Abstract
Recently, it has been discovered that one of the primary causes of a variety of inflammatory illnesses, including periodontitis, is an excess of Reactive Oxygen Species (ROS). It is recognised that the host’s response to pathogens plays an equal or even bigger part in determining how connective tissue breaks down. The process of Polymorphonuclear (PMN) phagocytosis greatly increases ROS formation through the metabolic pathway known as the “respiratory burst.” Because the antioxidant defense system is unable to neutralise these high levels or activities of ROS, Oxidative Stress (OS) and tissue damage ensue. ROS can directly affect tissue through Lipid Peroxidation (LPO), Deoxyribonucleic Acid (DNA) damage, protein breakdown, and the oxidation of essential enzymes. Numerous aldehydes can be produced as byproducts of LPO, including Malondialdehyde (MDA), propanal, hexanal, and 4-Hydroxynonenal (4-HNE). They can be detected in bodily fluids and suggest a pro-oxidant state. MDA is a by-product created by the enzymatic or non enzymatic breakdown of Arachidonic Acid (AA) and larger Polyunsaturated Fatty Acids (PUFAs). MDA is the most studied OS tissue damage indicator. After it is formed, MDA can either be broken down by enzymes or combine with DNA or proteins in cells and tissues to form adducts that can cause harm to biological molecules.
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