Reactive oxygen species and human inflammatory periodontal diseases

• Published in: Biochemistry (Moscow) Vol. 70; no. 6; pp. 619 - 628
• Main Authors: Canakci, C. F., Cicek, Y., Canakci, V.
• Format: Journal Article
• Language: English
• Published: United States Springer Nature B.V 01.06.2005
• Subjects: Animals; Apoptosis; Apoptosis - physiology; Cells; DNA Damage - physiology; Humans; Lipid Peroxidation - physiology; Mitochondria - metabolism; Neutrophils - metabolism; Oxidative Stress - physiology; Periodontal diseases; Periodontal Diseases - metabolism; Periodontal Diseases - pathology; Reactive Oxygen Species - metabolism; Signal Transduction
• ISSN: 0006-2979; 1608-3040; 0320-9725
• DOI: 10.1007/s10541-005-0161-9

Reactive oxygen species (ROS) have emerged as important signaling molecules in the regulation of various cellular processes. They can be generated by the mitochondrial electron transport chain in mitochondria and activation of polymorphonuclear leukocytes (PMN) during inflammatory conditions. Excessive generation of ROS may result in attack of and damage to most intracellular and extracellular components in a living organism. Moreover, ROS can directly induce and/or regulate apoptotic and necrotic cell death. Periodontal pathologies are inflammatory and degenerative diseases. Several forms of periodontal diseases are associated with activated PMN. Damage of tissues in inflammatory periodontal pathologies can be mediated by ROS resulting from the physiological activity of PMN during the phagocytosis of periodontopathic bacteria.