الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 150 |  |  |
| | | from | 150 | | |
Abstract
Alopecia areata (AA) is a non-scarring autoimmune skin disease in which antibodies attack one‘s own hair follicles, leading to hair loss. It commonly occurs on the scalp, but any hair bearing area of the skin can be affected. AA ranges from a single round/oval patch of hair loss (most likely on the scalp), or multiple patches, to complete scalp hair loss (alopecia totalis; AT), or complete scalp and body hair loss (alopecia universalis; AU).
There are several hypotheses proposed the etiology of AA, such as genetic susceptibility, atopic state, nonspecific autoimmune reactions, neurological factors, infectious agents and possible emotional stress. Current concepts of AA pathogenesis suggest that AA is a non-scarring, inflammatory, cell-mediated disease. A perifollicular and intrafollicular mononuclear cell infiltrate of primarily CD4+ and CD8+ cells are closely associated with dystrophic anagen stage hair follicle, which suggests that T cells and cytokines play an important role.
During inflammatory disorders, cells generate reactive oxygen species (ROS). When produced in excess, ROS brings about an imbalance in the antioxidant pathway. This imbalance of pro-oxidants and antioxidants in which prooxidants exceed in concentration is referred to as ―oxidative stress‖. Oxidative stress is very harmful to cells including cells of hair follicles.
Oxidative stress, which is an imbalance between ROS production and detoxification, may cause cellular damage by interacting with macromolecules such as protein, lipid, and DNA. Levels of ROS in the organism are maintained in a normal range through antioxidant agents such as SOD, GPX, GSH and vitamins C and E.