Open AccessReactive oxygen species in periodontitis
Author(s) -
Parveen Dahiya,
Reet Kamal,
Rajan Gupta,
Rohit Bhardwaj,
Karun Chaudhary,
Swayamjot Kaur
Publication year - 2013
Publication title -
journal of indian society of periodontology (print)/journal of indian society of periodontology (online)
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.309
H-Index - 28
eISSN - 0975-1580
pISSN - 0972-124X
DOI - 10.4103/0972-124x.118306
Subject(s) - reactive oxygen species , periodontitis , medicine , microbiology and biotechnology , immunology , population , oxidative stress , respiratory burst , superoxide , interleukin , inflammation , cytokine , biology , biochemistry , enzyme , dentistry , environmental health , endocrinology
Recent epidemiological studies reveal that more than two-third of the world's population suffers from one of the chronic forms of periodontal disease. The primary etiological agent of this inflammatory disease is a polymicrobial complex, predominantly Gram negative anaerobic or facultative bacteria within the sub-gingival biofilm. These bacterial species initiate the production of various cytokines such as interleukin-8 and TNF-α, further causing an increase in number and activity of polymorphonucleocytes (PMN) along with these cytokines, PMNs also produce reactive oxygen species (ROS) superoxide via the respiratory burst mechanism as the part of the defence response to infection. ROS just like the interleukins have deleterious effects on tissue cells when produced in excess. To counter the harmful effects of ROS, human body has its own defence mechanisms to eliminate them as soon as they are formed. The aim of this review is to focus on the role of different free radicals, ROS, and antioxidants in the pathophysiology of periodontal tissue destruction.