic adult periodontitis. Intracellular production and extracellular release of reactive oxygen species (ROS) by PMN stimulated by fusobacteria were evaluated. To estimate the potential extracellular damage that might be caused by the ROS, the lipid peroxidation (LPO) of an exogenous phospholipid, Intralipid, was assayed. The ROS production of PMN was studied by the nitroblue tetrazolium and chemiluminescence tests. The levels of malonaldehyde (MDA) and 4-hydroxyalkenals were used to indicate LPO. Fusobacterium nucleatum strains stimulated neutrophils to produce a large amount of ROS, independently of plasma complement factors. The two strains tested induced considerable intracellular, but no extracellular chemiluminescence responses during the first hour, indicating that ROS were released into phagosomes. However an incubation period of 4 h, in the presence of the extracellular lipid resulted in a high degree of LPO, presumably caused by ROS release from the Fusobacterium-stimulated PMN. ROS production and lipid peroxidation could be counteracted by vitamin E. In periodontitis local bacteria might stimulate PMN to release ROS, which cause inflammation and destruction.