Periodontal disease mechanisms - Reactive oxygen species: a potential rolein the pathogenesis of periodontal diseases

Citation
Rj. Waddington et al., Periodontal disease mechanisms - Reactive oxygen species: a potential rolein the pathogenesis of periodontal diseases, ORAL DIS, 6(3), 2000, pp. 138-151
Citations number
191
Categorie Soggetti
Dentistry/Oral Surgery & Medicine
Journal title
ORAL DISEASES
ISSN journal
1354523X → ACNP
Volume
6
Issue
3
Year of publication
2000
Pages
138 - 151
Database
ISI
SICI code
1354-523X(200005)6:3<138:PDM-RO>2.0.ZU;2-5
Abstract
The pathological events leading to the destruction of the periodontium duri ng inflammatory periodontal diseases are likely to represent complex intera ctions involving an imbalance in enzymic and non-enzymic degradative mechan isms. This paper aims to review the increasing body of evidence implicating reactive oxygen species (ROS), derived from many metabolic sources, in the pathogenesis of periodontal tissue destruction. ROS are generated predomin antly by polymorphonuclear leukocytes (PMN) during an inflammatory response and are regarded as being highly destructive in nature. The detection of R OS oxidation products, the elevation of iron and copper ions, which catalys e the production of the most reactive radical species, and the identificati on of an imbalance in the oxidant/antioxidant activity within periodontal p ockets, suggests a significant role for ROS in periodontal tissue destructi on. In vitro studies have shown that ROS are capable of degrading a number of extracellular matrix components including proteoglycans, resulting in th e modification of amino acid functional groups, leading to fragmentation of the core protein, whilst the constituent glycosaminoglycan chains undergo limited depolymerisation, The identification and characterisation of connec tive tissue metabolites in gingival crevicular fluid (GCF) resulting from t he degradation of periodontal tissues, notably alveolar bone, provides furt her evidence for a role for ROS in tissue destruction associated with infla mmatory periodontal diseases.